[leish-l] Fwd: Articles found by RefScout 2005/12/07 - 2005/49

[jeffreyj at usp.br]

    Date: Wed, 7 Dec 2005 00:40:35
    From: info at refscout.com


New!

Have a look at our new tool, the RefScout‘s PDF-Manager (PDFM)! The RefScout‘s
PDFM will revolutionize your life with PDF files!

Simply let your PDF files be organized by the RefScout‘s PDFM in a table and get
direct link to your local copy. In addition, the RefScout‘s PDFM will alert you
each time the NLM PubMed updates information concerning your specific
reference!
Get your free 2 months trial version now at RefScout’s PDF-Manager.

This is RefScout-Newsletter 49/2005.






REQUEST: [ leishmaniasis ]

(13 articles match this request. 2 articles matching other requests removed)



PMID: 16328954
 

TITLE: Calcium-dependent proteolytic activity of a cysteine protease caldonopain
is detected during Leishmania infection.

AUTHORS: Runu Dey, Jharna Bhattacharya, Salil C Datta

AFFILIATION: Department of Biological Chemistry, Infectious Diseases Group,
Indian Institute of Chemical Biology, Kolkata, India.

REFERENCE: Mol Cell Biochem 2006 Jan 281(1-2):27-33

A calcium-activated protease caldonopain in the cytosolic fraction of 
Leishmania donovani has been found to digest different endogenous 
proteins when subjected to SDS-PAGE. Gelatin-embedded gel 
electrophoresis confirms presence of calcium-dependent protease activity
. Ca(2+) affects proteolytic activity after 10 h. When host-parasite 
interaction was conducted in vitro, caldonopain was found to be active 
after 10 h of incubation with calcium. A 67-kDa protein is specifically 
digested during this time and two new proteins of 45 and 36 kDa appeared
 in SDS-PAGE electrophoregram. This belated action of calcium towards 
protease activity may be pre-requisite to facilitate invasion of host 
tissues and thereby mediate protein metabolism during survival of this 
pathogen both independently and intracellularly. It is likely that 
calcium metabolism in promastigotes and amastigotes does not propagate 
in the same manner. Involvement of calcium to initiate caldonopain 
activity may be critically associated with signal transduction pathways 
which may be responsible for the pathobiological action of this parasite
. We propose that caldonopain could be a potential target to develop new
 chemotherapeutic approach against leishmaniasis.








PMID: 16323101
 

TITLE: Parasitic central nervous system infections in immunocompromised hosts:
malaria, microsporidiosis, leishmaniasis, and african trypanosomiasis.

AUTHORS: Melanie Walker, James G Kublin, Joseph R Zunt

AFFILIATION: Department of Neurology, Infectious Diseases Division, University
of Washington School of Medicine, Seattle, WA, USA. jzunt at u.washington.edu.

REFERENCE: Clin Infect Dis 2006 Jan 42(1):115-25

Immunosuppression associated with HIV infection or following 
transplantation increases susceptibility to central nervous system (CNS
) infections. Because of increasing international travel, parasites that
 were previously limited to tropical regions pose an increasing 
infectious threat to populations at risk for acquiring opportunistic 
infection, especially people with HIV infection or individuals who have 
received a solid organ or bone marrow transplant. Although long-term 
immunosuppression caused by medications such as prednisone likely also 
increases the risk for acquiring infection and for developing CNS 
manifestations, little published information is available to support 
this hypothesis. In an earlier article published in Clinical Infectious 
Diseases, we described the neurologic manifestations of some of the more
 common parasitic CNS infections. This review will discuss the 
presentation, diagnosis, and treatment of the following additional 
parasitic CNS infections: malaria, microsporidiosis, leishmaniasis, and 
African trypanosomiasis.




PMID: 16299275
 

TITLE: Decreased in situ expression of interleukin-10 receptor is correlated
with the exacerbated inflammatory and cytotoxic responses observed in mucosal
leishmaniasis.

AUTHORS: Daniela R Faria, Kenneth J Gollob, José Barbosa, Albert Schriefer,
Paulo R L Machado, Hélio Lessa, Lucas P Carvalho, Marco Aurélio Romano-Silva,
Amélia R de Jesus, Edgar M Carvalho, Walderez O Dutra

AFFILIATION: Department of Morphology, Federal University of Minas Gerais, Belo
Horizonte, Brazil.

