Info

— Diplococcus

5 mm

— Diplococcus

5 mm

Figure 19.10 Capsules Can Prevent Phagocytosis The polysaccharide capsule of Streptococcus pneumoniae prevents phagocytosis. Antibodies that bind to the capsule allow phagocytosis to occur.

have Fc receptors are able to coat themselves with antibody molecules in a manner that obscures the cell from phagocytes. The phagocytic cell has no mechanism for recognizing the Fab region, which will be projecting outward on these cells.

Surviving Within the Phagocyte

Some bacteria make no attempt to avoid engulfment, instead using phagocytosis as an opportunity. It allows them to hide from antibodies, control some aspects of the immune response, and

19.7 Avoiding the Host Defenses 471

obtain a "free ride" to other locations in the body. Mechanisms used to survive within phagocytes include:

■ Escape from the phagosome. Some bacteria are able to escape from the phagosome before it fuses with the lysosome; these organisms are then able to multiply within the cytoplasm of the phagocyte, protected from other host defenses. Listeria monocytogenes, for example, produces a molecule that is activated to form pores in membranes once inside the phagosome, allowing the bacteria to escape to the cytoplasm. Shigella species are also able to lyse the phagosome before it fuses with the lysosome.

■ Preventing phagosome-lysosome fusion. Bacteria that prevent phagosome-lysosome fusion avoid the otherwise inevitable exposure to the degradative enzymes and other toxic components of the lysosome. Salmonella species are able to sense they have been ingested by a macrophage, and respond by producing a protein that blocks the fusion process.

■ Surviving within the phagolysosome. Relatively few organisms are able to survive the destructive environment within the phagolysosome. Coxsiella burnetii, however, an obligate intracellular parasite that causes Q fever, is able to withstand the conditions. It appears that once the organism has been ingested by a macrophage, it can delay the fusion of the phagosome with the lysosome, allowing it additional time to equip itself for growth within the phagolysosome.

Staphylococcus epidermidis

IgG antibody

Fc portion

Phagocytosis of S. epidermidis begins

w Epitopes U

IgG antibody

w Epitopes U

Fc portion

Phagocytosis of S. epidermidis begins

Figure 19.11 Foiling Opsonization by Antibodies (a) The host's intended orientation of antibody molecules on the surface of a bacterium (in this case, Staphylococcus epidermidis); note that the Fc region projects from the bacterial cell, making it available for the phagocyte to recognize and engage. (b) The effect of Fc receptors on a bacterial cell's surface; the receptors reverse the host's intended orientation of the antibody on the cell, preventing the Fc region from interacting with the phagocytic cell.

Stappyhyccccuu. aareeu

IgG antibody

Fc portion'

Fc receptors

Stappyhyccccuu. aareeu

Fc portion of IgG is not available for receptor

IgG antibody

Fc portion'

Fc receptors

Fc portion of IgG is not available for receptor

Figure 19.11 Foiling Opsonization by Antibodies (a) The host's intended orientation of antibody molecules on the surface of a bacterium (in this case, Staphylococcus epidermidis); note that the Fc region projects from the bacterial cell, making it available for the phagocyte to recognize and engage. (b) The effect of Fc receptors on a bacterial cell's surface; the receptors reverse the host's intended orientation of the antibody on the cell, preventing the Fc region from interacting with the phagocytic cell.

472 Chapter 19 Host-Microbe Interactions

Avoiding Antibodies

Pathogens that survive the initial assault of the innate defenses soon encounter an additional obstacle, the adaptive defenses.

For most bacteria, the most formidable of these are antibodies.

Mechanisms for avoiding antibodies include:

■ IgA protease. This enzyme cleaves IgA, the class of antibody found in mucus and other secretions. Neisseria gonorrhoeae and a variety of other pathogens produce IgA protease. This enzyme may also have other roles.

■ Antigenic variation. Some pathogens routinely alter the structure of their surface antigens; this allows them to stay ahead of antibody production by altering the very molecules that the antibodies would otherwise recognize. Neisseria gonorrhoeae is able to vary the antigenic structure of its pili; antibodies produced by the host in response to one variation of the pili cannot bind effectively to another. ■ antigenic variation, p. 187

■ Mimicking host molecules. An essential aspect of the immune system is the development of tolerance for molecules that the body perceives as healthy "self." Pathogens can exploit this by covering themselves with molecules that resemble normal "self" molecules. For example, certain strains of Streptococcus pyogenes have a capsule composed of hyaluronic acid, a polysaccharide found in tissues.

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