Immune response to bacteria Flashcards
what is immune evasion
strategy used by pathogenic organisms and tumours to evade a host’s immune response to maximize their probability of being transmitted to a fresh host or to continue growing, respectively.
surface defences against bacteria
- mucosal and epithelial surfaces
- can shed tissue/skin during infection, and then repair later
- microbial antagonism by normal flora
- good vascularity
- physical barriers e.g. tight junction
what are PAMPs
Pathogen-associated molecular pattern. generic structures located on bacteria to recognise foreign cells by phagocytes that contain PRR/TLR
what happens when a PAMP binds to a PRR
intracellular signalling cascade that activates transcription factors to start producing inflammatory cytokines and IFN. Start of immune response
what happens when bacteria gets in (passing surface barriers)
quickly recognised by neutrophils/macrophages as being foreign .’. activate and release cytokines/chemokines .’. recruit more cells, cause inflammation, activation of complement, transferrin and CRP influx (due to permeability of vessels)
what is CRP
C-reactive protein. CRP is classified as an acute phase reactant, which means that its levels will rise in response to inflammation
why does adaptive immune system take more time than innate
innate is generic and responds in same way to all pathogens. adaptive = antigen presented to B and T cells and THEN Th cells activate cells and macrophages
how do serum molecules reach site of infection in inflammation
incr. blood supply
inc capillary permeability
migration of cells from blood to tissue
what are virulence factors
produced by bacteria, viruses, fungi, protozoa that add to their effectiveness in colonisation, immunoevasion, immunosuppression, tissue damage
roles of complement
inducing inflammatory response, promoting chemotaxis, inc. phagocytosis via opsonisation, inc. vascular permeability, mast cell degranulation, lysis of cell membranes
why may N.meningitidis, Haemophilus influenza, Ecoli have serum resistance
have LPS layer and polysaccharide capsule which contains sialic acid/hyaluronic acid .’. stops complement from binding bc are nonspecific antigens that we do not produce antibodies towards bc do not want to attack own cells bc we also contain these components
what are opsonins
molecules that bind to foreign microorganisms or cells making them more susceptible to phagocytosis e.g. IgG1, IgG3,C3b, CRP
what is the principle of opsonisation
phagocytes have C3b and Fc receptors on their surface. so bacteria opsonised by Ig and other molecules .’. are flagged up as foreign .’. can be recognised by the respective receptors on phagocytes and be engulfed
what are M cells (microfold cells)
transport antigens from the GI tract to cells of the immune system, thereby initiating an immune response or tolerance.
what happens when a pathogen is recognised by a lymphocyte (mucosal immunity)
triggers immune response. T cell will migrate from peyers patch and drain local lymph node and bcells activated. mucosal lymphocytes home back to the mucosal immune system before they can produce Ig
