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====Complement====
 
====Complement====
Some bacteria, particularly those with an outer lipid bilayer (i.e. Gram-negative), are susceptible to [[Complement]] activated via the alternative pathway (the lytic complex: C5b-9). The release of C3a and C5a lead to histamine release, and attracts and activates [[Neutrophils|neutrophils]]. Components of C3 aid opsonisation of the bacteria.
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Some bacteria, particularly those with an outer lipid bilayer (i.e. Gram-negative), are susceptible to [[Complement|complement]] activated via the alternative pathway (the lytic complex: C5b-9). The release of C3a and C5a lead to histamine release, and attracts and activates [[Neutrophils|neutrophils]]. Components of C3 aid opsonisation of the bacteria.
    
====Phagocytosis====
 
====Phagocytosis====
 
Most bacteria are killed this way. [[Complement|Complement products]], bacterial components (e.g. f-Met-Leu-Phe) and locally released cytokines are chemotactic for phagocytes. The binding of the phagocyte can be mediated by the following:
 
Most bacteria are killed this way. [[Complement|Complement products]], bacterial components (e.g. f-Met-Leu-Phe) and locally released cytokines are chemotactic for phagocytes. The binding of the phagocyte can be mediated by the following:
**Lectins on the bacteria, e.g. mannose-binding lectin of E. coli.
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*Lectins on the bacteria, e.g. mannose-binding lectin of ''[[E. coli]]''.
**Lectins on the phagocyte, e.g. complement receptors such as CR3.
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*Lectins on the phagocyte, e.g. complement receptors such as CR3.
**[[Complement]] deposited on the organism, both classic and alternative pathways.
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*[[Complement]] deposited on the organism, both classic and alternative pathways.
**Fc receptors on phagocyte, bind to the antibody on bacteria.
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*Fc receptors on phagocyte, bind to the antibody on bacteria.
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==Immunopathology==
 
==Immunopathology==
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The release of endotoxins, typically LPS by Gram-negative bacteria, can cause the excessive production of [[Cytokines|cytokines]] that lead to 'endotoxin shock.' This can lead to fever, circulatory collapse and haemorrhagic necrosis, and eventually multiple organ failure and potentially death. Gram-positive bacteria can cause a similar reaction. The Koch phenomenon is the necrotic response observed in [[Mycobacterium tuberculosis|M. tuberculosis]] infections and is thought to be partly due to the release of [[Cytokines|cytokines]].  
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The release of endotoxins, typically LPS by Gram-negative bacteria, can cause the excessive production of [[Cytokines|cytokines]] that lead to 'endotoxin shock.' This can lead to fever, circulatory collapse and haemorrhagic necrosis, and eventually multiple organ failure and potentially death. Gram-positive bacteria can cause a similar reaction. The Koch phenomenon is the necrotic response observed in ''[[Mycobacterium tuberculosis]]'' infections and is thought to be partly due to the release of [[Cytokines|cytokines]].  
       
==Evading immune defences==
 
==Evading immune defences==
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Bacteria can avoid the [[Complement|complement]] reponse. Proteins can be expressed on the surface that divert the lytic complex from the cell membrane; The outer membrane can resist the lytic complex; Some bacteria have an outer membrane that inhibits complement activation and An enzyme found on the membrane of some bacteria is able to degrade complement.
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Bacteria can avoid the [[Complement|complement]] response. Proteins can be expressed on the surface that divert the lytic complex from the cell membrane or the outer membrane can resist the lytic complex. Some bacteria have an outer membrane that inhibits complement activation and an enzyme found on the membrane of some bacteria is able to degrade complement.
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Many can also avoid the phagocytic response by secreting repellents or toxins, some bacteria can inhibit chemotaxis. Once ingested, some bacteria inhibit lysosome fusion or proton pump action (preventing the phagocyte pH from falling), e.g. ''[[Mycobacterium tuberculosis|M. tuberculosis]]''. Some bacteria have outer coats that inhibit phagocyte attachment and some secrete catalase which breaks down hydrogen peroxide. The release of a phenolic glycolipid by ''M. leprae'' prevents damage by free radicals. Lipoarabinomannan, released by some [[:Category:Mycobacteria|Mycobacteria]], blocks [[Macrophage|macrophage]] response to IFN-γ and infected cells can lose their ability to present antigens.
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Many can also avoid the phagocytic response by secreting repellants or toxins, some bacteria can inhibit [http://www.cellsalive.com/chemotx.htm| chemotaxis]. Once ingested, some bacteria inhibit lysosome fusion or proton pump action (preventing the phagocyte pH from falling), e.g. [[Mycobacterium tuberculosis|M. tuberculosis]]. Some bacteria have outer coats that inhibit phagocyte attachment and some secrete catalase which breaks down hydrogen peroxide. The release of a phenolic glycolipid by M. leprae prevents damage by free radicals. Lipoarabinomannan, released by some Mycobacteria, blocks [[Macrophage|macrophage]] response to IFN-γ and infected cells can lose their ability to present antigens.
      
<big>'''Also see [[Innate Immunity to Bacteria]] and [[Adaptive Immunity to Bacteria]]'''</big>
 
<big>'''Also see [[Innate Immunity to Bacteria]] and [[Adaptive Immunity to Bacteria]]'''</big>
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[[Category:To Do - AimeeHicks]]
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[[Category:Bacteria]]
[[Category:To Do - AP Review]]
 
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