Changes

[[File:Extravasation.png|thumb|right|300px|Extravasation (the Movement of Leukocytes from the Bloodstream) - R.J. Francis, RVC 2012]]

[[File:Extravasation.png|thumb|right|300px|Extravasation (the Movement of Leukocytes from the Bloodstream) - R.J. Francis, RVC 2012]]

<p>Neutrophils are extremely motile and express a number of adhesion molecules on their surface which allows them to attach to the walls of capillaries. </p>

<p>Neutrophils are extremely motile and express a number of adhesion molecules on their surface which allows them to attach to the walls of capillaries. </p>

<p>Selection molecules expressed on the surface of neutrophil bind to receptors on the capillary endothelium causing a loose attachment. This allows the neutrophil to “roll” along the surface of capillaries. Stimulation by chemokines causes further attachment between the neutrophils intergrin molecules and associated receptors on the endothelium. Finally signalling molecules or [[Cytokines|cytokines]] such as tumour necrosis factor alpha (TNF-α) and interleukin 1 (IL-1) cause the expression of inter-cellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) on the enothelium enabling the neutrophils to form a firm attachment through the beta2 integrin adhesion molecules (in particular LFA-1). </p>

<p>Selection molecules expressed on the surface of neutrophil bind to receptors on the capillary endothelium causing a loose attachment. This allows the neutrophil to “roll” along the surface of capillaries. Stimulation by chemokines causes further attachment between the neutrophils intergrin molecules and associated receptors on the endothelium. Finally signalling molecules or [[Cytokines|cytokines]] such as tumour necrosis factor alpha (TNF-α) and interleukin 1 (IL-1) cause the expression of inter-cellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) on the enothelium enabling the neutrophils to form a firm attachment through the β2 integrin adhesion molecules (in particular LFA-1). </p>

<p>The neutrophil then exhibits amoeboid movement and can pass through holes in the capillary wall that are smaller than themselves ('''diapedesis'''). This is achieved by extending a small part of the cell (a pseudopodium) through the capillary; the neutrophil's cytoplasm and contents then passes through. This process is assisted by the release of histamine and other vasodilators by other inflammatory cells.</p>

<p>The neutrophil then exhibits amoeboid movement and can pass through holes in the capillary wall that are smaller than themselves ('''diapedesis'''). This is achieved by extending a small part of the cell (a pseudopodium) through the capillary; the neutrophil's cytoplasm and contents then passes through. This process is assisted by the release of histamine and other vasodilators by other inflammatory cells.</p>

<p>Once within the tissue, neutrophils respond to chemotactic substances such as [[Cytokines|cytokines]] or bacterial products which attract the neutrophil to the area of damage/ infection. This process is called '''chemotaxis''' (see below for a link to a video of this process). Once neutrophils have entered tissue they do not return to the blood stream but instead undergo cell death (see below) .</p>

<p>Once within the tissue, neutrophils respond to chemotactic substances such as [[Cytokines|cytokines]] or bacterial products which attract the neutrophil to the area of damage/ infection. This process is called '''chemotaxis''' (see below for a link to a video of this process). Once neutrophils have entered tissue they do not return to the blood stream but instead undergo cell death (see below) .</p>