[Leish-l] RefScout 4/2007

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  REQUEST: [ leishmania ]
(19 articles match this request)

PMID: 17223963<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17223963>
TITLE: Elevated levels of soluble non-classical major histocompatibility
class I molecule human leucocyte antigen (HLA)-G in the blood of
HIV-infected patients with or without visceral
leishmaniasis.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17223963>
AUTHORS: L Donaghy, F Gros, L Amiot, C Mary, A Maillard, C Guiguen, J-P
Gangneux
AFFILIATION: Inserm U522, Rennes, CHU de Rennes, France.
REFERENCE: Clin Exp Immunol 2007 Feb 147(2):236-40
The non-classical class I major histocompatibility complex molecules human
leucocyte antigen (HLA)-G have been shown to play a role in HIV persistence,
but no data are available on the expression of the soluble forms HLA-G5 and
sHLA-G1 in HIV-infected patients with and without opportunistic infections.
The soluble HLA-G isoform was measured with an enzyme-linked immunosorbent
assay (ELISA) method in plasma from 94 subjects: 31 HIV-1-seropositive, 17
with visceral leishmaniasis (VL), seven with both VL and HIV-1 infection and
39 healthy HIV-seronegative subjects. Between groups, the frequency of
sHLA-G positivity was statistically different: 81% of HIV-infected patients
were positive, as were 57% of HIV-*Leishmania* infantum co-infected
patients, 35% of HIV- seronegative patients with VL and 3% of healthy
controls. Levels of the soluble forms of the immunomodulatory molecules
HLA-G are elevated during HIV infection. In HIV-*Leishmania* co-infected
patients, sHLA-G secretion could contribute to the tolerogenic environment
and to *Leishmania* immune evasion.


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PMID: 16841091<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=16841091>
TITLE: Apoptosis is induced in leishmanial cells by a novel protein kinase
inhibitor withaferin A and is facilitated by apoptotic topoisomerase I-DNA
complex.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=16841091>
AUTHORS: N Sen, B Banerjee, B B Das, A Ganguly, T Sen, S Pramanik, S
Mukhopadhyay, H K Majumder
AFFILIATION: 1Division of Infectious Diseases, Indian Institute of Chemical
Biology, 4, Raja SC Mullick Road, Kolkata 700 032, India.
REFERENCE: Cell Death Differ 2007 Feb 14(2):358-67
Protein kinase C (PKC) is an important constituent of the signaling pathways
involved in apoptosis. We report here that like staurosporine, withaferin A
is a potent inhibitor of PKC. In *Leishmania* donovani, the inhibition of
PKC by withaferin A causes depolarization of DeltaPsi(m) and generates ROS
inside cells. Loss of DeltaPsi(m) leads to the release of cytochrome c into
the cytosol and subsequently activates caspase- like proteases and
oligonucleosomal DNA cleavage. Moreover, in treated cells, oxidative DNA
lesions facilitate the stabilization of topoisomerase I-mediated cleavable
complexes, which also contribute to DNA fragmentation. However, withaferin A
and staurosporine cannot induce cleavable complex formation in vitro with
recombinant topoisomerase I nor with nuclear extracts from control cells.
Taken together, our results indicate that inhibition of PKC by withaferin A
is a central event for the induction of apoptosis and that the stabilization
of topoisomerase I-DNA complex is necessary to amplify apoptotic process.
Cell Death and Differentiation (2007) 14, 358-367. doi:10.1038/sj.cdd.
4402002; published online 14 July 2006.


