L16-17 Flashcards
(42 cards)
Main defense against extracellular bacteria
opsonizing antibody and phagocytosis (esp for encapsulated bacteria), neutralizing antibody, complement
Encapsulated bacteria
hydrophilic capsule prevents phagocytosis unless opsonizing antibody + C3b are used to engulf bacteria
What complement molecule helps phagocytose encapsulated bacteria
C3b
neutropenic patients susceptible to
infections with extracellular pathogens
Splenectomized patients are susceptible to
sepsis (encapsulated bacteria)
Neutralizing antibody
inhibits attachment to receptors on host cells
Ig Deficiency patients are susceptible to
infections with extracellular pathogens
IgA defends
mucosal surfaces from infections
Anti-toxin antibodies
bind and neutralize toxin molecules by inhibiting them from binding to specific host cell receptors
endotoxins
LPS
Endotoxin is produced by
gram negative bacteria
Endotoxin structure
Lipid A core, highly variable carbohydrate side chains
Endotoxin vaccine?
no cannot be made into a toxoid due to stable Lipid A structure
Secondary immunity to endotoxin?
NO, highly variable structure will not recognized from another infection
Endotoxin triggers
alternative complement pathway
LPS is an exogenous pyrogen producing:
IL-1, TNF-alpha, IL-6
TLR4
PRR that binds CD14-LBP-LPS to induce macrophage response
Exotoxin is produced by
gram negative bacteria or gram positive bacteria
Exotoxin structure
distinct receptors, little variance, neutralizing antibodies are effective
Tetanus
disease doesn’t always lead to immunity because toxins cause disease long before inducing an antibody response
Exotoxin vaccine
yes, toxoid
Superantigens
exotoxin capable of inducing large quantities of cytokines, by binding HLA class II molecules at non-binding site and activate all T cells with TCR allele
Immunity to intracellular bacteria
CD4 producing IFN-gamma
IFN-gamma
restricts protein synthesis by decreasing a.a. pool
decreased membrane fluidity to prevent entrance
NO production for bacterial toxicity
altered cell metabolism to inhibit bacterial growth
increased HLA Class I
activation of macrophages