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Neurogenic Inflammation and Arthritis
Author(s) -
LEVINE JON D.,
KHASAR SACHIA G.,
GREEN PAUL G.
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1351.014
Subject(s) - extravasation , inflammation , hyperalgesia , sexual dimorphism , nociceptor , immune system , arthritis , medicine , immunology , neuroscience , endocrinology , nociception , biology , receptor
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.