Avoiding the Host Defenses

Inside the body, invading microorganisms soon encounter the innate and adaptive defenses. Pathogens as a group have evolved a variety of mechanisms to circumvent the otherwise lethal effects of these defenses.

Hiding Within a Host Cell

Some bacteria can evade some components of the host defenses by remaining inside host cells, out of the reach of the phagocytes, complement, and antibodies. An example is Shigella species; recall that these organisms induce their own uptake by intestinal epithelial cells. Once inside a host cell, the bacteria can orchestrate their transfer to adjacent cells. They do this by causing the rapid polymerization of host cell actin at one end of the bacterial cell, effectively forming an "actin tail" that propels the bacterium within the cell. This "tail" can also propel a cell with such force that it drives the bacterium out of one cell and into another. Listeria monocytogenes also polymerizes host cell actin to facilitate its own movement (figure 19.7). ■ actin, p. 74

Avoiding Killing by Complement Proteins

As we discussed in chapter 15, activation of the complement system leads to three primary outcomes—lysis of foreign cells by the membrane attack complex (MAC), opsonization, and inflammation (see figure 15.7). Because the latter two outcomes are associated with phagocytosis, mechanisms that bacteria use to subvert them will be discussed in the next sec-

Mucous membrane

Nester-Anderson-Roberts: I III. Microorganisms and I 19. Host-Microbe I I © The McGraw-Hill

Microbiology, A Human Humans Interactions Companies, 2003

Perspective, Fourth Edition

Figure 19.7 Actin Tail of Intracellular Listeria monocytogenes Rapid polymerization of host cell actin (green) at one end of the bacterial cell (orange) propels the bacterium within the cell.

19.7 Avoiding the Host Defenses 469

pathway of complement activation. This pathway is usually initiated when the complement component C3b binds to a cell surface (figure 19.8). The surfaces of host cells do not set off the pathway because they contain molecules that attach to complement regulatory proteins, resulting in the inactivation of the C3b. Some pathogens carry surface components such as sialic acid that capture the regulatory proteins; the surface components often mimic molecules that host cells use to attach to complement regulatory proteins. Because this leads to inactivation of any C3b that binds, it foils the alternative pathway of complement activation. Certain strains of Neisseria gonorrhoeae have sialic acid in the lipooligosaccharide (LOS) of their outer membrane (LOS is the functional equivalent of lipopolysaccharide) that binds the complement regulatory proteins. These serum-resistant strains cause disseminated gonococcal infection, a systemic disease characterized by symptoms including fever, rash, and arthritis. Certain strains of Neisseria meningitidis have a capsule composed of sialic acid. ■ disseminated gonococcal infection, p. 645

tion. Here, we will focus on mechanisms used to avoid the lethal effects of the MAC. Recall that Gram-negative bacteria are susceptible to the MAC because their outer membrane serves as a target; the MAC has little effect on Gram-positive organisms. ■ complement, p. 381

Gram-negative bacteria that circumvent killing by the complement proteins are said to be serum resistant. One mechanism these organisms use to avoid the effects of MAC is to thwart certain events that would normally lead to its formation. They do this by hijacking the mechanisms that host cells use to prevent their own surfaces from triggering the alternative

Avoiding Destruction by Phagocytes

Phagocytosis involves multiple steps—including chemotaxis, recognition and attachment, engulfment, and fUsion of the phagosome with the lysosome—that lead to the destruction and digestion of an invading microbe (see figure 15.9). Pathogenic bacteria have evolved a variety of ingenious mechanisms to avoid the destructive effects of phagocytosis (figure 19.9).

Preventing Encounters with Phagocytes

Some pathogens avoid the process of phagocytosis by avoiding macrophages and neutrophils altogether. One way they do this

(a) Bacterial surface

Complement regulatory protein

^ Other complement ^ proteins

C3b attaches to bacterial surface

Other complement proteins attach to C3b bound to the surface, forming an enzyme that initiates the complement cascade.

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Responses

  • cara tunnelly
    How do bacteria avoid hist defenses by avoiding killing by complement proteins?
    3 years ago

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