lecture 18 Flashcards
what are the 5 key events during infection
1) exposure to reservoir of organism
2) transmission to person
3) adhesion to initial site of infection
4) overcome barriers to establish infection
5) spread to other sites by changing initial site of infection
what are the 3 microbial factors
dose, type of organism and route of entry
what are the 3 host factors
integrity of innate barriers, competence of adaptive immune system, genetic capacity to respond to organism
what is type of organism as a microbial facor
how our body copes with the virus and what type of virus is it
what is dose as a microbial factor
degree of exposure (how large is the dose)
what is route of entry as a microbial factor
was it breathed in or ingested
what is integrity of innate barriers as a host factor
was there a cut on the hand which allowed for the microbe to come in
what is competence of adaptive immune system
is there a previous exposure such as a vaccination
what are anatomic barriers
skin, mucosa, respiratory epithelium, intestine, physical protection by bodies of epithelial surfaces
what are complement proteins
C3, defensins, chemical and enzymatic systems which act as a antimicrobials near the epithelium
what are innate immune cells
macrophages, granulocytes, NJK cells, if the epithelial is breached then innate cells provide rapid response
what are adaptive immune cells
slower acting cells needed if prior barriers fall including B cells, T cells and antibodies
what do sensor cells do
secrete cytokines that signal to other immune cells, and can lock on to bacteria and engulf them
what are TH1 cells
mature helper cells which promote inflammation and provide immunity against viral infections and intracellular bacteria
What are TH2 cells
mature helper T cells which promote allergic responses to IgE and provide immunity against extracellular organisms in particular helmiths
what are Treg cells
mature helper T cells that control TH1 and TH2 cells and ensure we dont respond to self
what happens when antibodies and complement work together
enhance bacteria destruction by phagocytosis
what are the 3 pathways which activate complement host defense
lectin pathway, alternative pathway and classical pathway
what is the lectin pathway
lectin binds to pathogen surface and mannose binding protein and ficolins recognise receptors and bind carbohydrates on pathogen surface.
what is classical pathway
antibody mediated pathway in which specific antibodies will recognise the outside of the bacteria and lead to C1q binding to the antibody and pathogen surface
what is the alternative pathway
some pathogen surfaces C3 undergo spontaneous hydrolysis to detect pathogens, the C3 then breaks apart and the process of C3 binding to the pathogen surface occurs
what happens once complement defence system is activated
opsonisation of pathogen occurs (phagocytosis)
what do all 3 pathways lead to
recruitment of inflammtory cells (chemotaxis) and killing of pathogens (lysis)
when do all these systems occur
at the same time at different parts of the pathogen surface resulting in C3 cleavage
what is C3 cleavage
activation of complement
what happens when C3 cleaves
it also cleaves to C3A and C3B
what is C3B
C3B binds to surface of the pathogen
what is C3A
C3A floats around as an immune signalling molecule
what mechanisms occur when C3 is cleaved
1) C3B and C5A signal the recuitment of phagocytic cells and promote inflammation at the site of infection
2) opsonisation of pathogens
3) lysis by formation of spore which can punch holes in surface of some bacteria
what is a capsule
layer that bacteria can have on their outside
how does a capsule work
its negativly charged so it creates a physical way for bacteria to repel the phagocyte as a phagocyte is also negativly charged
what is intracellular growth
being able to divide and grow inside the body
what are type 1 interferons
antiviral mechanism which provides a response when cells become infected
how does type 1 interferons work for neighbouring cells
interferons are sent out into the environment by infected cells which allow neighbouring cells to turn on some processes which make them more likely to be infected by the virus (down regulate molecules and receptors)
how does type 1 interferons work for NK cells
interferon type 1 can provide a signal to NK cells to kill neighboring infected cells
how do some viruses interfere with interferon response
by dampening interferon secreation by infected cells and by blocking the antiviral state of neighbouring cells from being activated
what happens if the interferon secretion is delayed
it can do more harm than good
