Bacterial Capsules and Evasion of Immune Responses

Bacterial surfaces include various structures that activate host defense and thus induce a host immune response. Bacterial capsules are one of the outermost structures on the surface of bacteria, which can completely encompass all antigenic molecules or can be co-expressed with other bacterial antigens. They include a wide range of biological processes such as prevention of drying, adhesion, and resistance to nonspecific and specific host immunity.

Gram-negative and gram-positive capsular polysaccharides contribute to bacterial tolerance to host's immune response through different mechanisms. In general, capsular polysaccharides that obscure the underlying cell surface structure are weakly activated or inactivated in all immune systems, while bacterial capsules co-expressed with other bacterial antigens activate the immune system , Cover the conditioning and interfere with the complement attack complex. Formation and phagocytosis.

Bacterial capsules completely enclose bacterial cells and enhance the ability of bacteria to cause disease

Polysaccharides are polymeric carbohydrate structures formed by repeating units of one or more sugar residues joined together by glycosidic linkages.

Antigenic mutations alter the surface structure of microorganisms and allow them to overcome the immune response

Phagocytosis is the process by which specific cells called phagocytes phagocytose and digest solid particles as bacteria.

The complement system is part of the innate immune system and consists of a number of small plasma proteins that circulate as inactive precursors and are linked as opsonin after their activation.

Key words: bacterial capsule, polysaccharide, antigen mutation, phagocytosis avoidance, supplementary tolerance

Extracellular enzymes and toxins can act as an attacking force to destroy the physical barrier, destroy the host cell and avoid phagocytosis and other innate immune defense. The bacterial capsule or alginate layer will also circumvent bacterial cells from antibody, complement and phagocytosis mediated antibody killing. Two extracellular proteases (elastase and alkaline protease) are closely related to toxicity during early invasion. Elastase regulates some toxic activity by cleaving collagen, IgG, IgA and complement. By cleavage of fibrin, elastase destroys respiratory epithelial cells and impair ciliary function. Alkaline protease destroys the formation of fibrin and dissolves fibrin. Thus, elastase and alkaline protease may destroy the base of the cornea and other support structures composed of fibrin and elastin.

Bacterial surfaces include various structures that activate host defense and thus induce a host immune response. Bacterial capsules are one of the outermost structures on the surface of bacteria, which can completely encompass all antigenic molecules or can be co-expressed with other bacterial antigens. They include a wide range of biological processes such as prevention of drying, adhesion, and resistance to nonspecific and specific host immunity.

Gram-negative and gram-positive capsular polysaccharides contribute to bacterial tolerance to host's immune response through different mechanisms. In general, capsular polysaccharides that obscure the underlying cell surface structure are weakly activated or inactivated in all immune systems, while bacterial capsules co-expressed with other bacterial antigens activate the immune system , Cover the conditioning and interfere with the complement attack complex. Formation and phagocytosis.

Bacterial pathogenic factors such as glycocalyx and various adhesins enable colonization in the host, immune evasion and establishment of disease. Septicemia caused by gram-negative bacteria is thought to be caused mainly by the reaction of the host to the lipid A component of lipopolysaccharide (also known as endotoxin). Septicemia caused by gram-positive bacteria may be caused by an immune reaction against cell wall lipoteichoic acid. Bacterial exotoxins as superantigens may also cause sepsis. In the absence of antigen presentation, the superantigen binds to both the major histocompatibility complex and the T cell receptor. This mandatory receptor interaction induces T cells to produce pro-inflammatory chemical signals (cytokines)