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Immunologic Defences Against Extracellular Microorganisms

Immunologic Defences Against Extracellular Microorganisms

 Many organisms exist primarily in an extracellular environment, whether in the circulation or within infected tissues. The immunologic systems attack such organisms in three ways: phagocytosis , inacti­vation of toxins, and bacteriolysis. 

Phagocytosis: Phagocytosis is the principal host mechanism for elimination of most microorganisms, and was first recognized by Metchnikoff in 1882. Neutrophils (polymorphonuclear leucocytes) and macrophages arc the principal cells involved in phagocytosis, and both of them are derived from a common stem cell in the bone marrow. Neutrophils are short lived cells and survive in tissues for only a few days. Macrophages, unlike the neutrophils, are long-lived and can persist in tissues for weeks and months. Most macrophages that are found in tissues come from blood monocytes which migrate from the blood into tissues.

Two types of mature macrophages are recognized: 1. Those wandering in tissues and body spaces (e. g. alveolar and peritoneal macrophages) and 2.Those fixed to vascular endothelium (e. g. Kupffer cells and fixed macrophages of the spleen and lymph nodes). The phagocytic process may be divided into two phases: 1. Attachment of the microorganisms to the cell membrane and 2. Injection and destruction of microorganisms: The mechanism by which phagocytic cells are attracted to injured tissue or invading microorganisms probably involves chemo­taxis. Chemotactic factors are either released from immune T-lymphocytes , or formed from complexes or cleavage products of complement components. Some organisms are easily attached, for example, Mycobacteria and Listeria. Others arc not attached easily and consequently are phagocytized with great difficulty. Many of these, for example, Streptococcus pneumoniae and Klebsiella pneumoniae, can only be phagocytized if the phagocyte traps the organism on a rough surface where it cannot slide away, and can be injected without prior attachment.

This is called surface phagocytosis. In the majority of cases the microbial surface is first coated with an antibody promoting its attachment to the phagocytic cell membrane, This is called opsonization. Opsonins are specific antibodies directed against the surface antigens of microorganisms which render microbial surfaces sticky, so that they are easily engulfed by phagocytic cells. After attachment, the phagocyte extends small pseudopods around the organism. These fuse and form a pouch which contains the organism surrounded by the cell membrane. This structure is now called a phagosome. Engulfment is followed by a process known as degranulation. The lysosomes containing hydrolytic enzymes and bactericidal substances fuse with the phagosome and discharge their contents. This Structure is now called the phagolysosome.

Within the phagolysosome the microorganism is attacked by degradative enzymes and digested. The process of phagocytosis is an energy-requiring one. In neutrophils and most macrophages, energy is obtained by glycolysis. Other macrophages, such as alveolar macrophages, utilize aerobic oxidative mechanisms for energy production. How microbial cells are killed is not precisely known. Enzymes involved are lysozyme, alkaline phosphatase, ribonuclease, and β-glucuronidase. Other antimicrobial substances present in phagocytes include basic protein, lactic acid and lactoferrin. Another, as yet poorly characterized protein, called phagocytin, is also thought to be active in the phagocytic killing process. One intracellular microbicidal mechanism studied in some detail is the myeloperoxidase system. This system involves the production of a highly reactive oxygen molecule called the singlet oxygen (0) by the oxidation of chloride ions in presence of excess peroxide. This is highly unstable and reacts with microbial constitnents, exerting microbicidal activity.

Inactivation of toxins:The pathogenic effects of some organisms are due to the production of soluble exotoxins. These toxins are highly antigenic and evoke antitoxins. The toxins, stimulate IgQ ( IgM, and , IgA production. However, only IgA can inactivate the biologic activity of most, exotoxins. The antibody binds to the toxin and blocks the binding of toxin to its substrate. Inactivation of endotoxins is not clearly understood. Endotoxins will initial1y stimulate increased phagocytic activity by reticuloendo­thelial cells and leucocytes. However, the reticuloendothelial system rapidly removes endotoxins from the blood, and thereby cells-are damaged. Thus, phagocytic activity as well as antibody formation is temporarily suppressed. Some endotoxins, like those of the plague bacillus Yesinia pestis, do induce inactivating antibody. Salmonella lipopolysaccharides (LPS) endotoxin is a potent activator of the, alternate complement (properdin) pathway, and there is some evidence that this is facilitated by the natural antibody to LPS. Complement mediated opsonization may thus occur. This explains the nonimmune clearance of LPS by the reticuloendothelial system.

Bacteriolysis: A specific antibody with complement can bring about the lysis of infecting organisms, especially gram negative bacilli. IgG or IgM can generate such lytic complement activity. IgA can activate the terminal complement components through the properdin pathway, but requires the additional presence of lysozyme to effect bacteriolysis. Immune lymphocytes and some lymphokines can directly destroy cells, and may thus bring about bacteriolysis.

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