PMID: 17027989<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17027989>
TITLE: The *Leishmania* donovani complex: Genotypes of five metabolic
enzymes (ICD, ME, MPI, G6PDH, and FH), new targets for multilocus sequence
typing.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17027989>
AUTHORS: Eva Zemanová, Milan Jirků, Isabel L Mauricio, Ales Horák,
Michael A Miles, Julius Lukes
AFFILIATION: Biology Centre, Institute of Parasitology, Czech Academy of
Sciences and Faculty of Biology, University of South Bohemia, CeskÃ(c)
Budejovice, (Budweis), Czech Republic.
REFERENCE: Int J Parasitol 2007 Feb 37(2):149-60
Flagellates of the *Leishmania* donovani complex are causative agents of
human cutaneous and visceral leishmaniasis. The complex is comprised of L.
donovani, *Leishmania* infantum and *Leishmania* archibaldi, although the
latter is not now considered to be a valid species. Morphological
distinction of *Leishmania* species is impractical, so biochemical,
immunological and DNA-based criteria were introduced. Multilocus enzyme
electrophoresis (MLEE) is the present gold standard. We have sequenced the
genes encoding five metabolic enzymes used for MLEE, both to resolve the DNA
diversity underlying isoenzyme mobility differences and to explore the
potential of these targets for higher resolution PCR-based multilocus
sequence typing. The genes sequenced were isocitrate dehydrogenase, malic
enzyme, mannose phosphate isomerase, glucose-6- phosphate dehydrogenase, and
fumarate hydratase, for 17 strains of L. infantum, seven strains of L.
donovani, and three strains of L. archibaldi. Protein mobilities predicted
from amino acid sequences did not always accord precisely with reported MLEE
profiles. A high number of heterozygous sites was detected. Heterozygosity
was particularly frequent in some strains and indirectly supported the
presence of genetic exchange in *Leishmania*. Phylogenetic analysis of a
concatenated alignment based on a total of 263kb protein-coding sequences
showed strong correlation of genotype with geographical origin. Europe and
Africa appear to represent independent evolutionary centres.


PMID: 17107676<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17107676>
TITLE: *Leishmania* major metacaspase can replace yeast metacaspase in
programmed cell death and has arginine-specific cysteine peptidase
activity.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17107676>
AUTHORS: Iveth J González, Chantal Desponds, CÃ(c)dric Schaff, Jeremy C
Mottram, Nicolas Fasel
AFFILIATION: Department of Biochemistry, University of Lausanne, 155 Chemin
des Boveresses, CH-1066 Epalinges, Switzerland.
REFERENCE: Int J Parasitol 2007 Feb 37(2):161-72
The human protozoan parasite *Leishmania* major has been shown to exhibit
several morphological and biochemical features characteristic of a cell
death program when differentiating into infectious stages and under a
variety of stress conditions. Although some caspase-like peptidase activity
has been reported in dying parasites, no caspase gene is present in the
genome. However, a single metacaspase gene is present in L. major whose
encoded protein harbors the predicted secondary structure and the catalytic
dyad histidine/cysteine described for caspases and other metacaspases
identified in plants and yeast. The Saccharomyces cerevisiae metacaspase
YCA1 has been implicated in the death of aging cells, cells defective in
some biological functions, and cells exposed to different environmental
stresses. In this study, we describe the functional heterologous
complementation of a S. cerevisiae yca1 null mutant with the L. major
metacaspase (LmjMCA) in cell death induced by oxidative stress. We show that
LmjMCA is involved in yeast cell death, similar to YCA1, and that this
function depends on its catalytic activity. LmjMCA was found to be
auto-processed as occurs for caspases, however LmjMCA did not exhibit any
activity with caspase substrates. In contrast and similarly to Arabidopsis
thaliana metacaspases, LmjMCA was active towards substrates with arginine in
the P1 position, with the activity being abolished following H147A and C202A
catalytic site mutations. These results suggest that metacaspases are
members of a family of peptidases with a role in cell death conserved in
evolution notwithstanding possible differences in their catalytic activity.