REFERENCE: Infect Immun 2005 Dec 73(12):7853-9

Human infection with Leishmania braziliensis can lead to cutaneous 
leishmaniasis (CL) or mucosal leishmaniasis (ML). We hypothesize that 
the intense tissue destruction observed in ML is a consequence of an 
uncontrolled exacerbated inflammatory immune response, with cytotoxic 
activity. For the first time, this work identifies the cellular sources 
of inflammatory and antiinflammatory cytokines, the expression of 
effector molecules, and the expression of interleukin-10 (IL-10) 
receptor in ML and CL lesions by using confocal microscopy. ML lesions 
displayed a higher number of gamma interferon (IFN-gamma)-producing 
cells than did CL lesions. In both ML and CL, CD4+ cells represented the
 majority of IFN-gamma-producing cells, followed by CD8+ cells and CD4- 
CD8- cells. The numbers of tumor necrosis factor alpha-positive cells, 
as well as those of IL-10-producing cells, were similar in ML and CL 
lesions. The effector molecule granzyme A showed greater expression in 
ML than in CL lesions, while inducible nitric oxide synthase did not. 
Finally, the expression of IL-10 receptor was lower in ML than in CL 
lesions. Thus, our data identified distinct cytokine and cell population
 profiles for CL versus ML patients and provide a possible mechanism for
 the development of ML disease through the demonstration that low 
expression of IL-10 receptor is present in conjunction with a cytotoxic 
and inflammatory profile in ML.




PMID: 16299292
 

TITLE: Chronic Leishmania donovani infection promotes bystander CD8+-T-cell
expansion and heterologous immunity.

AUTHORS: Rosalind Polley, Stephanie L Sanos, Sara Prickett, Ashraful Haque, Paul
M Kaye

AFFILIATION: Department of Infectious and Tropical Diseases, London School of
Hygiene and Tropical Medicine, London WC1E 7HT, United Kingdom.

REFERENCE: Infect Immun 2005 Dec 73(12):7996-8001

It has been proposed that long-lived memory T cells generated by 
vaccination or infection reside within a memory compartment that has a 
finite size. Consequently, in a variety of acute infection models 
interclonal competition has been shown to lead to attrition of 
preexisting memory CD8+ T cells. Contrary to expectations, therefore, we
 found that chronic Leishmania donovani infection of Listeria-immune 
mice results in heightened protection against subsequent Listeria 
challenge. This protection was associated with bystander expansion of 
Listeria-specific CD8+ T cells and a bias in these cells toward a 
central memory T-cell phenotype with an enhanced capacity for gamma 
interferon production. We propose that splenomegaly, which is 
characteristic of visceral leishmaniasis and other tropical infections, 
may help promote heterologous immunity by resetting the size of the 
memory compartment during chronic infection.




PMID: 16299331
 

TITLE: Regulation of impaired protein kinase C signaling by chemokines in murine
macrophages during visceral leishmaniasis.

AUTHORS: Ranadhir Dey, Arup Sarkar, Nivedita Majumder, Suchandra Bhattacharyya
Majumdar, Kaushik Roychoudhury, Sandip Bhattacharyya, Syamal Roy, Subrata
Majumdar

AFFILIATION: Department of Microbiology, Bose Institute, P1/12, C.I.T. Scheme
VII-M, Kolkata-700 054, India.

REFERENCE: Infect Immun 2005 Dec 73(12):8334-44

The protein kinase C (PKC) family regulates macrophage function involved
 in host defense against infection. In the case of Leishmania donovani 
infection, the impairment of PKC-mediated signaling is one of the 
crucial events for the establishment of parasite into the macrophages. 
Earlier reports established that C-C chemokines mediated protection 
against leishmaniasis via the generation of nitric oxide after 48 h. In 
this study, we investigated the role of MIP-1alpha and MCP-1 in the 
regulation of impaired PKC activity in the early hours (6 h) of 
infection. These chemokines restored Ca2+-dependent PKC activity and 
inhibited Ca2+-independent atypical PKC activity in L. donovani-infected
 macrophages under both in vivo and in vitro conditions. Pretreatment of
 macrophages with chemokines induced superoxide anion generation by 
activating NADPH oxidase components in infected cells. Chemokine 
administration in vitro induced the migration of infected macrophages 
and triggered the production of reactive oxygen species. In vivo 
treatment with chemokines significantly restricted the parasitic burden 
in livers as well as in spleens. Collectively, these results indicate a 
novel regulatory role of C-C chemokines in controlling the intracellular
 growth and multiplication of L. donovani, thereby demonstrating the 
antileishmanial properties of C-C chemokines in the disease process.




PMID: 16318433
 

TITLE: Treatment of visceral leishmaniasis.

AUTHORS: Shyam Sundar, Madhukar Rai

AFFILIATION: Department of Medicine, Institute of Medical Sciences, Banaras
Hindu University, Varanasi- 221005, India. shyam_vns at sify.com;
drshyamsundar at hotmail.com.

