Research Projects

Tuberculosis (TB) is a communicable disease caused by Mycobacterium tuberculosis(M.tb), and it infects 1/3rd of the population all over the world and only 10-15% of the individuals will develop active disease in their lifetime and household contacts (HHCs) of TB patients are at higher risk1 Both innate and acquired immune responses play a role in host defense mechanism against M.tb which involves an inflammatory reactions. When the pathogen is not eliminated by the initial response then a multiple metabolic and neuroendocrine changes takesplace and releases proinflammatory cytokines which further allows for the secretion of Corticotropin-releasing hormone(CRH) in hypothalamus. The CRH release into the hypophyseal portal stimulates the secretion of adrenocorticotropin hormone (ACTH) from anterior pituitary gland and it reaches adrenal glands and synthesis further for the release of glucocorticoids (GCs) and adrenal androgens-dehydroepiandrosterone (DHEA)2,3,4. The high ratio of cortisol/DHEA will change the concentration of gonadal steroids which may lead to imbalance of Th1 (IFN-γ, IL-6)/Th2↑ ( IL-4, TGF-β) cytokine pathway which is affecting the control of infection. The present study is proposed to demonstrate the importance of immunoendocrine changes in TB patients & HHCs in TB pathogenesis.