PMID: 17178178<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17178178>
TITLE: Immunogenicity of the P-8 amastigote antigen in the experimental
model of canine visceral
leishmaniasis.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17178178>
AUTHORS: E Carrillo, S Ahmed, K Goldsmith-Pestana, J Nieto, Y Osorio, B
Travi, J Moreno, D McMahon-Pratt
AFFILIATION: WHO Collaborating Centre for Leishmaniasis, Instituto de Salud
Carlos III, Ctra. Majadahonda-Pozuelo km. 2, 28220 Madrid, Spain.
REFERENCE: Vaccine 2007 Feb 25(8):1534-43
The P-8 proteoglycolipid complex (P-8 PGLC), an amastigote antigen of *
Leishmania* pifanoi, has been demonstrated to induce protection in mouse
models, as well as to induce Tc1/Th1-like cellular responses in American
cutaneous leishmaniasis patients. Because the immunization with P-8 PGLC in
the murine model does not appear to be genetically restricted, we have
studied the reactivity of the P-8 PGLC in *Leishmania* infantum infected
dogs. In this study, it is shown that PBMC from experimentally infected dogs
(asymptomatic, oligosymptomatic) significantly proliferated in response to
soluble leishmanial antigen (SLA) or the P-8 PGLC. Further, quantification
of the gene expression induced by the stimulation with P-8 in
asymptomatically infected dogs showed an up- regulation of IFN-gamma and
TNF-alpha, which were three to 4-fold higher than that induced by soluble *
Leishmania* antigen (SLA). While no measurable induction of IL-10 was
observed, low levels of IL-4 mRNA were observed in response to both P-8 and
SLA antigens. Thus, our studies establish that P-8 is recognized by infected
canines and elicits a potentially curative/protective Th1-like immune
response. The identification of *Leishmania* antigens that elicit
appropriate immune responses across different host species (humans, canine)
and disease manifestations (cutaneous or visceral) could be an advantage in
generating a general vaccine for leishmaniasis.


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PMID: 17233673<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17233673>
TITLE: Identification of New World *Leishmania* species from Peru by
biochemical techniques and multiplex PCR
assay.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17233673>
AUTHORS: Isabel Rodríguez-González, Clotilde Marín, Silvia S Longoni,
Hector Mateo, JosÃ(c) M Alunda, Gloria Minaya, Ramón GutiÃ(c)rrez-Sánchez,
Franklin Vargas, Manuel Sánchez-Moreno
AFFILIATION: Instituto de Biotecnología, Departamento de Parasitología,
Facultad de Ciencias, Universidad de Granada, Granada, Spain.
REFERENCE: FEMS Microbiol Lett 2007 Feb 267(1):9-16
We have characterized diverse strains or species of *Leishmania* isolated in
humans that are currently circulating throughout Peru, by means of
isoenzymatic characterization, kDNA analysis by restriction enzymes, and
multiplex PCR assay. The cluster analysis gave five groups. Cluster 1
includes L. (L.) donovani together with the isolates LP4 and LP7, forming
the donovani complex. Thus, this complex corresponds to the New World
visceral form, L. (L.) chagasi. Cluster 2 is formed by the isolates LP1-LP3,
LP6, LP10, LP9, and LP11, phylogenetically intermediate between Cluster 1
and Cluster 3, or they can be treated as hybrids. Cluster 3 is divided into
two subgroups: one formed by L. (V.) peruviana, together with the isolates
LP14 and LP5, and the second one formed by L. (V.) brazilensis and the
isolate LP8. These two subgroups form part of the brazilensis complex. The
three strains of L. (L.) infantum [L. (L.) infantum I and II and la LSI]
make up Cluster 4. In Cluster 5, we include the three Mexican strains
(LM1-LM3) forming one subgroup while we would place L. (L.) amazonensis in
another subgroup. These two subgroups would comprise the complex mexicana.


PMID: 16797076<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=16797076>
TITLE: Laryngeal leishmaniasis in
Malta.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=16797076>
AUTHORS: C Fsadni, P Fsadni, T Piscopo, C Mallia Azzopardi
AFFILIATION: Infectious Diseases Unit (STZ), St. Luke's Hospital,
Gwardamangia, Malta. claudia_7 at excite.com
REFERENCE: J Infect 2007 Feb 54(2):e61-3
The localization of *Leishmania* spp. in the larynx is rare especially when
not associated with immunosuppression or with visceral or cutaneous
leishmaniasis. We present a case of isolated laryngeal leishmaniasis, the
first of its kind documented in Malta and infrequently reported from the
Mediterranean basin.