REFERENCE: Expert Opin Pharmacother 2005 Dec 6(16):2821-9

The Leishmania donovani complex includes L. chagasi and L. infantum, and
 causes visceral leishmaniasis (VL), a disseminated and potentially 
fatal form of leishmaniasis. The treatment options for VL are limited. 
Pentavalent antimonials (Sb(v)) are the first-line treatment options 
worldwide except for in Europe and Sb(v)-unresponsive regions of India. 
Amphotericin B deoxycholate is the drug of choice in India, as are its 
lipid formulations in Europe. However, liposomal amphotericin B (
AmBisome((R)), Gilead Sciences, Inc.) is the best antileishmanial 
formulation, but its prohibitive cost limits its use in endemic 
countries. Preferential pricing of AmBisome for patients with VL may 
provide hope for these underprivileged patients. Oral miltefosine and 
paromomycin are the other drugs that have been recently developed. 
Limited therapeutic options, the potential for development of resistance
 and serious toxicity associated with antileishmanial drugs necessitates
 a change in the treatment policy. A shift from monotherapy to multi-
drug combinations of short courses delivered at no or affordable cost, 
through directly observed therapy, seems to be the only way to develop 
the treatment of this disease.








PMID: 15936088
 

TITLE: Atypical multifocal cutaneous leishmaniasis in an immunocompetent patient
treated by liposomal amphotericin B.

AUTHORS: A Paradisi, R Capizzi, A Zampetti, I Proietti, C De Simone, C
Feliciani, P L Amerio

AFFILIATION: Department of Dermatology, Catholic University of Rome, Rome,
Italy. iclde at rm.unicatt.it

REFERENCE: J Infect 2005 Dec 51(5):e261-4

Multifocal cutaneous leishmaniasis (MCL) is an extremely rare disease in
 South Europe, and it mainly affects immunosuppressed patients. We 
report a case of MCL in an immunocompetent patient affected by type II 
diabetes mellitus that clinically presented with three large ulcers on 
the legs with a non-linear distribution and several months later with an
 erythematous-crusty lesion on the left cheek. Diagnosis of 
leishmaniasis due to Leishmania infantum was formulated by PCR analysis
. Given the diffuse and wide lesions, the unresponsiveness to previous 
local and systemic treatments, a parenteral i.v. therapy with liposomal 
amphotericin B at a dosage of 3mg/kg/day for 5 days was started and then
 repeated on the 14th and 21st days, leading to a clear improvement in 
the clinical picture. The different clinical expression and the 
evolution of leishmaniasis depend on both the parasite subtype and the 
host's immunity status. L. infantum manifests with an atypical clinical 
feature more frequently than other species. The differential diagnosis 
for multiple ulcers must include several skin diseases, such as 
cutaneous TBC, bacterial ulcers, traumatic ulcers, deep mycoses, and 
sarcoidosis. However, an MCL should always be considered in subjects 
coming from endemic areas. In our case, the multifocality, the size of 
the lesions and the unresponsiveness to other treatment indicate a short
 course treatment with liposomal B amphotericin that proved to be a 
suitable alternative to traditional drugs used in MCL.




PMID: 16261353
 

TITLE: Intramuscular immunization with p36(LACK) DNA vaccine induces IFN-gamma
production but does not protect BALB/c mice against Leishmania chagasi
intravenous challenge.

AUTHORS: Eduardo A Marques-da-Silva, Eduardo A F Coelho, Daniel C O Gomes,
Márcia C Vilela, Cássio Z Masioli, Carlos A P Tavares, Ana Paula Fernandes,
Luis Carlos C Afonso, Simone A Rezende

AFFILIATION: Laboratório de Imunoparasitologia, DECBI/NUPEB-ICEB, Campus Morro
do Cruzeiro, Universidade Federal de Ouro Preto, CEP 35400-000, Ouro Preto, MG,
Brazil.

REFERENCE: Parasitol Res 2005 Dec 98(1):67-74

Acute visceral leishmaniasis is a progressive disease caused by 
Leishmania chagasi in South America. The acquisition of immunity 
following infection suggests that vaccination is a feasible approach to 
protect against this disease. Since Leishmania homologue of receptors 
for activated C kinase (LACK) antigen is of particular interest as a 
vaccine candidate because of the prominent role it plays in the 
pathogenesis of experimental Leishmania major infection, we evaluated 
the potential of a p36(LACK) DNA vaccine in protecting BALB/c mice 
challenged with L. chagasi. In this study, mice received intramuscular (
i.m.) or subcutaneous (s.c.) doses of LACK DNA vaccine. We evaluated the
 production of vaccine-induced cytokines and whether this immunization 
was able to reduce parasite load in liver and spleen. We detected a 
significant production of interferon gamma by splenocytes from i.m. 
vaccinated mice in response to L. chagasi antigen and to rLACK protein. 
However, we did not observe a reduction in parasite load neither in 
liver nor in the spleen of vaccinated animals. The lack of protection 
observed may be explained by a significant production of IL-10 induced 
by the vaccine.




