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SAKINAH NUR FADILLAH
CONETA WULANDARI
SUB POKOK BAHASAN
4. In many infections, tissue injury and disease may be caused by the host
response to the microbe and its products rather than by the microbe itself
IMMUNITY TO MICROBES
(BACTERIA, FUNGI,VIRUSES, AND
PARASITE)
IMMUNITY TO
EXTRACELLULER BACTERIA
IMMUNITY TO
EXTRACELLULER BACTERIA
Extracellular bacteria are capable of replicating outside host cells, for example, in the circulation, 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. This is how
pyogenic (pusforming) cocci cause a large number of suppurative infections in humans.
Second, many of these bacteria produce toxins, which have diverse pathologic effects.
Bacteria that express mannose on their surface may bind mannose-binding lectin, thereby leading to
complement activation by the lectin pathway.
In addition, activated phagocytes secrete cytokines, which induce leukocyte infiltration into sites of infection
(inflammation). Injury to normal tissue is a pathologic side effect of inflammation. Cytokines also induce the
systemic manifestations of infection, including fever and the synthesis of acute-phase proteins.
ADACTIVE IMMUNITY TO EXTRACELLULER BACTERIA
HUMMORAL IMMUNITY IS THE PRINCIPAL PROTECTIVE RESPONSE AGAINTS
EXTRACELLLER BACTERIA, AND IT FUNCTIONS TO BLOCK INFECTION, ELIMINATE THE
MICROBES, AND 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.
The effector mechanisms used by antibodies to combat these infections include neutralization,
opsonization and phagocytosis, and activation of complement by the classical pathway
Neutralization is mediated by high-affinity immunoglobulin G (IgG) and IgA isotypes, opsonization by some
subclasses of IgG, and complement activation by IgM and subclasses of IgG. The protein antigens of
extracellular bacteria also activate CD4+ helper T cells, which produce cytokines that stimulate antibody
production, induce local inflammation, and enhance the phagocytic and microbicidal activities of
macrophages and neutrophils
Figure 1. Addactive Immune Respones to Extracelluler Microbes
INJURIOUS EFFECTS OF IMMUNE RESPONSES
The principal injurious consequences of host responses to extracellular bacteria are inflammation and
septic shock
INFLAMMATION
tissue damage by local production of reactive oxygen species and lysosomal enzymes
SEPTIC SHOCK
severe pathologic consequence of disseminated infection by gram-negative and some gram-positive bacteria.
IMMUNITY TO
INTRASELLULER BACTERIA
INNATE IMMUNITY TO INTRACELLULER BACTERIA
The principal mediators of innate immunity against fungi are neutrophils and macrophages
Virulent strains of Cryptococcus neoformans inhibit the production of cytokines such as TNF and
IL-12 by macrophages and stimulate production of IL-10, thus inhibiting macrophage activation. .
Neutrophils
Neutrophils (also called polymorphonuclear leukocytes [PMNs]) are the most abundant leukocytes in
the blood, numbering 4000 to 10,000 per μL.
Production of neutrophils from the bone marrow increases rapidly, and their number may rise to
20,000 per μL of blood.
Production of neutrophils is stimulated by cytokines,
Neutrophils are the first cell type to respond to most infections, particularly bacterial and fungal
infections
Ingest microbes in the circulation
Rapidly enter extravascular tissues at sites of infection, where they also ingest microbes and die after
a few hours.
ADAPTIVE IMMUNITY TO FUNGI
Cell-mediated immunity is the major mechanism of adaptive immunity against fungal infections.
Histoplasma capsulatum, is eliminated by the same celluler mechanisms that are effective againt
intracelluler bacteria.
CD4+ and CD8+ T cells cooperate to eliminate the yeast forms of C. neoformans, which tend to
colonize the lungs and brain in immunodeficient hosts. Candida infections often start at mucosal
surfaces, and cell-mediated immunity is believed to prevent spread of the fungi into tissues .
In many of these situations, TH1 responses are protective and TH2 responses are detrimental to the
host.
IMMUNITY TO VIRUSES
VIRUSES
viruses can cause tissue injury and disease by any of several mechanisms.
Viral replication interferes with normal cellular protein synthesis and function and leads to injury and
ultimately death of the infected cell.
Viruses may also cause latent infections, during which viral DNA persists in host cells and produces
proteins that may or may not alter cellular functions.
IMMUNITY TO VIRUSES
INNATE IMMUNITY TO VIRUSES
THE PRINCIPAL MECHANISMS OF INNATE IMMUNITY AGAINST VIRUSES ARE INHIBITION OF
INFECTION BY TYPE I IFNS AND NK CELL-MEDIATED KILLING OF INFECTED CELLS.
Virus-specific CTLs are CD8+ T cells that recognize cytosolic, usually endogenously synthesized,
viral antigens in association with class I MHC molecules on any nucleated cell.
IMMUNITY TO PARASITES
INNATE IMMUNITY TO PARASITE
PROTOZOA
The principal innate immune response to protozoa is phagocytosis, but many of these parasites are resistant to
phagocytic killing and may even replicate within macrophages .
Some protozoa may express surface molecules that are recognized by TLRs and activate phagocytes.
HELMINTH
Phagocytes also attack helminthic parasites and secrete microbicidal substances to kill organisms that are
too large to be phagocytosed. .
Some helminths may also activate the alternative pathway of complement
ADAPTIVE IMMUNITY TO PARASITE
PROTOZOA
The principal defense mechanism against protozoa that survive within macrophages is cell-mediated
immunity, particularly macrophage activation by TH1 cell-derived cytokines
HELMINTH
Defense against many helminthic infections is mediated by the activation of TH2 cells, which results in production
of IgE antibodies and activation of eosinophils
IgE antibodies that bind to the surface of the helminths may activate mast cells
Extracellular bacteria
Intracellular bacteria