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a Department of Medicine, NIH Pain Center, University of California, San Francisco, San Francisco, California 94143-0440, USA b Oral and Maxillofacial Surgery, NIH Pain Center, University of California, San, Francisco, San Francisco, California 94143-0440, USA
Key Words: nociception • pain • hyperalgesia • inflammation • inflammatory diseases • sympathoadrenal axis • adrenal medulla • hypothalamic-pituitary-adrenal axis • plasma extravasation • sex differences • 17  -estradiol • testosterone • chemotaxis • -adrenergic receptor • polymorphonuclear leukocytes
Address for correspondence: Jon D. Levine, NIH Pain Center, C522 Box 0440, UCSF, 521 Parnassus Avenue, San Francisco, CA 94143-0440, USA. Voice: +1-415-476-5108; fax: +1-415-476-6305. e-mail: Jon.Levine{at}ucsf.edu
Inflammation and inflammatory diseases are sexually dimorphic, but the underlying causes for this observed sexual dimorphism are poorly understood. We discuss neural-immune mechanisms that underlie sexual dimorphism in three critical aspects of the inflammatory process—plasma extravasation, neutrophil function, and inflammatory hyperalgesia. Plasma extravasation and accumulation/activation of leukocytes into tissues are critical components in inflammation and are required for several other aspects of the inflammatory response. Pain (hyperalgesia) also markedly influences the magnitude of other components of the inflammatory response and induces a feedback control of plasma extravasation and neutrophil function. More important, this feedback control itself is powerfully modulated by vagal afferent activity and both the function of the primary afferent nociceptor and the modulation of inflammatory hyperalgesia by vagal afferent activity are highly sexually dimorphic.
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