Macrophages in Inflammation

Abstract

The inflammatory process is usually tightly regulated, involving both signals that initiate and maintain inflammation and signals that shut the process down. An imbalance between the two signals leaves inflammation unchecked, resulting in cellular and tissue damage. Macrophages are a major component of the mononuclear phagocyte system that consists of closely related cells of bone marrow origin, including blood monocytes, and tissue macrophages. From the blood, monocytes migrate into various tissues and transform macrophages. In inflammation, macrophages have three major function; antigen presentation, phagocytosis, and immunomodulation through production of various cytokines and growth factors. Macrophages play a critical role in the initiation, maintenance, and resolution of inflammation. They are activated and deactivated in the inflammatory process. Activation signals include cytokines (interferon gamma, granulocyte-monocyte colony stimulating factor, and tumor necrosis factor alpha), bacterial lipopolysaccharide, extracellular matrix proteins, and other chemical mediators. Inhibition of inflammation by removal or deactivation of mediators and inflammatory effector cells permits the host to repair damages tissues. Activated macrophages are deactivated by anti-inflammatory cytokines (interleukin 10 and transforming growth factor beta) and cytokine antagonists that are mainly produced by macrophages. Macrophages participate in the autoregulatory loop in the inflammatory process. Because macrophages produce a wide range of biologically active molecules participated in both beneficial and detrimental outcomes in inflammation, therapeutic interventions targeted macrophages and their products may open new avenues for controlling inflammatory diseases.

Anti‐inflammatory and anti‐insulin resistance activities of aqueous extract from Anoectochilus burmannicus

“…It is noteworthy that effective therapeutic agents on controlling a variety of inflammatory diseases mostly target macrophages and their products (Fujiwara & Kobayashi, 2005). Many studies have extensively focused on anti‐inflammation and metabolic syndrome.…”

Lung carcinogenesis induced by chronic tuberculosis infection: the experimental model and genetic control

“…Formation and maintenance of the granulomas are mediated by an active immune response and require the production of interferon-g and other cytokines by antigen-specific T lymphocytes. Subsequent macrophage activation by combination of cytokines and mycobacterial products results in the massive local production of reactive nitrogen and oxygen species, prostaglandins, proteases and inflammatory cytokines representing an attempt of the host to clear the bacteria (Fujiwara and Kobayashi, 2005;Russell, 2007;Saunders and Britton, 2007), which may also cause an extensive host tissue damage. Unfolding tissue repair processes lead to a varying degree of fibrosis in the vicinity of granulomas.…”

Pulmonary intravascular monocytes/macrophages in a rat model of sepsis

“…Precise reasons for enhanced susceptibility for lung injury following a secondary microbial challenge are not well understood. Because activated monocytes and macrophages can produce inflammatory mediators (Fujiwara and Kobayashi, 2005), we speculated that recruited PIMMs may contribute to increased susceptibility for lung inflammation following a secondary challenge in a rat model of sepsis. Therefore, the objectives of our study were to characterize recruited PIMMs in sepsis and their contributions to lung inflammation following a secondary challenge with E. coli lipopolysachharide (LPS).…”