PMID: 16318709
 

TITLE: Canine leishmaniasis, Italy.

AUTHORS: Ezio Ferroglio

AFFILIATION: University of Turin, Turin, Italy.

REFERENCE: Emerg Infect Dis 2005 Oct 11(10):1618-20

We report the results of a survey to determine the prevalence of canine 
leishmaniasis and the presence of sand flies in northwestern Italy, 
where autochthonous foci of canine leishmaniasis have not been reported
. Active foci of canine leishmaniasis were identified, which suggests 
that the disease is now also endemic in continental climate areas.




PMID: 16312721
 

TITLE: Visceral leishmaniasis therapy.

AUTHORS: G Cascio, L Titone

AFFILIATION: Institute of Infectious Diseases - Palermo University, Italy.

REFERENCE: J Chemother 1989 Jul 1(4 Suppl):956-9




PMID: 16312722
 

TITLE: Our experiences in visceral leishmaniasis therapy.

AUTHORS: L Titone, F Scarlata, A Cascio, S Giordano, G Mancuso

AFFILIATION: Institute of Infectious Diseases - Palermo University, Italy.

REFERENCE: J Chemother 1989 Jul 1(4 Suppl):960-1




REQUEST: [ leishmania ]

(17 articles match this request. 8 articles matching other requests removed)



PMID: 16219371
 

TITLE: Roles for mitochondria in pentamidine susceptibility and resistance in
Leishmania donovani.

AUTHORS: Angana Mukherjee, Prasad K Padmanabhan, Mayurbhai H Sahani, Michael
Peter Barrett, Rentala Madhubala

AFFILIATION: School of Life Sciences, Jawaharlal Nehru University, New Delhi
110067, India.

REFERENCE: Mol Biochem Parasitol 2006 Jan 145(1):1-10

Pentamidine resistant Leishmania donovani was raised in the laboratory 
by stepwise exposure to increasing drug pressure until a line capable of
 growth in 8muM pentamidine (R8) had been selected. An IC(50) value of 
40muM was determined for this line, some 50-fold higher than that 
recorded for the parental wild-type line. The pentamidine resistant 
promastigotes were cross-resistant to other toxic diamidine derivatives 
but not to antimonials or substrates of multidrug resistance pumps. 
Decreased mitochondrial transmembrane potential was observed in 
pentamidine resistant promastigotes. A substantial net decrease in 
accumulation of [(3)H]-pentamidine accompanied the resistance phenotype
. Inhibitors of P-glycoprotein pumps, including prochlorperazine and 
trifluoperazine, did not reverse this decreased drug uptake, which 
distinguishes the L. donovani resistant line studied here from L. 
mexicana promastigotes previously studied for pentamidine resistance. 
Kinetic analysis identified a carrier with an apparent K(m) value of 
6muM for pentamidine. No significant difference between wild-type and 
resistant parasites could be detected with respect to this transporter 
in rapid uptake experiments. However, in longer-term uptake experiments 
and also using concentrations of pentamidine up to 1mM, it was 
demonstrated that wild-type cells, but not resistant cells, could 
continue to accumulate pentamidine after apparent saturation via the 
measured transporter had been reached. Agents that diminish the 
mitochondrial membrane potential inhibited this secondary route. A 
fluorescent analogue of pentamidine, 2,5-bis-(4-amidophenyl)-3,4-
dimethylfuran (DB99), accumulated in the kinetoplast of wild-type but 
not resistant parasites indicating that uptake of this cationic compound
 into mitochondria of wild-type cells was more pronounced than in the 
resistant line. These data together indicate that resistance to 
pentamidine in L. donovani is associated with alterations to the 
mitochondria of the parasites, which lead to reduced accumulation of 
drug.








PMID: 16240129
 

TITLE: Characterization of two different mucolipin-like genes from Leishmania
major.

AUTHORS: Mehdi Chenik, Feriel Douagi, Yosser Ben Achour, Noureddine Ben Khalef,
Meriem Ouakad, Hechmi Louzir, Koussay Dellagi

AFFILIATION: Laboratoire d'Immunopathologie, Vaccinologie et Génétique
Moléculaire, Institut Pasteur de Tunis, 13, Place Pasteur, 1002,
Tunis-Belvédère, Tunisia, mehdi.chenik at pasteur.rns.tn.

