398 PART I The Immune System in Health and Disease TABLE 17-3 Host immune responses to bacterial infection and bacterial evasion mechanisms Infection proces Host defense Bacterial evasion mechanism Attachment to host Blockage of attachment by Secretion of proteases that cleave secretory igA dimers secretory IgA antibodies neisseria meningitidis, N gonorrhoeae, Haemophilus influenzae Antigenic variation in attachment structures(pili of Proliferation sis(Ab-and fibrin coat)that inhibit phagocytic els aride capsule, M protein, Mechanisms for surviving within phagocytic cells Induction of apoptosis in macrophages( Shigella flexneri Complement-mediated lysis and Generalized resistance of gram-positive bacteria to complement localized inflammatory respons mediated lysis Insertion of membrane-attack complex prevented by long side hain in cell-wall LPS(some gram-negative bacteria) Invasion of host tissues Ab-mediated agglutination Secretion of elastase that inactivates C3a and C5a(Pseudomonas) Toxin-induced damage Neturalization of toxin by antibody Secretion of hyaluronidase, which enhances bacterial invasiveness to host cells uring infection, the host produces antibody against the Mechanisms for interfering with the complement system infecting serotype. This antibody protects against reinfection help other bacteria survive. In some gram-negative bacteria, with the same serotype but will not protect against infection for example, long side chains on the lipid a moiety of the by a different serotype. In this way, S. pneumoniae can cause cell-wall core polysaccharide help to resist complement disease many times in the same individual. On other bacteria, mediated lysis. Pseudomonas secretes an enzyme, elastase such as Streptococcus pyogenes, a surface protein projection that inactivates both the C3a and C5a anaphylatoxins, there called the M protein inhibits phagocytosis. Some pathogenic by diminishing the localized inflammatory reaction staphylococci are able to assemble a protective coat from hos A number of bacteria escape host defense mechanisms by proteins. These bacteria secrete a coagulase enzyme that pre- their ability to survive within phagocytic cells. Some, such as cipitates a fibrin coat around them, shielding them from Listeria monocytogenes, do this by escaping from the phago- phagocytic cells lysosome to the cytoplasm, which is a more favorable environ- ment for their growth. Other bacteria, such as Mycobacterium avium, block lysosomal fusion with the phagolysosome; and some mycobacteria are resistant to the oxidative attack that takes place within the phagolysosome Immune Responses Can Contribute to Bacterial Pathogenesis In some cases, disease is caused not by the bacterial pathogen itself but by the immune response to the pathogen. As described in Chapter 12, pathogen-stimulated overproduce tion of cytokines leads to the symptoms of bacterial septic shock, food poisoning, and toxic-shock syndrome. For in stance, cell-wall endotoxins of some gram-negative bacteria activate macrophages, resulting in release of high levels of IL-l and TNF-a, which can cause septic shock. In staphylo- coccal food poisoning and toxic-shock syndrome, exotoxins produced by the pathogens function as superantigens, which FIGURE17-9 Electron micrograph of Neisseria gonorhoeae at- can activate all T cells that express T-cell receptors with a par- taching to urethral epithelial cells. Pili(P)extend from the gonococ- ticular VB domain(see Table 10-4). The resulting overpro- al surface and mediate the attachment / From M. E. Ward and P J duction of cytokines by activated TH cells causes many of the at.1972.nt.Dis.126601J symptoms of these diseasesDuring infection, the host produces antibody against the infecting serotype. This antibody protects against reinfection with the same serotype but will not protect against infection by a different serotype. In this way, S. pneumoniae can cause disease many times in the same individual. On other bacteria, such as Streptococcus pyogenes, a surface protein projection called the M protein inhibits phagocytosis. Some pathogenic staphylococci are able to assemble a protective coat from host proteins. These bacteria secrete a coagulase enzyme that pre￾cipitates a fibrin coat around them, shielding them from phagocytic cells. Mechanisms for interfering with the complement system help other bacteria survive. In some gram-negative bacteria, for example, long side chains on the lipid A moiety of the cell-wall core polysaccharide help to resist complement￾mediated lysis. Pseudomonas secretes an enzyme, elastase, that inactivates both the C3a and C5a anaphylatoxins, there￾by diminishing the localized inflammatory reaction. A number of bacteria escape host defense mechanisms by their ability to survive within phagocytic cells. Some, such as Listeria monocytogenes, do this by escaping from the phago￾lysosome to the cytoplasm, which is a more favorable environ￾ment for their growth. Other bacteria, such as Mycobacterium avium, block lysosomal fusion with the phagolysosome; and some mycobacteria are resistant to the oxidative attack that takes place within the phagolysosome. Immune Responses Can Contribute to Bacterial Pathogenesis In some cases, disease is caused not by the bacterial pathogen itself but by the immune response to the pathogen. As described in Chapter 12, pathogen-stimulated overproduc￾tion of cytokines leads to the symptoms of bacterial septic shock, food poisoning, and toxic-shock syndrome. For in￾stance, cell-wall endotoxins of some gram-negative bacteria activate macrophages, resulting in release of high levels of IL-1 and TNF-, which can cause septic shock. In staphylo￾coccal food poisoning and toxic-shock syndrome, exotoxins produced by the pathogens function as superantigens, which can activate all T cells that express T-cell receptors with a par￾ticular V domain (see Table 10-4). The resulting overpro￾duction of cytokines by activated TH cells causes many of the symptoms of these diseases. 398 PART IV The Immune System in Health and Disease TABLE 17-3 Host immune responses to bacterial infection and bacterial evasion mechanisms Infection process Host defense Bacterial evasion mechanisms Attachment to host Blockage of attachment by Secretion of proteases that cleave secretory IgA dimers cells secretory IgA antibodies (Neisseria meningitidis, N. gonorrhoeae, Haemophilus influenzae) Antigenic variation in attachment structures (pili of N. gonorrhoeae) Proliferation Phagocytosis (Ab- and Production of surface structures (polysaccharide capsule, M protein, C3b-mediated opsonization) fibrin coat) that inhibit phagocytic cells Mechanisms for surviving within phagocytic cells Induction of apoptosis in macrophages (Shigella flexneri) Complement-mediated lysis and Generalized resistance of gram-positive bacteria to complement￾localized inflammatory response mediated lysis Insertion of membrane-attack complex prevented by long side chain in cell-wall LPS (some gram-negative bacteria) Invasion of host tissues Ab-mediated agglutination Secretion of elastase that inactivates C3a and C5a (Pseudomonas) Toxin-induced damage Neturalization of toxin by antibody Secretion of hyaluronidase, which enhances bacterial invasiveness to host cells FIGURE 17-9 Electron micrograph of Neisseria gonorrhoeae at￾taching to urethral epithelial cells. Pili (P) extend from the gonococ￾cal surface and mediate the attachment. [From M. E. Ward and P. J. Watt, 1972, J. Inf. Dis. 126:601.]