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Tag words: innate immunity, natural immunity, antimicrobial defense, individual resistance, cellular defense, lysozyme, complement, normal flora, inflammation, inflammatory exudate, phagocytosis, opsonization, neutrophils, macrophages, oxidative burst, mast cells.

Kenneth Todar currently teaches Microbiology 100 at the University of Wisconsin-Madison.  His main teaching interest include general microbiology, bacterial diversity, microbial ecology and pathogenic bacteriology.

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Immune Defense against Bacterial Pathogens: Innate Immunity (page 4)

(This chapter has 6 pages)

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Of all the defense mechanisms in the animal host, the inflammatory response may be the most important for dealing with microbial infection. Inflammation is necessary for the proper functioning of all the host defenses, including the immune defenses, because it focuses all circulating antimicrobial factors on the site of infection. These include phagocytes, lymphocytes, antibodies, complement and other antimicrobial components of plasma. However, inflammation is also an important aspect of bacterial pathogenesis since the inflammatory response induced by a microbe can result in considerable damage to the host and, therefore, be part of the pathology of microbial disease.

Inflammation is a tissue reaction to infection or injury, the characteristic symptoms of which are redness, swelling, heat and pain. These are sometimes called the cardinal signs of inflammation. The redness is due to increased blood flow to the area of injury. The swelling (edema) is due to increased extravascular fluid and phagocyte infiltration to the damaged area. The heat is due to the increased blood flow and the action of pyrogens (fever-inducing agents). The pain is caused by local tissue destruction and irritation of sensory nerve receptors. If a whole organ or tissue is involved, loss of function may occur.

Inflammation can be induced by certain immunological reactions, tissue damage, or the entry of an injurious agent (microbial or nonmicrobial). Certain bacterial cells and/or their products (e.g. structural components or toxins) can induce an inflammatory response. Inflammation increases the blood supply and temperature in the inflamed tissues, which favors maximal metabolic activity of the leukocytes, and lowers the pH slightly, which tends to inhibit the multiplication of many microorganisms.

Inflammation is mediated by mast cells in fixed tissues (the GI tract, respiratory tract, conjunctiva), giving rise to a localized response; or by basophils in the blood giving rise to a systemic response. The response may be initiated in a variety of ways. Some of the main events involved in the induction and maintenance of an inflammatory response during a microbial infection are summarized below.

(1) The inflammatory response is triggered by pathogen invasion or tissue injury. Injured and dying cells release cytoplasmic constituents which lower the pH in the surrounding extracellular environment.

(2) The increased acidity activates an extracellular enzyme kallikrein which in turn activates bradykinin.

(3a) Bradykinin binds to receptors on the capillary walls opening junctions between cells to allow leakage of plasma components collectively referred to as the inflammatory exudate.

Increased capillary permeability allows leukocytes to pass from the vessels into tissues (this process is called diapedisis). The first cells to appear, and the most dominant, are neutrophils, which are actively phagocytic. The other components of the inflammatory exudate and their functions are described in Table 2 below).

(3b) Bradykinin also binds to mast cells of the connective tissue that are associated with the small vessels of most tissues. This initiates other events that are associated with the process of inflammation.

Initially, in the mast cell,  there is a rapid influx of Ca++, intracellular cAMP levels drop, and mediator-rich lysosomal granules migrate to the cell surface, fuse with the cell membrane, and discharge their contents (preformed mediators of inflammation such as histamine, heparin, etc.) to the exterior by exocytosis

The change in mast cell permeability activates an enzyme, phospholipase A2 to synthesize a substance called arachidonic acid. This compound can be acted upon subsequently by the cyclooxygenase pathways or lipooxygenase pathways of the mast cell leading to new synthesis of prostaglandins, leukotrienes, and other mediators of inflammation. These substances contribute to the inflammatory exudate.

Component Function
Bradykinin, histamine, leukotrienes, serotonin, prostaglandins Inflammatory Agents (IA) which act on the vascular system to produce increased blood flow and permeability
Fibrin: (formed from fibrinogen in plasma) coagulates and may localize an invading pathogen
Lysozyme causes lysis of bacterial cell walls
Complement various activities increase the inflammatory response and lead to increased phagocytosis and complement-mediated lysis of cells
Antibodies (in immune individuals) block colonization by pathogens; neutralize microbial toxins or viruses; opsonize pathogens making them more susceptible to phagocytosis; activate complement
Pyrogens, including endogenous pyrogen (Interleukin 1) cause fever acting on the thermo-regulatory control centers in the hypothalamus. (Interleukin-1, which is produced by macrophages, also promotes activation and mitosis of B-cells and T-cells)
Neutrophils migrate to focus of infection and ingest and destroy foreign agents by phagocytosis
Macrophages engulf and destroy infective agents, process antigenic components and convey them to lymphocytes
Immunocompetent lymphocytes (B-cells and T-cells) for direct participation in immunological responses (AMI and CMI)

The overall effect of an inflammatory reaction is to recruit various cells and components to the actual site of microbial invasion. Many of these cells and plasma components have a direct role in defense against the intruding microorganism. These include neutrophils (phagocytes which engulf and destroy the microbes); macrophages and lymphocytes which are the cells necessary to initiate immunological responses against the pathogen; pre-existing antibodies which can neutralize microbial pathogens or their toxins; and plasma components such as lysozyme, complement and fibrin, which have a variety of antimicrobial activities.

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Kenneth Todar has taught microbiology to undergraduate students at The University of Texas, University of Alaska and University of Wisconsin since 1969.

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