title: Innate immunity and glucocorticoids: potential regulatory mechanisms in epididymal biology.
abstract: Inflammation is a primordial host response to invasion by pathogens or  tissue injury. During infection, microbes can activate immune cells through  pattern-recognition receptors, such as Toll-like receptors, an evolutionarily  conserved family of receptors that mediate innate immunity in a wide range of  organisms. Infection also triggers an increase in glucocorticoid levels as  part of the stress response. The scenario indicates that these signals have to  be well integrated to mount an effective host response to infection and  injury. The mechanisms by which innate and adaptive immunity are regulated, as  well as the intersection of these responses with glucocorticoids and the  glucocorticoid receptor (GR) in the epididymis, an organ essential for the  transport, maturation, storage, and protection of the spermatozoa, are not  well understood. In this review we bring together recent data demonstrating  the cellular and biochemical machinery involved in the response of the adult  rat epididymis to a bacterial product challenge. We also illustrate the basic  aspects of the expression, localization, function, and regulation of the GR by  steroid hormones (androgens and glucocorticoids) within the epididymis. We  conclude with considerations of controversial or still unanswered topics about  GR, now emerging as a regulatory step in epididymal biology, its functional  relationship with androgens and androgen receptor, and the innate immune  response of the epididymis. How these topics may be of interest as part of  future research in the area, and how they ultimately can help us to better  understand the epididymal function under noninflammatory and inflammatory  conditions, are also discussed.
authors.affiliation: Section of Experimental Endocrinology, Department of Pharmacology, Universidade Federal de São Paulo-Escola Paulista de Medicina, Rua 03 de maio 100, INFAR, Vila Clementino, São Paulo, SP, Brazil.
authors.forename: Erick José R
authors.initials: EJ
authors.lastname: Silva
authors.forename: Daniel B C
authors.initials: DB
authors.lastname: Queiróz
authors.forename: Alexandre
authors.initials: A
authors.lastname: Rodrigues
authors.forename: Luciana
authors.initials: L
authors.lastname: Honda
authors.forename: Maria Christina W
authors.initials: MC
authors.lastname: Avellar
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000276:immunology; D004822:Epididymis / Q000276:immunology*; D004823:Epididymitis / Q000276:immunology / Q000382:microbiology; D005938:Glucocorticoids / Q000276:immunology* / Q000378:metabolism*; D006801:Humans; D007113:Immunity, Innate; D008297:Male; D051379:Mice; D051381:Rats; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D051193:Toll-Like Receptors / Q000276:immunology / Q000378:metabolism
chemical_list: D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D051193:Toll-Like Receptors