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| ==[[Neutrophils|Neutrophils]]== | | ==[[Neutrophils|Neutrophils]]== |
| [[Image:Neutrophil 2.jpg|thumb|right|150px|Neutrophils - J. Bredl, RVC 2008]] | | [[Image:Neutrophil 2.jpg|thumb|right|150px|Neutrophils - J. Bredl, RVC 2008]] |
− | * Neutrophils are the principal, highly active '''phagocytes''' in the blood
| + | [[Neutrophils|Neutrophils]] are the principal, highly active '''[[Phagocytosis|phagocytes]]''' in the blood and comprise 30-70% of all white blood cells depending on species. Their main function is to kill and digest microbes in a similar way as macrophages. They also have another function of extracellular bacterial killing by disrupting bacterial membranes by the secretion of small antibacterial peptides, for example defensins and bactenecins. |
− | ** Comprise 30-70% of white blood cells depending on species
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− | ** Kill and digest microbes in a similar way as macrophages
| + | <br /> |
− | * Neutrophils can also cause extracellular bacterial killing by disrupting bacterial membranes
| + | Neutrophils also produce vasoactive peptides, for example, histamine and bradykinin which, as their name suggests, activate the endothelium to become more "leaky" causing a great increase in extravasation of blood granulocytes and [[Monocytes|monocytes]], and the diffusion of plasma proteins to the site of infection. These peptides, released from other cells as well as neutrophils, are responsible for the classical signs of inflammation: redness ('''rubor'''), heat ('''calor'''), swelling ('''tumor'''), and pain ('''dolor'''), often accompanied by loss of function. Neutrophil activation in an inflammatory lesion also results in the release of '''prostaglandins''' which are responsible for vasoactive changes and for pain (N.B. These are reduced with cyclo-oxygenase (COX) inhibition for example with the NSAID(non-steriodal anti-inflammatory drugs)'s Aspirin and Ibuprofen). |
− | ** Secrete small antibacterial peptides
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− | *** E.g. defensins and bactenecins
| + | <br /> |
− | * Neutrophils produce vasoactive peptides
| + | It is for the reasons above that neutrophils have been described as the archetypal cell associated with [[:Category:Inflammation|acute inflammation]]. |
− | ** E.g. histamine and bradykinin
| + | <br /> |
− | ** Cause a great increase in extravasation of blood granulocytes and [[Monocytes|monocytes]] and plasma proteins at the site of infection
| + | <br /> |
− | * Neutrophils are the archetypal cell associated with [[:Category:Inflammation|acute inflammation]]
| + | To move the neutrophils from the blood to the sites of inflammation a system of various chemoattractants exist. These include [[Complement|complement components]], in particular C3a and C5a; [[Cytokine|cytokine]] production, in particular the chemokine class of cytokines, for example CXCL8 (IL-8); and the activation of the endothelium of post-capillary venules. |
− | ** Are attracted to sites of inflammation by:
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− | *** Complement activation
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− | *** Cytokine production
| + | Their removal from the site after the removal of infection is an important step in the resolution of the lesion. Under physiological conditions the neutrophils undergo a process called '''apoptosis''' (or ''Programmed Cell Death''), and are then cleared by tissue macrophages (see above). However, if there are too few macrophages to clear the cells, or the infection is resulting in the death of the neutrophils, they undergo a process called '''necrosis'''. When these neutrophils accumulate at the site of infection it forms '''pus'''. |
− | *** Changes to vascular endothelium
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− | ** Neutrophil activation in an inflammatory lesion results in the release of '''prostaglandins'''
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− | *** Responsible for vasoactive changes and for pain
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− | * The accumulation of dead and dying [[Neutrophils|neutrophils]] at the site of infection is called '''pus'''
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− | ** Their removal from the site after the removal of infection is an important step in the resolution of the lesion
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| ==[[Eosinophils|Eosinophils]]== | | ==[[Eosinophils|Eosinophils]]== |