REFERENCE: Parasitol Res 2005 Dec 98(1):5-13

Here, we report the existence of two different mucolipin-like genes in 
Leishmania parasites. The Leishmania major mucolipin-like A and B genes
 (lmmlA and lmmlB) encode two proteins of 776 and 590 amino acids, 
respectively, and may be classified among the mucolipins family [
transient receptors potential mucolipin (TRPML)] because (1) they 
include a large region that exhibits significant similarities with 
specific domains of ion transport proteins and transient receptors 
potential (TRP) channels, (2) they contain at least 173 residues that 
display significant homologies with conserved regions of different 
mucolipins from several species, and (3) as TRPMLs, they include six 
predicted transmembrane domains. Gene expression analysis reveals that 
lmmlB is upregulated in metacyclics and amastigotes relative to 
procyclics, while lmmlA is constitutively expressed in the three 
Leishmania developmental stages. These genes could constitute potential 
drug targets.




PMID: 16214217
 

TITLE: Complexation of antimony (Sb(V)) with guanosine 5'-monophosphate and
guanosine 5'-diphospho-d-mannose: Formation of both mono- and bis-adducts.

AUTHORS: Yi Chai, Siucheong Yan, Iris L K Wong, Larry M C Chow, Hongzhe Sun

AFFILIATION: Department of Chemistry and Open Laboratory of Chemical Biology,
The University of Hong Kong, Pokfulam Road, Hong Kong, PR China.

REFERENCE: J Inorg Biochem 2005 Dec 99(12):2257-63

In spite of the extensive use of pentavalent antimony chemotherapy, the 
mechanism of its anti-leishmania action is still not clear. Here, we 
report the interactions of Sb(V), including the clinically used drug 
stibogluconate, with guanosine 5'-monophosphate (5'-GMP) and guanosine 5
'-diphospho-d-mannose (5'-GDP-mannose) in aqueous solution. The 
deprotonated hydroxyl groups (-OH) of the ribose ring are shown to be 
the binding site for Sb(V), probably via chelation. Both mono- and bis-
adducts were formed as determined by NMR, high performance liquid 
chromatography (HPLC) and electrospray ionization mass spectrometry (ESI
-MS), and both of them are stable in the pH range of 4 to around 9.5. 
The formation of the mono-adduct (k(1)=1.67x10(-3) and 3.43x10(-3) mM(-1
) min(-1) for Sb(5'-GMP) and Sb(5'-GDP-mannose), respectively, at 298 K
) was 10-fold faster than that of the bis-adduct (k(2)=0.16x10(-3) and 0
.21x10(-3) mM(-1) min(-1), for Sb(5'-GMP)(2) and Sb(5'-GDP-mannose)(2), 
respectively), and the mono-adduct was the major species in solution 
with the [bis-adduct]/[mono-adduct]<0.5. The reactions of 
stibogluconate with 5'-GMP and 5'-GDP-mannose were slower than that of 
antimonate under similar conditions.




PMID: 16315106
 

TITLE: Evolutionary relationships and protein domain architecture in an expanded
calpain superfamily in kinetoplastid parasites.

AUTHORS: Klaus Ersfeld, Helen Barraclough, Keith Gull

AFFILIATION: Department of Biological Sciences, University of Hull, Hull, HU6
7RX, UK, k.ersfeld at hull.ac.uk.

REFERENCE: J Mol Evol 2005 Dec 61(6):742-57

Employing whole-genome analysis we have characterized a large family of 
genes coding for calpain-related proteins in three kinetoplastid 
parasites. We have defined a total of 18 calpain-like sequences in 
Trypanosoma brucei, 27 in Leishmania major, and 24 in Trypanosoma cruzi
. Sequence characterization revealed a well-conserved protease domain in
 most proteins, although residues critical for catalytic activity were 
frequently altered. Many of the proteins contain a novel N-terminal 
sequence motif unique to kinetoplastids. Furthermore, 24 of the 
sequences contain N-terminal fatty acid acylation motifs indicating 
association of these proteins with intracellular membranes. This 
extended family of proteins also includes a group of sequences that 
completely lack a protease domain but is specifically related to other 
kinetoplastid calpain-related proteins by a highly conserved N-terminal 
domain and by genomic organization. All sequences lack the C-terminal 
calmodulin-related calcium-binding domain typical of most mammalian 
calpains. Our analysis emphasizes the highly modular structure of 
calpains and calpain-like proteins, suggesting that they are involved in
 diverse cellular functions. The discovery of this surprisingly large 
family of calpain-like proteins in lower eukaryotes that combines novel 
and conserved sequence modules contributes to our understanding of the 
evolution of this abundant protein family.




PMID: 16299330
 

TITLE: Leishmania pifanoi amastigotes avoid macrophage production of superoxide
by inducing heme degradation.

