Immune defense against extracellular bacteria

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Defense against extracellular bacteria depends on well-functioning mechanisms of phagocytosis, functional antibodies, complement, and intracellular killing.

  • In particular, opsonization with complement components , lectins and antibodies is required to eliminate bacteria . The final elimination is most often provided by neutrophils .
  • Absorbed bacteria are killed intracellularly by oxidative products of NADPH-oxidase (so-called oxidative flare -up ), or by some oxygen-independent mechanisms (lysosomal proteases, nucleases, lipases, lower pH).
  • Cytokines produced by phagocytes , such as interleukin-1, interleukin-6 , TNF , induce fever , metabolic response and increased acute phase protein synthesis .
  • This is followed by stimulation of antigen-specific components of immunity , stimulation first of T-lymphocytes , then B-lymphocytes and IgM production . With the help of T-ly, there is an isotype rearrangement and the promotion of B-ly proliferation and the production of more affine IgG or IgA.

Encapsulated bacterial strains (e.g., pneumococcus ) directly stimulate B cells by aggregating their BCRs and induce T-independent production of IgM antibodies; these, when bound to bacteria, activate the classical complement activation pathway .


Only gram-negative bacteria (eg Neisseria ) are sensitive to the action of the complement membranolytic complex .


Some bacteria produce toxins . Neutralizing antibodies are crucial protection.


IgG and IgA memory antibodies remain in the body after infection , which have a protective role. Memory T and B cells rapidly activate upon further infection and initiate an anamnestic antibody response ( secondary immune response ).


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References[edit | edit source]

  • HOŘEJŠÍ, Václav. Základy imunologie. 3. edition. Triton, 2008. 280 pp. ISBN 80-7254-686-4.


Categorie:Imunology