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General features of immune responses to microbes

responses always involve innate and adpative immunity

the immune system responds in distinct and specialized ways to different types of microbes to be most effective

microbes evade or resist the effector mechanisms of immunity

many microbes establish latent, or presistent, infections. The immuner esponse controls but does not eliminate the microbe and the microbe survives without propagating the infection

in many infections, tissue injury and disease may be caused by the host response rather than by the microbe itself


First line of defnse

mechanical barrier


commensal bacteria

low pH

physical mechanisms


second line of defnse

innate immunty: nonsepcific, macrophages, neutrophils, complement

adaptive immunty: antigen specific, lymphocytes (B and T cells) antibodies


Extracellular bacteria

extracellular bacteria may either induce inflammation or produce toxins

they are ony capable of replicating and surviving outside of host cells

Innate response, adaptive repsonses, bacterial toxins, evasion of immune responses, overreaction of immune response


Bacterial toxins

exotoxins: secreted by bacteria. neutralized by IgG and IgA

endotoxins: not secreted. LPS of cell wall


Extracellular bacteria evasion of immune response

bacterial capsules: external polysaccharide structure. prevent desiccation and resist phagocytosis

biofilms: prevents phagocytosis. increase tolerance to antibiotics. Pseudomonas


Extracellular bacteria evasion of immune system

antigenic variation

complement inhibtion

neutralization of reactive : catalase producing bacteria

protein A (staph) and protein G (strep): bind antibody and block opsonization and phagocytosis


overreaction to extracellular bacteria

abscess: collection of immune cells with a surrounding capsule

Septic shock


intracellular bacteria

surivive and replicate in host cells

they require cell mediated immunity to be eliminated as they are not able to be seen by antibodies and complement: innate response, adaptive response, evasion of immune response, overreaction of immune response.


Intracellular bacteria: innate immune response

phagocytes (DC/macrophages) become infected with intracellular bacteria

they release IL 12 which activate NK cells

NK cells then release IFN which activates phagocyte to kill the bacteria


Intracellular bacteria: adaptive immune response

innate immune response often fails to control intracellular infections

t cell mediate immunity is the primary protective response

CD4 cells (TH1) release IFN (activates phagocytes to kill bacteria)

TH1 cells have CD40L which activates phagocyte via CD40

CD8 cells kill infected cells


phagocyte activation

following IFN stimulation of infected phagocyte, microbes are eliminated by the fusion of hte phagosome and lysosome and exposure to reactive nitrogen intermediates (RNI) and reactive oxygen intermediates (ROI)


Intracellular bacteria evasion of immune system

escape from phagosomes

inhibition of phagosome and lysosome fusion

detoxification of RNI and ROI (catalse neutralized h202)

diminish phagosome's ability to present antigens to CD4 T cells


overreaction to intracellular bacteria

granulom: collection of immune cells. Tuberculosis

promotes survival of bateria



survive and replicate inside host cells

they require cell mediated immunity to be eliminated as they are not able to be seen by antibodies and complement


Viruses: innate immune response

host cell pattern recognition receptors (PRR) recognize viral pathogen associated molecular pattern (PAMPS)

infected cell produces cytokines (IFN a and B) which elicit antiviral properties in neighboring cells

NK cells recognize loss of MHC and kill infected cell


Virus: adaptive immune response

humoral response is effective when virus in outside of host cells

antibodies can neutralize virus and prevent its entry into cells


Viral evasion: antigenic drift vs shift

antigenic shift vs drift. anitgenic drift creates influenza viruses with slightly modified antigens, while antigenic shift generate viruses with entirely new antigens


viral evasion of immune system

code for anitbody receptors to block effector anitbody functions

inhibit IFN synthesis

produce soluble IFN receptors to block IFN function

mimic MHC molecuels, thus avoid being killed by NK cells (remember that NK cells kill cells that lack MHC)

Inhibit MHC I molecule expression, thus avoid CD8 cell recognition

decreases production of IL 12 (IL 12 stimulates IFN production by NK)

T cells and increases cytotoxic acitivity

viral latency EBV and herpes


Overreaction to virus: cirrhosis in hep B

HBV is not directly toxic to hepatocytes and people with imparied cellular immunity will have no inflammation

hepatocytes adre damaged by the immunological response

if the infection is not cleared, the insufficient immune response will continue and cause progressive liver damage.



Can occur as yeast or mold (hypae)


Fungi: innate immune response

antibdoy opsonization

neutrophil and macrophage phagocytosis of yeast

pattern recognition receptors recognize pathogen associated molecules patterns

release of proinflammatory cytokines (IL12). Phagosome and lysosome fusion

neutrophils release NETS (neutrophil exracellular traps) for hyphae


Fungi adaptive immune response

T helper subsets are important

TH1 cells secrete IFN gamma and promote fungal clearance

TH17 cells recruits neutrophils

TH2 cells inhibit fungal clearance and have a role in allergic disease

T helper cell importance is seen in AIDS, where a lack of CD4 helper cells leads to increase susceptibility to fungal infections


Fungi evasion of immune response

stimulate production of Il 10 (inhibitory cytokine)

inhibit IL-12

inhibit phagolysosome

change cell wall composition: changing surface glycoproteins


Overreaction of fungi




protozoa (one cell organisms)

helminths (multicellular worm)


parassite innate immune response

PRRS recognize PAMPs mobilizes and activates macrophages

antigen presentation and activation of adaptive immune system

rarely eliminates parasites, just slows the growth


parasites: adaptive immune response

antibodies neutralize the extracellular protozoa

CD8 t cells can kill infected cells directly

TH1 serete IFN and activate macrophages to kill intracellular protozoa

th2 cells are the primary response to helminth infections


Parasites adaptive imune response

IL13: cell turnover mucus

IL5: recruit eosinophils

IgE: regulates mast cells and enhance elimination

mast cells: inflammatory response. Mucus production. Muscle contraction.


Parasite evasion of immune system

antigenic variation

stage specific: different antigens see at different stages in the life cycle. COntinual alteration of antigens with replication

production of IL 10

prevention of lysosome and phagosome fusion

produce antioxidants to neutralize lysosome effects


overreaction to parasites


increase in size and number of macrophages and engorgement of blood vessels