PMID: 17126422<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17126422>
TITLE: Analysis of telomere length variation in *Leishmania* over
time.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17126422>
AUTHORS: Paul-AndrÃ(c) Genest, Piet Borst
AFFILIATION: The Netherlands Cancer Institute, Divison of Molecular Biology
and Centre of Biomedical Genetics, Plesmanlaan 121, 1066 CX Amsterdam, The
Netherlands.
REFERENCE: Mol Biochem Parasitol 2007 Feb 151(2):213-5


PMID: 16889626<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=16889626>
TITLE: *Leishmania* promastigotes activate PI3K/Akt signalling to confer
host cell resistance to
apoptosis.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=16889626>
AUTHORS: Aaron Ruhland, Nicole Leal, Peter E Kima
AFFILIATION: Department of Microbiology and Cell Science, University of
Florida, Gainesville, FL 326111, USA.
REFERENCE: Cell Microbiol 2007 Jan 9(1):84-96
Previous reports have shown that cells infected with promastigotes of some *
Leishmania* species are resistant to the induction of apoptosis. This would
suggest that either parasites elaborate factors that block signalling from
apoptosis inducers or that parasites engage endogenous host signalling
pathways that block apoptosis. To investigate the latter scenario, we
determined whether *Leishmania* infection results in the activation of
signalling pathways that have been shown to mediate resistance to apoptosis
in other infection models. First, we showed that infection with the
promastigote form of *Leishmania* major, *Leishmania* pifanoi and *
Leishmania* amazonensis activates signalling through p38 mitogen-activated
protein kinase (MAPK), NFkappaB and PI3K/Akt. Then we found that inhibition
of signalling through the PI3K/Akt pathway with LY294002 and Akt IV
inhibitor reversed resistance of infected bone marrow-derived macrophages
and RAW 264.7 macrophages to potent inducers of apoptosis. Moreover,
reduction of Akt levels with small interfering RNAs to Akt resulted in the
inability of infected macrophages to resist apoptosis. Further evidence of
the role of PI3K/Akt signalling in the promotion of cell survival by
infected cells was obtained with the finding that Bad, which is a substrate
of Akt, becomes phosphorylated during the course of infection. In contrast
to the observations with PI3K/Akt signalling, inhibition of p38 MAPK
signalling with SB202190 or NFkappaB signalling with wedelolactone had
limited effect on parasite- induced resistance to apoptosis. We conclude
that *Leishmania* promastigotes engage PI3K/Akt signalling, which confers to
the infected cell, the capacity to resist death from activators of
apoptosis.


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PMID: 17222179<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17222179>
TITLE: *Leishmania* donovani bisubunit topoisomerase I gene fusion leads to
an active enzyme with conserved type IB enzyme
function.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17222179>
AUTHORS: Benu B Das, Somdeb Bose Dasgupta, Agneyo Ganguly, Saumyabrata
Mazumder, Amit Roy, Hemanta K Majumder
AFFILIATION: Department of Molecular Parasitology, Indian Institute of
Chemical Biology, Kolkata, India.
REFERENCE: FEBS J 2007 Jan 274(1):150-63
All eukaryotic topoisomerase I enzymes are monomeric enzymes, whereas the
kinetoplastid family (Trypanosoma and *Leishmania*) possess an unusual
bisubunit topoisomerase I. To determine what happens to the enzyme
architecture and catalytic property if the two subunits are fused, and to
explore the functional relationship between the two subunits, we describe
here in vitro gene fusion of *Leishmania* bisubunit topoisomerase I into a
single ORF encoding a new monomeric topoisomerase I (LdTOPIL- fus-S). It was
found that LdTOPIL-fus-S is active. Gene fusion leads to a significant
modulation of in vitro topoisomerase I activity compared to the wild-type
heterodimeric enzyme (LdTOPILS). Interestingly, an N- terminal truncation
mutant (1-210 amino acids) of the small subunit, when fused to the intact
large subunit [LdTOPIL-fus-Delta(1-210)S], showed reduced topoisomerase I
activity and camptothecin sensitivity in comparison to LdTOPIL-fus-S.
Investigation of the reduction in enzyme activity indicated that the
nonconserved 1-210 residues of LdTOPIS probably act as a 'pseudolinker'
domain between the core and catalytic domain of the fused
*Leishmania*enzyme, whereas mutational analysis of conserved His453 in
the core
DNA-binding domain (LdTOPIL) strongly suggested that its role is to
stabilize the enzyme-DNA transition state through hydrogen bonding to one of
the nonbridging oxygens. Taken together, our findings provide an insight
into the details of the unusual structure of bisubunit topoisomerase I of *
Leishmania* donovani.