AUTHORS: Nam-Kha Pham, Jennifer Mouriz, Peter E Kima

AFFILIATION: Department of Microbiology and Cell Science, Building 981, Box
110700, University of Florida, Gainesville, FL 32611, USA.

REFERENCE: Infect Immun 2005 Dec 73(12):8322-33

Whereas infections of macrophages by promastigote forms of Leishmania 
mexicana pifanoi induce the production of superoxide, infections by 
amastigotes barely induce superoxide production. Several approaches were
 employed to gain insight into the mechanism by which amastigotes avoid 
eliciting superoxide production. First, in experiments with nitroblue 
tetrazolium, we found that 25% of parasitophorous vacuoles (PVs) that 
harbor promastigotes are positive for the NADPH oxidase complex, in 
contrast to only 2% of PVs that harbor amastigotes. Second, confocal 
microscope analyses of infected cells labeled with antibodies to 
gp91phox revealed that this enzyme subunit is found in PVs that harbor 
amastigotes. Third, in immunoblots of subcellular fractions enriched 
with PVs from amastigote-infected cells and probed with antibodies to 
gp91phox, only the 65-kDa premature form of gp91phox was found. In 
contrast, subcellular fractions from macrophages that ingested zymosan 
particles contained both the 91- and 65-kDa forms of gp91phox. This 
suggested that only the immature form of gp91phox is recruited to PVs 
that harbor amastigotes. Given that gp91phox maturation is dependent on 
the availability of heme, we found that infections by Leishmania 
parasites induce an increase in heme oxygenase 1 (HO-1), the rate-
limiting enzyme in heme degradation. Infections by amastigotes performed
 in the presence of metalloporphyrins, which are inhibitors of HO-1, 
resulted in superoxide production by infected macrophages. Taken 
together, we propose that Leishmania amastigotes avoid superoxide 
production by inducing an increase in heme degradation, which results in
 blockage of the maturation of gp91phox, which prevents assembly of the 
NADPH oxidase enzyme complex.




PMID: 16168668
 

TITLE: Isolation of infective promastigotes of Leishmania major from long-term
culture by cocultivation with macrophage cell line.

AUTHORS: Mirjalili Ali, Sarkari Bahador

AFFILIATION: Cell and Gene Bank of Razi Institute (CGBRI), Biotechnology
Department, Razi Vaccine and Serum Research Institute (RVSRI), Hesarrak, Karaj,
Iran.

REFERENCE: Biologicals 2005 Dec 33(4):257-60

Research on Leishmania-macrophage interaction is mainly focused on the 
impact of the parasite on macrophages and several known virulent factors
 have been described. Furthermore, studies on macrophage revealed 
several defense mechanisms including various cytokines which are 
released by macrophages to defend against parasite. In the present study
, a new aspect of this interaction was evaluated: parasite 
characteristics, which emerge when they were cocultivated with 
macrophage. Two promastigote characteristics, survival at high 
temperature (32 degrees C) and infectivity rate were the focus of this 
study. In this study, an in vitro coculture model for promastigotes with
 macrophage cell line, J774 A1, was introduced using a cell culture 
chamber system which separates both cell types by a microporous 
polycarbonate membrane. After 5-7 days of coculturing at 32 degrees C, a
 few promastigotes survived longer than control group. Once this 
population of parasite was cultured at optimal temperature (26 degrees C
), the emerged new clone was much more infective for J774 A1 cell line 
in comparison with the original one. Having this system and using the 
new clone of promastigotes, parasite infectivity rate was raised from 1-
2% of original clone to 35-45%. Using this new introduced technique, 
infective promastigotes were isolated from 9 month old frequently sub-
cultured clone of Leishmania major. This coculturing system allows 
investigators to prepare infective promastigotes from the frequently 
cultured parasites. Molecular and biochemical mechanisms of this 
phenomenon need to be investigated.




PMID: 16188262
 

TITLE: Retardation of cell cycle progression of macrophages from G1 to S phase
by ICAM-L from Leishmania.

AUTHORS: Oleg I Kuzmenok, Su-Chi Chiang, Yi-Chun Lin, Sho Tone Lee

AFFILIATION: Division of Infectious Diseases, Institute of Biomedical Sciences,
Academia Sinica, (IBMS), No.128, Academia Road Sec.2, Nan-Kang, Taipei 11529,
Taiwan, ROC.

