Interaction of Inflammatory Molecules in Tuberculosis and Sars Cov-2 Infection

The Hyper-inflammatory immune response is a chief reason for disease severity and mortality in patients. Generally, macrophages and dendritic cells sense and react to microbial or viral invasion by making inflammatory molecules that remove pathogens and help in tissue repair. During tuberculosis infection, alveolar macrophages activate alveolar dendritic cells, which move to lymph nodes. In lymph nodes, the proliferation of CD4+ T cells, CD8+ cells and γδ T cells occur. Mycobacterium tuberculosis (MTB) bacteria further modify the host's immune system for their long survival period. Meanwhile, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infects alveolar macrophages and releases inflammatory cytokine to produce and activate T-cells. MTB and SARS-CoV-2 infections together lead to an increase in the rate of pathogenesis. This type of co-infection in macrophages causes the production of pro- and anti-inflammatory cytokines, which further play an important role in immune-pathogenesis. However, the abnormal or dysregulated response of macrophages leads to harmful effects of the host, as observed in the macrophage activation syndrome induced by severe infections, including the virus SARSCoV-2. Unlike macrophages, dendritic cells (DCs) act as antigen presenting cells. They connect innate and adaptive immunity cells. They are susceptible to cytokine-mediated activation and lead to cytokine production. The cytokine Interleukin-6 (IL6) is an important and unique molecule that can act pro- as well as anti-inflammatory and helps in the development and differentiation of macrophages associated with numerous inflammatory diseases. In this review paper, we have emphasized the vital pathological role of macrophages, dendritic cells and IL-6 in tuberculosis and SARS-CoV-2 infection and prospective therapeutic strategies based upon IL-6 as the main target for preventing the cytokine storm and associated organ failure.