Role of macrophages in prevention and control of diseases and their upregulation through cowpathy

Abstract

Mammalian macrophages are present from mid gestation onwards, helping to maintain physiologic homeostasis. During embryonic development in the mouse, macrophages emerge from yolk sac and foetal liver progenitors and survive as diverse, self-renewing tissue-resident populations in many organs. After birth, bone marrow-derived blood monocytes are recruited to replenish tissue resident populations and to meet additional demands during inflammation, infection, and metabolic changes. Signals that generate and maintain inflammation, as well as signals that shut down the process, are normally controlled carefully in the inflammatory process. Inflammation goes uncontrolled when the two signals are out of sync, causing cellular and tissue damage. Macrophages are a key component of the mononuclear phagocyte system, which includes blood monocytes and tissue macrophages. Monocytes travel from the bloodstream into various organs and convert into macrophages. Antigen presentation, phagocytosis, and immunomodulation through the production of different cytokines and growth factors are three key functions of macrophages in inflammation. Macrophages are critical in the onset, maintenance, and resolution of inflammation. During the inflammatory process, they are activated and deactivated. Cytokines (interferon, granulocyte-monocyte colony stimulating factor, and tumour necrosis factor), bacterial lipopolysaccharide, extracellular matrix proteins, and other chemical mediators are all examples of activation signals. The elimination or deactivation of mediators and inflammatory effector cells inhibits inflammation, allowing the host to heal damaged tissues. Anti-inflammatory cytokines (interleukin 10 and transforming growth factor ß) and cytokine antagonists, which are primarily generated by macrophages, deactivate active macrophages. Macrophages are involved in the inflammatory process' autoregulatory loop. We outline macrophage activities in inflammation and healing in response to