REFERENCE: Int J Parasitol 2005 Dec 35(14):1547-55

Leishmania, an obligate intracellular parasite of host macrophages, 
infects the macrophage through receptor-mediated phagocytosis that 
either activates or deactivates macrophages to eliminate the parasite or
 allow the parasite to grow intracellularly. ICAM-L, an intercellular 
adhesion molecule from L. amazonensis, results in lower MTT tests and 
proliferative responses of macrophages when incubated in vitro. The 
inhibition of cell proliferation, however, results from temporary 
retardation of the cell cycle progression at the G1 to S phase 
transition rather than cell death. The retardation is due to the 
upregulation of two CKI proteins, p21 and p27, in a p53-independent 
manner which, control the G(1) to S phase transition checkpoint.








PMID: 16305434
 

TITLE: Targeted drug delivery to macrophages in parasitic infections.

AUTHORS: M Owais, C M Gupta

AFFILIATION: Interdisciplinary Biotechnology Unit, Aligarh Muslim University,
Aligarh 202 002, India.

REFERENCE: Curr Drug Deliv 2005 Oct 2(4):311-8

Successful homing of drugs to the desired biological compartment of the 
host usually depends on the intrinsic properties of the drug molecules. 
However, it can always be manipulated by appropriate designing of the 
carrier/delivery system, as little can be done to influence the target 
and its surroundings. Various carrier systems have emerged to deliver 
drugs to macrophages, albeit the efficacy, reliability and selectivity 
of these carriers are still in question. To date, the most extensively 
studied carriers are liposomes and microspheres. In fact, 
physicochemical properties of these carriers can alter their efficacy 
and specificity to a great extent. These properties include 
hydrophilicity, surface charge, composition, concentration, and presence
 of various target specific ligands on their surface. Incidentally, the 
particulate nature of these vehicles may facilitate passive homing of 
the entrapped drug molecules to the macrophages, which may harbour many 
of the important pathogens in their intracellular compartments, such as 
Mycobacterium sps, Leishmania and dengue virus etc., belonging to three 
different major classes of microbes. Moreover, macrophages upon 
interaction with particulate drug delivery vehicles may act as secondary
 drug depot, thus helping in localized delivery of the drug at the 
infected site. In the present article, a comprehensive review of 
literature is presented on the suitability of some lipid-based and 
polymeric materials as vehicles in delivery of drugs to macrophages in 
parasitic infections.




PMID: 16313440
 

TITLE: In Vitro and Ex Vivo Permissivity of Hepatocytes for Leishmania
donovani.

AUTHORS: Jean-Pierre Gangneux, Olivier Lemenand, Yannick Reinhard, Claude
Guiguen, Christiane Guguen-Guillouzo, Philippe Gripon

AFFILIATION: Institut National de la Santé et de la Recherche Médicale
(INSERM) U-522, and Laboratoire de Parasitologie-Mycologie, Faculte de Medicine
de Rennes, 35000 Rennes, France.

REFERENCE: J Eukaryot Microbiol 2005 Nov-Dec 52(6):489-91

Using models of ex vivo infection of murine, rat, and human primary 
hepatocytes by Leishmania donovani, we showed that hepatocytes are 
permissive for Leishmania at a low level. We then modeled the in vitro 
infection of a human hepatoma-derived cell line to examine the parasite'
s capability to proliferate and to cause direct damage to hepatocytes. 
Results showed that L. donovani can infect hepatocytes, but do not 
massively proliferate. This slight infection under our experimental 
conditions resulted in limited damage to hepatocytes. These results 
bring into question a possible role for hepatocytes as a parasite 
reservoir during latent infection.




REQUEST: [ sand fly ]

(2 articles match this request)



PMID: 16313571
 

TITLE: Characterization of a blood activated chitinolytic system in the midgut
of the sand fly vectors Lutzomyia longipalpis and Phlebotomus papatasi.

AUTHORS: J M Ramalho-Ortigão, S Kamhawi, M B Joshi, D Reynoso, P G Lawyer, D M
Dwyer, D L Sacks, J G Valenzuela

AFFILIATION: Intracellular Parasite Biology Section, Laboratory of Parasitic
Diseases, National Institute for Allergy and Infectious Diseases, National
Institutes of Health, Bethesda, MD, USA.

REFERENCE: Insect Mol Biol 2005 Dec 14(6):703-12

We characterized a cDNA from Phlebotomus papatasi, PpChit1, which 
encodes a midgut specific chitinase and show the presence of a 
functional, blood-induced chitinolytic system in sand flies. PpChit1 is 
detected only in the midgut and is regulated by blood feeding. A 
recombinant protein (rPpChit1) produced in HEK 293-F cells exhibited a 
similar activity profile to that found in the native protein against 
several specific substrates, including an oligomeric glycol chitin and 
synthetic 4-methyl-umbelliferone labelled substrates. Western blotting 
showed that the native protein is recognized by mouse polyclonal 
antibodies against rPpChit1. Additionally, the rPpChit1 and the native 
chitinase displayed similar retention times in a HPLC size fractionation
 column. When added to rPpChit1 or to midgut lysates, PpChit1 sera 
reduced chitinolytic activity by 65-70%.




