Macrophage Polarization Is Decisive for Chronic Bacterial Infection-Induced Carcinogenesis

Abstract

Macrophages are the special cells of the immune system and play both immu-nological and physiological role. One of the peculiar characteristics of macrophages is that they are double-edged and highly plastic component of immune system. Due to this characteristic, they are responsible for both progressions as well control of a variety of inflammatory, infectious and metabolic diseases and cancer. These are found in the body in three major phenotypes, which are known as M0 (also known as naïve); M1 (classically activated macrophages); and/or M2 (alternatively activated macrophages) at normal physiological conditions. We have been exploring macrophages in context of bacterial infection and previ-ously demonstrated that M2 polarization of M1 effector alveolar macrophages during chronic/persistent Chlamydia pneumonia , Mycobacterium tuberculosis and Helicobacter pylori pathogens are decisive for the infection induced cancer development in host. Since chronic infection with these pathogens has been associated with adenocarcinoma, therefore, we feel that disruption of macrophage plasticity plays crucial role in the host for the development of cancer. On the basis of this, we propose that in such pathological conditions, management of M1/M2 imbalance is paramount for minimizing the risk of developing cancer by chronic and persistent infection. macrophage for subverting effector mechanisms during latency. Pathogenic bacteria interfere with various key signaling pathways which are important for the effector responses, e.g., recognition by receptors, uptake, and phagocytosis, lysosomal degradation, and alter signaling pathways and secretion of Th1 cytokines for establishing Th2 bias.