PMID: 17222186<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17222186>
TITLE: Elongation of polyunsaturated fatty acids in
trypanosomatids.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17222186>
AUTHORS: Verónica I Livore, Karina E J Tripodi, Antonio D Uttaro
AFFILIATION: Instituto de Biología Molecular y Celular de Rosario (IBR),
CONICET, Departamento de Microbiología, Facultad de Ciencias Bioquímicas y
FarmacÃ(c)uticas, Universidad Nacional de Rosario, Santa Fe, Argentina.
REFERENCE: FEBS J 2007 Jan 274(1):264-74
*Leishmania* major synthesizes polyunsaturated fatty acids by using Delta6 ,
Delta5 and Delta4 front-end desaturases, which have recently been
characterized [Tripodi KE, Buttigliero LV, Altabe SG & Uttaro AD ( 2006)
FEBS J273, 271-280], and two predicted elongases specific for C18 Delta6 and
C20 Delta5 polyunsaturated fatty acids, respectively. Trypanosoma brucei and
Trypanosoma cruzi lack Delta6 and Delta5 desaturases but contain Delta4
desaturases, implying that trypanosomes use exogenous polyunsaturated fatty
acids to produce C22 Delta4 fatty acids. In order to identify putative
precursors of these C22 fatty acids and to completely describe the pathways
for polyunsaturated fatty acid biosynthesis in trypanosomatids, we have
performed a search in the three genomes and identified four different
elongase genes in T. brucei, five in T. cruzi and 14 in L. major. After a
phylogenetic analysis of the encoded proteins together with elongases from a
variety of other organisms, we selected four candidate polyunsaturated fatty
acid elongases. *Leishmania* major CAJ02037, T. brucei AAX69821 and T. cruzi
XP_808770 share 57-52% identity, and group together with C20 Delta5
polyunsaturated fatty acid elongases from algae. The predicted activity was
corroborated by functional characterization after expression in yeast. T.
brucei elongase was also able to elongate Delta8 and Delta11 C20
polyunsaturated fatty acids. L. major CAJ08636, which shares 33% identity
with Mortierella alpinaDelta6 elongase, showed a high specificity for C18
Delta6 polyunsaturated fatty acids. In all cases, a preference for n6
polyunsaturated fatty acids was observed. This indicates that L. major has,
as predicted, Delta6 and Delta5 elongases and a complete pathway for
polyunsaturated fatty acid biosynthesis. Trypanosomes contain only Delta5
elongases, which, together with Delta4 desaturases, allow them to use
eicosapentaenoic acid and arachidonic acid, a precursor that is relatively
abundant in the host, for C22 polyunsaturated fatty acid biosynthesis.


PMID: 17182338<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17182338>
TITLE: Oral miltefosine to treat new world cutaneous
leishmaniasis.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17182338>
AUTHORS: Jaime Soto, Julia T Toledo
REFERENCE: Lancet Infect Dis 2007 Jan 7(1):7


