Cytokine gene polymorphisms in type I and type II reactions in Hansen's disease.

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Date: Sept-Oct 2020
Publisher: Medknow Publications and Media Pvt. Ltd.
Document Type: Article
Length: 3,932 words
Lexile Measure: 1280L

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Byline: Vijendran. Pragasam, Biju. Vasudevan, Nikhil. Moorchung

Introduction: Leprosy or Hansen's disease is a chronic debilitating disease caused by Mycobacterium leprae. Host genetics are believed to strongly influence the course of the disease. It is known that cytokines play an important role in leprosy and cytokine gene polymorphisms probably influence the course of the disease. Methods: In the present study, we evaluated 70 patients with leprosy and 243 controls. DNA was extracted from the peripheral blood and genotyping was done for the following polymorphisms: IL-1 RA intron 2, IL-1ß-511 C/T and TNF-a A/G. Results: A strong association of TNF-a-308 G/A polymorphism with Hansen's disease with both genotypes and alleles was found. However, no correlation was identified between the other two polymorphisms and Hansen's disease. A strong association between the IL-1ß gene polymorphisms and the type of reactions seen in leprosy was found. In contrast, the other two polymorphisms did not show any such association. Limitations: Genetic polymorphisms are association studies. They are not a direct reflection of the transcriptome or proteome and this is a major limitation of this study. Conclusion: In conclusion, cytokine gene polymorphisms appear to influence the susceptibility and course of Hansen's disease. An evaluation of the cytokine levels in the skin during lepra reactions would confirm this observation. Possibly, in future, this would be a guide to therapeutic decisions in cases of lepra reactions.

Introduction

Leprosy or Hansen's disease is a chronic debilitating disease caused by an obligate intracellular pathogen-- Mycobacterium leprae ( M. leprae ). The clinical spectrum of the disease varies and it depends on the host immunity; one pole is tuberculoid leprosy in which the patients have a strong cellular immune response and the other pole is lepromatous leprosy (LL) where patients have a limited cellular immune response leading to a disseminated disease with diffuse infiltration of skin and nerves and bacilli-loaded foamy macrophages. Between the two poles, the majority of patients are borderline classified as borderline tuberculoid (BT), mid-borderline (BB) or borderline lepromatous (BL).[1],[2]

Factors influencing the type of leprosy are not well understood. Host genetics are believed to strongly influence the course of the disease. Cytokines play a critical role in triggering host-pathogen interaction in leprosy. The onset of tuberculoid leprosy is correlated with cytokine production by Th1 cells (IFN a productions) and lepromatous leprosy is correlated with a Th 2 response (IL-4 production). Besides IFN and IL-4, other cytokines produced by T cells such as tumor necrosis factor-alpha (TNF-a), IL-6 and IL-10 and by macrophages such as IL-1 family also regulate M. leprae cell-mediated and humoral immune responses.[3],[4],[5],[6],[7]

Leprosy reactions are immune inflammatory-related phenotypes that may occur before diagnosis, during treatment or after Multi Drug Therapy (MD T). Lepra reactions require immediate treatment to prevent permanent disabilities. There are 2 major types of lepra reactions. Type I reaction is characterized by acute inflammation of preexisting skin lesions or by the appearance of new lesions and/or neuritis. Systemic symptoms are rare. Type I reactions are seen in patients who have an...

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Gale Document Number: GALE|A633604974