| Evaluation of localized and systemic immune responses in cutaneous leishmaniasis caused by Leishmania tropica: interleukin-8, monocyte chemotactic protein-1 and nitric oxide are major regulatory factors. | |
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MedLine Citation:
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PMID: 20102417 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We have established Leishmania tropica as the causative agent of cutaneous leishmaniasis (CL) in the region of India where the disease is endemic. The association between localized and circulating levels of immune-determinants in CL patients was evaluated. Reverse transcription-polymerase chain reaction analysis revealed up-regulation of interferon-gamma (IFN-gamma), interleukin (IL)-1beta, IL-8, tumour necrosis factor-alpha (TNF-alpha), IL-10 and IL-4 in dermal lesions at the pretreatment stage (n = 31) compared with healthy controls (P < 0.001) and a significant down-regulation after treatment (n = 14, P < 0.05). The results indicated that an unfavourable clinical outcome in CL was not related to an inadequate T helper 1 (Th1) cell response, but rather to impairment in multiple immune functions. Comparative assessment of treatment regimes with rifampicin (RFM) or sodium antimony gluconate (SAG) revealed tissue cytokine levels to be significantly reduced after treatment with RFM (P < 0.005), while no significant decrease was evident in the levels of IFN-gamma, TNF-alpha and IL-10 (P > 0.05) as a result of treatment with SAG. Increased transcripts of monocyte chemoattractant protein-1 (MCP-1) (P < 0.001) and inducible nitric oxide synthase (iNOS) (P < 0.05) were evident before treatment in tissue lesions and remained high after treatment. Immunohistochemistry demonstrated strong expression of myeloperoxidase (MPO) and IL-8, and moderate expression of iNOS in dermal lesions. The expression levels of IL-8, MCP-1 and nitric oxide (NO) were high in patient sera before treatment, as determined using cytokine bead array and enzyme-linked immunosorbent assay (ELISA). At the post-treatment stage, the serum IL-8 levels had decreased; however, the levels of MCP-1 and NO remained high. These data suggest that IL-8 is an effector immune-determinant in the progression of CL, whereas NO facilitates the parasite killing by macrophages via MCP-1-mediated stimulation. |
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Authors:
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Rajesh Kumar; Ram A Bumb; Poonam Salotra |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-01-22 |
Journal Detail:
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Title: Immunology Volume: 130 ISSN: 1365-2567 ISO Abbreviation: Immunology Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-06-18 Completed Date: 2010-07-09 Revised Date: 2011-10-27 |
Medline Journal Info:
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Nlm Unique ID: 0374672 Medline TA: Immunology Country: England |
Other Details:
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Languages: eng Pagination: 193-201 Citation Subset: IM |
Affiliation:
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Institute of Pathology (ICMR), Safdarjung Hospital Campus, New Delhi. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adolescent Adult Antimony Sodium Gluconate / administration & dosage Antiprotozoal Agents / administration & dosage Chemokine CCL2 / blood, immunology* Child Child, Preschool Female Humans India / epidemiology Interferon-gamma / blood, immunology Interleukin-10 / blood, immunology Interleukin-4 / blood, immunology Interleukin-8 / blood, immunology* Leishmania tropica / immunology*, metabolism Leishmaniasis, Cutaneous / blood, drug therapy, epidemiology, immunology* Macrophages / immunology*, metabolism, pathology Male Middle Aged Nitric Oxide / blood, immunology Nitric Oxide Synthase Type II / biosynthesis, immunology Nucleic Acid Synthesis Inhibitors / administration & dosage Peroxidase / biosynthesis, immunology Retrospective Studies Rifampin / administration & dosage Th1 Cells / immunology, metabolism, pathology Tumor Necrosis Factor-alpha / blood, immunology Up-Regulation / drug effects, immunology* |
| Chemical | |
Reg. No./Substance:
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0/Antimony Sodium Gluconate; 0/Antiprotozoal Agents; 0/CCL2 protein, human; 0/Chemokine CCL2; 0/IL10 protein, human; 0/IL4 protein, human; 0/IL8 protein, human; 0/Interleukin-8; 0/Nucleic Acid Synthesis Inhibitors; 0/Tumor Necrosis Factor-alpha; 10102-43-9/Nitric Oxide; 130068-27-8/Interleukin-10; 13292-46-1/Rifampin; 207137-56-2/Interleukin-4; 82115-62-6/Interferon-gamma; EC 1.11.1.7/Peroxidase; EC 1.14.13.39/NOS2 protein, human; EC 1.14.13.39/Nitric Oxide Synthase Type II |
| Comments/Corrections | |
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