PMID: 17118349<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17118349>
TITLE: Acute cysticercosis favours rapid and more severe lesions caused by *
Leishmania* major and *Leishmania* mexicana infection, a role for
alternatively activated
macrophages.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17118349>
AUTHORS: Miriam Rodríguez-Sosa, Irma Rivera-Montoya, Arlett Espinoza,
Miriam Romero-Grijalva, Roberto López-Flores, Jorge González, Luis I
Terrazas
AFFILIATION: Laboratory of Immunoparasitology, Unidad de Biomedicina,
Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de
MÃ(c)xico, Mexico.
REFERENCE: Cell Immunol 2006 Aug 242(2):61-71
Parasitic helminths have developed complex mechanisms to modulate host
immunity. In the present study we found that previous infection of mice with
the cestode Taenia crassiceps favours parasitemia and induces larger
cutaneous lesions during both *Leishmania* major and *Leishmania* mexicana
co-infections. Analysis of cytokine responses into draining lymph nodes
indicated that co-infection of T. crassiceps-*Leishmania* did not inhibit
IFN-gamma production in response to *Leishmania* antigens, but significantly
increased IL-4 production. Additionally, anti-*Leishmania*- specific IgG1
antibodies and total IgE increased in co-infected mice, whereas, IgG2a
titers remained similar. Macrophages from Taenia-infected mice displayed
increased mRNA transcripts of arginase-1, Ym1, and Mannose Receptor, as well
as greater production of urea (all markers for an alternate activation
state) compared to macrophages from *Leishmania*- infected mice. In
contrast, lower mRNA transcripts for IL-12p35, IL- 12p40, IL-23p19, and iNOS
were detected in macrophages obtained from cestode-infected mice compared to
uninfected and *Leishmania*-infected mice after LPS stimulation. The
presence of cestode also generated impaired macrophage anti-leishmanicidal
activity in vitro, as evidenced by the inability of these macrophages to
prevent *Leishmania* growth compared to macrophages from uninfected mice.
This was observed despite the fact that both groups of cells were exposed to
IFN-gamma. Flow cytometry showed high IFN-gammaR expression on
Taenia-induced macrophages. Thus, lack of response to IFN-gamma is not
associated with the absence of its receptor. Our data suggest that cestode
infection may favour *Leishmania* installation by inducing alternatively
activated macrophages rather than inhibiting Th1-type responses.


PMID: 16951815<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=16951815>
TITLE: Polymerase chain reaction with lesion scrapping for the diagnosis of
human American tegumentary
leishmaniasis.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=16951815>
AUTHORS: Eneide Aparecida Sabaini Venazzi, AndrÃ(c)a Claudia Bekner Silva
Roberto, Ione Parra Barbosa-Tessmann, Paulo Donizeti Zanzarini, Maria
Valdrinez Campana Lonardoni, Thaís Gomes Verzignassi Silveira
AFFILIATION: Departamento de Análises Clínicas, Departamento de
Bioquímica, Universidade Estadual de Maringá, Maringá, PR, Brasil.
REFERENCE: Mem Inst Oswaldo Cruz 2006 Jun 101(4):427-30
The objective of this work was to compare the polymerase chain reaction
(PCR) using lesion scrapping with other conventional techniques for the
diagnosis of the American tegumentary leishmaniasis (ATL). For this,
patients with cutaneous lesions suspected to be ATL were studied. The DNA
was amplified with the MP1L/MP3H primers. From the 156 studied patients, 79
(50.6%) presented positive parasite direct search (PD), 81 (51.9%) had
positive Montenegro skin test (MST), and 90 (57.7%) presented PD and/or MST
positive. The PCR was positive in all of the positive-PD patients (100%
sensitivity), in 91.1% of the positive PD and /or MST patients, and in
27.3%of the patients that presented negative PD and positive MST. The
PCR
positivity was similar to the PD (P = 0. 2482) and inferior to the MST (P =
0.0455), and to the PD/MST association (P = 0.0133). The high PCR
sensitivity, and positivity in those cases where the PD was negative,
highlights the importance of this technique as an auxiliary tool for the
diagnosis of ATL.


