The Principal Functions Of Mononuclear Phagocytes

Macrophages play a significant role in host defence mechanisms. When activated, they inhibit the growth of a wide variety of tumour cells and microorganisms [14]. Macrophages phagocytose foreign particles, such as microbes, macromolecules, including antigens, and even self-tissues that are injured or dead, such as senescent erythrocytes.

Phagocytosis is an evolutionarily conserved process utilized by many cells to ingest microbial pathogens, and apoptotic and necrotic corpses. By ingesting microbial pathogens, phagocytes accomplish two essential immune functions. Firstly, they initiate a microbial death pathway, in part by routing ingested pathogens to lysosomes rich in hydrolytic enzymes, and by targeting the phagocyte to oxidize a complex in the phagolysosome. Second, phagocytes, in particular dendritic cells, utilize phagocytosis to direct antigens to both MHCI and II compartments. Thus, phagocytosis serves a dual role: as an innate immune effector, and as a bridge between the innate and acquired immune responses [15]. This phylogenetically conserved process is critical for innate immunity, and mononuclear phagocytes play important roles in the recognition, activation and effector phases of specific immunity. Mononuclear phagocytes also are important participants in the bidirectional interactions between innate and specific immunity. Macrophages that respond to microbes as a reaction of innate immunity also function to trigger microbe-specific lymphocyte responses. Conversely, effector lymphocytes and their products enhance the antimicrobial functions of macrophages.

The phagocytic capacity of the macrophage is determined by the action of a composite of cell surface receptors, which can be classified generally as opsonic-dependent and opsonic-independent [16]. Opsonized pathogens may be recognized and internalized by receptors of the Fc portion of immunoglobulin, iC3b, and/or fibronectin. In the absence of opsonization, the clearance of micro-organisms, including Candida sp., Cryptococcus neoformans, Pseudomonas aeroginosa, Pneumococcus carnii, Neiseria sp., Leischmanisa sp., Histoplasma sp., and Mycobacterium sp., has been shown to be accomplished by lectinophagocytosis through the action of macrophage mannan and c-glucan receptors.

Macrophages produce cytokines that recruit other inflammatory cells, especially neutrophils, and are responsible for many of the systemic effects of inflammation, such as fever. One of the most potent inducers of these macrophage responses is a bacterial cell wall component called endotoxin [17], which binds to a macrophage surface molecule called CD14. Macrophages also produce growth factors for fibroblasts and vascular endothelium that promote the repair of injured tissues. Activated macrophages secrete proteolytic enzymes, active metabolites of oxygen (including superoxide anion and other oxygen radicals), arachidonic acid metabolites, cyclic adenosine monophosphate (cAMP), and cytokines such as interleukin-1 (IL-1), IL-6, IL-8 and tumour necrosis factor-a (TNF-a), among others. Many tissue-specific cells arc of macrophage lineage, and function to process and present antigen (e.g. Langerhans cells, oligodendrocytes, etc.).

Neutrophils, monocytes, and tissue-based macrophages are major cellular components of the innate immune system, which serve as the initial line of host defence against infections by pathogenic bacteria, fungi and parasites. Cytokines such as granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF), and interferon (IFN)-yhave received increasing attention as potential adjunctive immunomodulatory agents for the treatment of infectious diseases. In vitro and in vivo studies have shown that G-CSF, GM-CSF and IFN-y can augment the functional antimicrobial activities of neutrophils [17,18].

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