Changes

Neutrophils are the first inflammatory cells to enter damaged tissue from the blood after tissue damage has being caused. They are the predominant cell 4 - 6 hours after the beginning of an inflammatory reaction; at 12 hours there are also substantial numbers of [[Macrophages|macrophages]] and at 24 hours there are equal numbers of neutrophils and macrophages.  

Neutrophils are the first inflammatory cells to enter damaged tissue from the blood after tissue damage has being caused. They are the predominant cell 4 - 6 hours after the beginning of an inflammatory reaction; at 12 hours there are also substantial numbers of [[Macrophages|macrophages]] and at 24 hours there are equal numbers of neutrophils and macrophages.  

===Phagocytosis===

===Phagocytosis===

<p>The main role of the neutrophil is to engulf and destroy foreign material through [[Phagocytosis|phagocytosis]]. They uptake this material via endocytosis and this surrounds the material in the neutrophil membrane forming a '''phagosome'''. Lysosomes inside the neutrophil then fuse with the phagosome and release their contents degrading the foreign material. Phagocytosing material shortens the lifespan of the neutrophil due to the build up of toxins both from the degraded bacteria etc. and also from its own lysosomes contents.  Most neutrophils die after phagocytosing 5-25 bacteria; sufficient numbers of dead neutrophils form [[Necrosis - Pathology#Pus Formation|pus]].</p>

<p>The main role of the neutrophil is to engulf and destroy foreign material through [[Phagocytosis|phagocytosis]]. They uptake this material via endocytosis and this surrounds the material in the neutrophil membrane forming a '''phagosome'''. Lysosomes inside the neutrophil then fuse with the phagosome and release their contents degrading the foreign material. Phagocytosing material shortens the lifespan of the neutrophil due to the build up of toxins both from the degraded bacteria etc. and also from its own lysosomes contents.  Most neutrophils undergo programmed cell death after phagocytosing 5-25 bacteria (see below) </p>

<p>Neutrophils do not always destroy engulfed particles and may instead transport them to local lymph nodes to be dealt with by other host defence mechanisms. This means that acute inflammation in tissue can be accompanied by an acute inflammation in the lymph nodes.</p>

<p>Neutrophils do not always destroy engulfed particles and may instead transport them to local lymph nodes to be dealt with by other host defence mechanisms. This means that acute inflammation in tissue can be accompanied by an acute inflammation in the lymph nodes.</p>

====Recognition====

====Recognition====

====Further amplification of inflammation====

====Further amplification of inflammation====

Neutrophils have many mechanisms to increase inflammation. These include [[Cytokines|cytokine]] release and exocytosis of vasoactive peptides as mentioned above.  Neutrophil activation in an inflammatory lesion can also result in the release of prostaglandins, through synthesis by cyclo-oxygenase 2, 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).

Neutrophils have many mechanisms to increase inflammation. These include [[Cytokines|cytokine]] release and exocytosis of vasoactive peptides as mentioned above.  Neutrophil activation in an inflammatory lesion can also result in the release of prostaglandins, through synthesis by cyclo-oxygenase 2, 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).

===Interactions===

===Interactions===

<p>Il-6, Il-8 and C5a are all chemoattractants for neutrophils.</p>

<p>Il-6, Il-8 and C5a are all chemoattractants for neutrophils.</p>