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PMID: 17083857<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17083857>
TITLE: Sensitivity of leishmanin skin test in patients of acute cutaneous
leishmaniasis.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17083857>
AUTHORS: A Manzur, Arfan ul Bari
AFFILIATION: Department of Dermatology, PAF Hospital Sargodha, Pakistan.
REFERENCE: Dermatol Online J 2006 12(4):2
BACKGROUND: The leishmanin skin test (LST) is frequently used for clinical
diagnosis of cutaneous leishmaniasis (CL). Although, LST is highly sensitive
for CL, no definitive data exists as to how early in the disease does the
test becomes positive. OBJECTIVE: The study was aimed to evaluate the
sensitivity of LST in early cases of CL. PATIENTS AND METHODS: One hundred
male patients with CL of not more than 2-weeks duration and having
parasitologically proven diagnosis were enrolled in this study, carried out
in a military hospital in Balochistan, Pakistan . LST was done by
intradermal injection of 0.1 ml leishmanin on the volar surface of the
forearm. The skin test reaction was read after 48 hours and then at 72 hours
if the first reading was negative or marginal . If the initial test was
negative, the LST was repeated after every 7 days until a positive reaction
was produced. The total time from the onset of skin lesions until a positive
LST was obtained was recorded for every patient. RESULTS: A positive LST was
demonstrated in 78/100 patients with skin lesions of <or= 2 weeks duration,
thus showing a sensitivity of 78 percent for this short duration. The
sensitivity of LST increased to 94 percent and 98 percent for CL lesions of
4 and 6 weeks duration, respectively. CONCLUSION: LST is sensitive even in
those CL patients who present with lesions of very recent onset. Thus the
test can be employed with confidence, for the diagnosis of CL, even in early
disease.


PMID: 17221131<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17221131>
TITLE: Kinetics of growth of *Leishmania* (*Leishmania*) chagasi cycle in
McCoy cell culture.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17221131>
AUTHORS: Yeda L Nogueira, Paulo M Nakamura, Eunice A B Galati
AFFILIATION: Departamento de Epidemiologia, Faculdade de Saúde Pública,
Universidade de São Paulo, Avenida Dr. Arnaldo 715, 01246-902 São Paulo,
SP, Brasil. ynogueir at usp.br
REFERENCE: Rev Inst Med Trop Sao Paulo 2006 Nov-Dec 48(6):337-41
The kinetics of growth of *Leishmania* performed in vitro after
internalization of the promastigote form in the cell and the occurrence of
the transformation of the parasite into the amastigote form have been
described by several authors. They used explants of macrophages in hamster
spleen cell culture or in a human macrophage lineage cell, the U937. Using
microscopy, the description of morphologic inter- relationship and the
analysis of the production of specific molecules, it has been possible to
define some of the peculiarities of the biology of the parasite. The present
study shows the growth cycle of *Leishmania* chagasi during the observation
of kinetic analysis undertaken with a McCoy cell lineage that lasted for a
period of 144 hours. During the process, the morphologic transformation was
revealed by indirect immunofluorescence (IF) and the molecules liberated in
the extra cellular medium were observed by SDS-PAGE at 24-hour intervals
during the whole 144-hour period. It was observed that in the first 72 hours
the promastigote form of L. chagasi adhered to the cell membranes and
assumed a rounded (amastigote-like) form. At 96 hours the infected cells
showed morphologic alterations; at 120 hours the cells had liberated soluble
fluorescent antigens into the extra cellular medium. At 144 hours, new
elongated forms of the parasites, similar to promastigotes, were observed.
In the SDS-PAGE, specific molecular weight proteins were observed at each
point of the kinetic analysis showing that the McCoy cell imitates the
macrophage and may be considered a useful model for the study of the
infection of the *Leishmania*/cell binomial.


PMID: 17226519<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=17226519>
TITLE: Immunostimulant Activity of Picroliv, the Iridoid Glycoside Fraction
of Picrorhiza kurroa, and its Protective Action against
*Leishmania*donovani Infection in
Hamsters1.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17226519>
AUTHORS: A Puri, R P Saxena, P Y Guru, D K Kulshreshtha, K C Saxena, B N
Dhawan
AFFILIATION: ICMR Centre for Advanced Pharmacological Research on
Traditional Remedies, Central Drug Research Institute, Post Box No. 173,
Lucknow 226001 (U.P.), India.
REFERENCE: Planta Med 1992 Dec 58(6):528-32
Picroliv, a standardised fraction from root and rhizome of PICRORHIZA
KURROA, consisting of iridoid glycosides and shown to be responsible for its
hepatoprotective activity, was studied for immunostimulant activity . Oral
administration of Picroliv (10 mg/kg x 7 days) in mice prior to immunization
with sheep red blood cells (SRBC) resulted in a significant increase in
haemagglutinating antibody (HA) titre, plaque forming cells (PFC), and
delayed hypersensitivity (DTH) response to SRBC. Picroliv enhanced the
non-specific immune response characterized by an increase in macrophage
migration index (MMI), [ (14)C]-glucosamine uptake, phagocytosis of [
(14)C]-leucine labelled ESCHERICHIA COLI, chemiluminescence of peritoneal
macrophages, and higher uptake of [ (3)H ]-thymidine in the lymphocytes of
treated mice. It also induced a high degree of protection in golden hamsters
against challenge infection with *LEISHMANIA* DONOVANI promastigotes.


