Infection immunity: bacterial, virus, parasites and fungus
Posted by beauty33 on May 28th, 2019
Immunity to Bacteria
Extracellular bacteria are capable of replicating outside host cells, for example, in the blood, in connective tissues, and in tissue spaces such as the lumens of the airways and gastrointestinal tract. Many different species of extracellular bacteria are pathogenic, and disease is caused by two principal mechanisms. First, these bacteria induce inflammation, which results in tissue destruction at the site of infection. Second, bacteria produce toxins, which have diverse pathologic effects. The toxins may be endotoxins, which are components of bacterial cell walls, or exotoxins, which are secreted by the bacteria. The endotoxin of gram-negative bacteria, also called lipopolysaccharide (LPS), is a potent activator of macrophages, dendritic cells, and endothelial cells. Many exotoxins are cytotoxic, and others cause disease by various mechanisms. For instance, diphtheria toxin shuts down protein synthesis in infected cells, cholera toxin interferes with ion and water transport, tetanus toxin inhibits neuromuscular transmission, and anthrax toxin disrupts several critical biochemical signaling pathways in infected cells. Other exotoxins interfere with normal cellular functions without killing cells, and yet other exotoxins stimulate the production of cytokines that cause disease.
The principal mechanisms of innate immunity to extracellular bacteria are complement activation, phagocytosis, and the inflammatory response.
Complement activation: Peptidoglycans in the cell walls of Gram-positive bacteria and LPS in Gram-negative bacteria activate complement by the alternative pathway. Bacteria that express mannose on their surface may bind mannose-binding lectin, which activates complement by the lectin pathway. One result of complement activation is opsonization and enhanced phagocytosis of the bacteria. In addition, the membrane attack complex generated by complement activation lyses bacteria, Phagocytes and inflammation: Phagocytes (neutrophils and macrophages) use surface receptors, including mannose receptors and scavenger receptors, to recognize extracellular bacteria, and they use Fc receptors and complement receptors to recognize bacteria opsonized with antibodies and complement proteins, respectively. In addition, dendritic cells and phagocytes that are activated by the microbes secrete cytokines, which induce leukocyte infiltration into sites of infection (inflammation). The recruited leukocytes ingest and destroy the bacteria.
Humoral immunity is a major protective immune response against extracellular bacteria, and it functions to block infection, to eliminate the microbes, and to neutralize their toxins. Antibody responses against extracellular bacteria are directed against cell wall antigens and secreted and cell-associated toxins, which may be polysaccharides or proteins.
Figure 1. Adaptive immune responses to extracellular microbes. Adaptive immune responses to extracellular microbes such as bacteria and their toxins consist of antibody production and the activation of CD4+ helper T cells.
A characteristic of facultative intracellular bacteria is their ability to survive and even to replicate within phagocytes. Because these microbes are able to find a niche where they are inaccessible to circulating antibodies, their elimination requires the mechanisms of cell-mediated immunity.
The innate immune response to intracellular bacteria is mediated mainly by phagocytes and natural killer (NK) cells. Intracellular bacteria activate NK cells by inducing expression of NK cell–activating ligands on infected cells and by stimulating dendritic cell and macrophage production of IL-12 and IL-15, both of which are NK cell activating cytokines. The NK cells produce IFN-γ, which in turn activates macrophages and promotes killing of the phagocytosed bacteria. Thus, the NK cells provide an early defense against these microbes, before the development of adaptive immunity. (Figure 2a)
The major protective immune response against intracellular bacteria is T cell–mediated recruitment and activation of phagocytes (cell-mediated immunity). Phagocytosed bacteria stimulate CD8+ T cell responses if bacterial antigens are transported from phagosomes into the cytosol or if the bacteria escape from phagosomes and enter the cytoplasm of infected cells. In the cytosol, the microbes are no longer susceptible to the microbicidal mechanisms of phagocytes, and for eradication of the infection, the infected cells have to be killed by CTLs.
Figure 2 Innate and adaptive immunity to intracellular bacteria.
Immunity to Virus
Viruses are obligatory intracellular microorganisms that use components of the nucleic acid and protein synthetic machinery of the host to replicate and spread. Viruses typically infect various cell types by using normal cell surface molecules as receptors to enter the cells. After entering cells, viruses can cause tissue injury and disease by any of several mechanisms.
The principal mechanisms of innate immunity against viruses are inhibition of infection by type I interferons and NK cell–mediated killing of infected cells. NK cells kill other cells infected with a variety of viruses and are an important mechanism of immunity against viruses early in the course of infection, before adaptive immune responses have developed (Figure 3a).
Adaptive immunity against viral infections is mediated by antibodies, which block virus binding and entry into host cells, and by CTLs, which eliminate the infection by killing infected cells. Antibodies are effective against viruses only during the extracellular stage of the lives of these microbes. Viruses may be extracellular early in the course of infection, before they infect host cells, or when they are released from infected cells by virus budding or if the infected cells die. Antiviral antibodies bind to viral envelope or capsid antigens and function mainly as neutralizing antibodies to prevent virus attachment and entry into host cells. Elimination of viruses that reside within cells is mediated by CTLs, which kill the infected cells. The principal physiologic function of CTLs is surveillance against viral infection.
Article source: https://www.creative-diagnostics.com/Infection-Immunity.htm
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About the Authorbeauty33
Joined: July 10th, 2017
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