Tuberculosis (TB) is a contagious and airborne disease caused by Mycobacterium tuberculosis (M.tb) in human beings. Commonly, the host immune response (IR) controls Mtb replication, which ultimately depends on a fine balance between the pathogen persistence and the specific IR. Cell-mediated immunity plays a major role against TB infection. Regulatory T cells (Tregs) are also relevant in IR and varies throughout the course of TB treatment and its relationship with immuno-endocrine mediators dealing with disease immunopathology. This chronic infection accompanied by prolonged cytokine production, which might affect the immuno-endocrine communication and favor the establishment of an adverse state. Cytokines released by activated immune cells subsequently lead to hormonal secretion from the hypothalamic pituitary-adrenal axis (HPA) or the hypothalamic pituitary-gonadal (HPG) axis, which regulates immune response against the pathogen and the control of the chronic inflammation induced during infection. If the immune response fails to eradicate the pathogen, a chronic state of inflammation is established. Generally, in TB infection, immuno-endocrine alterations changes the interleukin-6, cortisol, estradiol, prolactin and thyroid hormone concentrations in plasma. Moreover, it also changes the interferon gamma (IFN-γ) and transforming growth factor beta (TGF- β) production by lymphoid cells. The present review focuses on the immuno-endocrine interactions that play a detrimental role during TB infection which might affect the control of tissue damage and the protective immune responses.
Keywords:Immune Response, Immune-endocrine mediators, HPA axis, Immuno-endocrine interaction, Chronic inflammation.