********************************************************************************************************************
The following references are revised files and are brought to you in
accordance to license agreement with the NLM.
********************************************************************************************************************

PMID: 16728320<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=16728320>
TITLE: New world cutaneous leishmaniasis in
travellers.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=16728320>
AUTHORS: Eli Schwartz, Cristoph Hatz, Johannes Blum
AFFILIATION: The Center for Geographic Medicine and Tropical Diseases, Chaim
Sheba Medical Center, Sackler School of Medicine, Tel Aviv University,
Israel. elischwa at post.tau.ac.il
REFERENCE: Lancet Infect Dis 2006 Jun 6(6):342-9
As travel to Latin America has become increasingly common, cutaneous
leishmaniasis is increasingly seen among returning travellers--eg, the
number of observed cases has doubled in the Netherlands and tripled in the
UK in the past decade. A surprisingly high proportion of cases were acquired
in rural or jungle areas of the Amazon basin in Bolivia. The clinical
manifestations range from ulcerative skin lesions (cutaneous leishmaniasis)
to a destructive mucosal inflammation (mucocutaneous leishmaniasis), the
latter usually being a complication of infection with *Leishmania* (Viannia)
braziliensis. PCR is now the diagnostic method of choice, since it has a
high sensitivity and gives a species-specific diagnosis, allowing
species-specific treatment. Treatment of cutaneous leishmaniasis aims to
prevent mucosal invasion, to accelerate the healing of the skin lesion(s),
and to avoid disfiguring scars. Pentavalent antimonials drugs are still the
drug of choice for many patients. However, a high rate of adverse events,
length of treatment, and relapses in up to 25% of cases highlight the
limitations of these drugs. Although only used in a small number of patients
thus far, liposomal amphotericin B shows promising results. Further studies
are needed to find efficacious and better-tolerated drugs for new world
leishmaniasis.


PMID: 15657967<http://refscout.com/cgi-bin/exportAbstract.pl?base=medline-2007-04.xml&id=15657967>
TITLE: Dithiol proteins as guardians of the intracellular redox milieu in
parasites: old and new drug targets in trypanosomes and malaria-causing
plasmodia.<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=15657967>
AUTHORS: R Luise Krauth-Siegel, Holger Bauer, R Heiner Schirmer
AFFILIATION: Universität Heidelberg, Biochemie-Zentrum, Im Neuenheimer Feld
504, D-69120 Heidelberg, Germany. krauth-siegel at urz.uni-heidelberg.de
REFERENCE: Angew Chem Int Ed Engl 2005 Jan 44(5):690-715
Parasitic diseases such as sleeping sickness, Chagas' heart disease, and
malaria are major health problems in poverty-stricken areas. Antiparasitic
drugs that are not only active but also affordable and readily available are
urgently required. One approach to finding new drugs and rediscovering old
ones is based on enzyme inhibitors that paralyze antioxidant systems in the
pathogens. These antioxidant ensembles are essential to the parasites as
they are attacked in the human host by strong oxidants such as
peroxynitrite, hypochlorite, and H2O2. The pathogen-protecting system
consists of some 20 thiol and dithiol proteins, which buffer the
intraparasitic redox milieu at a potential of -250 mV. In trypanosomes and *
leishmania* the network is centered around the unique dithiol trypanothione
(N1,N8-bis(glutathionyl )spermidine). In contrast, malaria parasites have a
more conservative dual antioxidative system based on glutathione and
thioredoxin. Inhibitors of antioxidant enzymes such as trypanothione
reductase are, indeed, parasiticidal but they can also delay or prevent
resistance against a number of other antiparasitic drugs.


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