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Complement C3a receptors in the pituitary gland: a novel pathway by which an innate immune molecule releases hormones involved in the control of inflammation
Author(s) -
Francis Karen,
Lewis B. Mary,
Akatsu Hiroyasu,
Monk Peter N.,
Cain Stuart A.,
Scanlon Maurice F.,
Morgan B. Paul,
Ham Jack,
Gasque Philippe
Publication year - 2003
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.02-1103fje
Subject(s) - innate immune system , hormone , endocrinology , medicine , immune system , receptor , prolactin , inflammation , biology , corticosterone , anterior pituitary , immunology
Two‐way communication exists between the endocrine and immune systems using molecules such as hormones and cytokines. Here we describe a new pathway by which C3a, a complement‐ derived cytokine, stimulates anterior pituitary hormone release and activates the hypothalamic‐ pituitary‐adrenal axis, a reflex central to the stress response and to the control of inflammation. We show that C3a receptors are expressed in pituitary hormone secreting and non‐hormone secreting (folliculostellate) cells and that both C3a and C3adesArg (a non‐inflammatory metabolite) stimulate pituitary cell cultures to release prolactin, growth hormone, and adrenocorticotropin. Serum levels of these hormones, together with adrenal corticosterone, increase dose dependently with recombinant C3a and C3adesArg administration in vivo. Pertussis toxin blocks the response to C3a but not C3adesArg, which indicates the presence of two receptors, only one of which is coupled to Gαi‐proteins. We propose that the complement innate immune molecules (cytokines) modulate tissue‐specific and systemic inflammatory responses through communication with the endocrine pituitary gland.