Abstract
The lifespan of neutrophils is longer than expected and has been reported to be deeply involved in the pathophysiology of various chronic inflammatory diseases. In endometriosis patients, aberrant expression, and function of neutrophil chemokines, change in peripheral blood neutrophil count, and dysfunction of neutrophils in the local endometriotic tissues have been reported. These findings together with animal endometriosis models have indicated deep neutrophil involvement in the pathology of endometriosis. Various therapeutic targets for endometriosis related to neutrophils have been proposed. Those include cabergoline, formyl peptide receptor 1, cyclooxygenase-2 inhibitor, and all-transretinoic acid. Other candidates are drugs which have been shown to modify neutrophil function and are now in practical use for other chronic inflammatory diseases.
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