PMID: 16324569
 

TITLE: [Infections due to Toscana virus, West Nile virus, and other arboviruses
of interest in Europe.]

AUTHORS: Mari Paz Sánchez-Seco, José María Navarro

AFFILIATION: Unidad de Alerta y Emergencia. Laboratorio de Arbovirus y
Enfermedades Víricas Importadas. Centro Nacional de Microbiología. Instituto
de Salud Carlos III. Majadahonda. Madrid.

REFERENCE: Enferm Infecc Microbiol Clin 2005 Nov 23(9):560-8

Arbovirosis, viral infection transmitted by arthropods, is a widespread 
health problem. Recurrent outbreaks caused by some of these viruses such
 as dengue or West Nile strains in regions where they do not appear 
frequently, justify the establishment of global control measures. Tick-
borne encephalitis viruses, sand fly fever viruses (Toscana, Naples and 
Sicily) and occasionally West Nile and Crimean-Congo fever viruses are 
the most frequent causes of arbovirosis in Europe, although circulation 
of other potentially pathogenetic viruses such as Chikungunya has also 
been detected. The only native arbovirosis described in Spain is 
infection produced by Toscana virus, which causes aseptic, usually 
benign meningitis. Nevertheless, some West Nile virus-associated meningo
-encephalitis cases have been described in France, Portugal and 
countries in the Magreb region, increasing the risk of sporadic 
occurrence of these processes in our country. To achieve an accurate 
diagnosis, high clinical suspicion is required as well as highly 
specific laboratory techniques, mainly based on IgM detection, RT-PCR 
and viral culture of CSF and/or serum.




REQUEST: [ sandfly ]

(2 articles match this request)



PMID: 16318715
 

TITLE: Emergence of toscana virus in europe.

AUTHORS: Rémi N Charrel

AFFILIATION: Université de la Méditerranée, Marseille, France.

REFERENCE: Emerg Infect Dis 2005 Nov 11(11):1657-63

Toscana virus (TOSV) is an arthropodborne virus first identified in 1971
 from the sandfly Phlebotomus perniciosus in central Italy. Many case 
reports in travelers and clinical research and epidemiologic studies 
conducted around the Mediterranean region have shown that TOSV has a 
tropism for the central nervous system (CNS) and is a major cause of 
meningitis and encephalitis in countries in which it circulates. In 
central Italy, TOSV is the most frequent cause of meningitis from May to
 October, far exceeding enteroviruses. In other northern Mediterranean 
countries, TOSV is among the 3 most prevalent viruses associated with 
meningitis during the warm seasons. Therefore, TOSV must be considered 
an emerging pathogen. Here, we review the epidemiology of TOSV in Europe
 and determine questions that should be addressed in future studies. 
Despite increasing evidence of its major role in medicine as an emerging
 cause of CNS infections, TOSV remains an unstudied pathogen, and few 
physicians are aware of its potential to cause CNS infections.




PMID: 16318721
 

TITLE: Toscana virus in Spain.

AUTHORS: Sara Sanbonmatsu-Gámez

AFFILIATION: Hospital Universitario Virgen de las Nieves, Granada, Spain.

REFERENCE: Emerg Infect Dis 2005 Nov 11(11):1701-7

Toscana virus (TOSV, Phlebovirus, family Bunyaviridae) infection is one 
of the most prevalent arboviruses in Spain. Within the objectives of a 
multidisciplinary network, a study on the epidemiology of TOSV was 
conducted in Granada, in southern Spain. The overall seroprevalence rate
 was 24.9%, significantly increasing with age. TOSV was detected in 3 of
 103 sandfly pools by viral culture or reverse transcription-polymerase 
chain reaction from a region of the L gene. Nucleotide sequence homology
 was 99%-100% in TOSV from vectors and patients and 80%-81% compared to 
the Italian strain ISS Phl.3. Sequencing of the N gene of TOSV isolates 
from patients and vectors indicated 87%-88% and 100% homology at the 
nucleotide and amino acid levels, respectively, compared to the Italian 
strain. These findings demonstrate the circulation of at least 2 
different lineages of TOSV in the Mediterranean basin, the Italian 
lineage and the Spanish lineage.















You receive this email because you requested RefScout&#174;'s literature
update.
If you would like to change or add requests, please go to your user
profile.

If you can't read our newsletter, please resend newsletter back to us to
info at refscout.com, including information
about your operating system and mail client software you use, and we will do
our
best to solve the problem.

If you would like to be removed from RefScout&#174;'s literature service, please
press the
remove button.



DISCLAIMER







----- End forwarded message -----