05_defence-systems-of-pathogens

• inhibition of mucus removal through toxin production (Tracheal cytotoxin TCT)

• release of toxin from cell wall during groth -> paralyses mucocilary escalator & loss of ciliated cells => bacterial colonisation of epithelium

killing bacteria by insertion of cationic peptides (found at mucosal surfaces, within granules found in phagocytic cells) into microbial membranes

1. defensins

2. cathelicidins

3. thrombocidins (from platelets)

1. modification of membrane charge

   catalysation of additional palymitoyl residues to lipid A by bacterial pagP in Salmonella enterica -> less suspectible to binding of cationic peptides

   -> less destruction, shown through creation of gene knockouts in pagP

2. direct destruction of peptides

   • Staphylococcus aureus: binding and complex formation of Staphylokinase for neutralisation

   • Streptococcus pyogenes: sequestion of peptides by M1 protein to prevent activity

3. efflux pump

   • less effective CAMPs by acidification of cytoplasm

   • active pumping of peptides from cell (RosAB efflux pump: CAMPs out, K+ in)

4. bacterial biofilms formation: consortium of surface-attached bacterial cells embedded into the matrix composed of EC proteins, EC DNA and EPS

   • higher resistance to AMPs than planktonic bacteria

   • partly mediation of increased resistance via decreased penetration of AMPs through matrix

1. production of various glycosilidases -> sigA heavy glycosylated

2. IgA1 proteases produced by several bacteria -> cleavage of IgA1 H chain near chain region => falling apart of AB

   • Streptococcus pneuomoniae

   • Haemophilus

   • influenzae

   • Neisseria meningitidis

• toxin release -> killing phagocyte with toxin

• opsonization prevented -> preventing interaction btw. opsonizing antibody and phagocyte => preventing phagocytosis

• prevention of contact with phagocyte -> difficult/prevention of uptake of organism by phagocyte due to capsule (its charge, confirmation, mimicry of host cell structure, etc.)

• multiple point evasion

  • engagement with defined surface receptors

  • modification of signal transduction pathways

  • survival under hostile conditions

  • escape from phagosome

  • DNAse -> break-down of DNA, dissolving nets

kind of toxin

brdges macrophage and Tell-cell -> stimulation -> tons of hyperactivation of immune system -> host system own destrcution and cells to feed pathogen => proinflammatory cytokines

• bacterial cpasules : limited recognition of surface structures of bacteria & limited direct binding of C3b

• LPS (Lipopolysaccharide): reduction of complement availability, limiting successful lysis of gram negative bacteria

• modification of non-sialyted surface

• antigenic determinants very similar/identical to norm host cell components

  -> initial step in autoimmune diseases

=> thinks own host cells attack immune system -> defence against them => less phagocytotic cells

• Cytochrome B 561 (Burkholderia sp)

• FimH (Escherichia sp., Klebsiella sp.)

• Lipoligosaccharides (Campylobacter jejuni)

• surface proteins (Haemophilus influenca, Neisseria gonorrhoeae)

• Exopolysaccharide (Streptococcus pneumoniae)

alteration of surface proteins in order to avoid host immune response (those determined by specific antibodies)

-> alteration of surface structore on a regular basis

e. g. N. gonorrhoeae

• hijacking of host signalling pathways to inhibit inflammation -> supress cellular activation, increase bacterial survival)

  e. g. N. meningitidis: inhibition of co-engaged TLR-2 signaling and cytokine release

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poor recognition: allows pathogen to prosper

desensitisation of response

• due to presence of large amount of antigen/ antigen/antibody complexes

• anergic state pf T-cells through lack of second signal => ineffective T-cells

• generation of regulatory T-Cells (Treg) produce anti-inflammatory IL-10

inhibition of secondary immune signal

• lack of second signal activation -> no T-cell receptor activation -> no (appropriate) T-cell response