Literature DB >> 26989708

Comparison of Th1 and Th2 responses in non-healing and healing patients with cutaneous leishmaniasis.

Maryam Shahi1, Masoud Mohajery2, Seyyed Ali Akbar Shamsian2, Hossein Nahrevanian3, Seyyed Mohammad Javad Yazdanpanah2.   

Abstract

BACKGROUND: Cutaneous leishmaniasis is an endemic disease in many regions of Iran, including the city of Mashhad. In recent years, some cases have not responded to Glucantime, the usual treatment for this disease. The cellular immune response caused by T-helper type 1 (Th1) cells has an important role in protection against leishmaniasis, and activation of the T-helper type 2 (Th2) response causes progression of the disease. By analyzing these responses we hope to find a more effective treatment than that currently in use for leishmaniasis patients.
METHODS: The cellular immune responses in 60 cases of non-healing and healing cutaneous leishmaniasis, and individuals in a control group, were analyzed by measuring cytokines released by peripheral blood mononuclear cells (PBMCs) when stimulated with Leishmania major antigens by Enzyme Linked Immuno Sorbent Assay (ELISA).
RESULTS: Subjects from the healing group secreted more interleukin-12 (IL-12) and interferon gamma (IFN-γ) (p<0.05) and less interleukins -4, -5, -10 (IL-4, IL-5, and IL-10) (p<0.005) and -18 (IL-18) (p=0.003) than the non-healing group.
CONCLUSIONS: The results demonstrate that secretion of cytokines that activate Th2 response including IL-4, IL-5 and IL-10 in non-healing subjects was higher than healing subjects and secretion of cytokines that activate Th1 response including IL-12 and IFN-γ in healing subjects was higher relative to the non-healing subjects. In this study it has been shown that the level of IL-18 progresses disease in non-healing patients when the level of IL-12 gets decreased.

Entities:  

Keywords:  Cutaneous leishmaniasis; Cytokines; Glucantime

Year:  2013        PMID: 26989708      PMCID: PMC4757055     

Source DB:  PubMed          Journal:  Rep Biochem Mol Biol        ISSN: 2322-3480


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