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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).

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 [[Introduction - Inflammation|inflammation]]: redness ('''rubor'''), heat ('''calor'''), swelling ('''tumour'''), 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).

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