{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T18:01:00Z","timestamp":1778781660485,"version":"3.51.4"},"reference-count":30,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2012,5,10]],"date-time":"2012-05-10T00:00:00Z","timestamp":1336608000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Neuroendocrinology"],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:p>The hypothalamic\u2010pituitary\u2010adrenocortical (HPA) responses to bacterial infection are mediated, in part, by the actions of lipopolysaccharide (LPS) on pituitary folliculostellate (FS) cells that release pro\u2010inflammatory cytokines [e.g. interleukin (IL)\u20106] and thereby facilitate adrenocorticotrophic hormone (ACTH) release from neighbouring corticotrophs. In the present study, two murine pituitary cell lines [TtT\/GF (FS cells) and AtT20 D16:16 (corticotrophs)], alone and in co\u2010culture, and an <jats:italic>in vivo<\/jats:italic> model of endotoxaemia were used to examine the potential role of nuclear factor\u2010kappa B (NF\u2010\u03baB) in mediating LPS\u2010induced ACTH secretion. Both cell lines expressed mRNAs for the key components of the LPS signalling system. LPS stimulated IL\u20106 release from TtT\/GF cells via a glucocorticoid\u2010sensitive, NF\u2010\u03baB\u2010dependent mechanism; it also activated NF\u2010\u03baB in AtT20 cells, as did corticotrophin\u2010releasing hormone (CRH). IL\u20106 potentiated (but LPS reduced) the stimulatory effects of CRH on ACTH release from AtT20 cells, whereas blockade of NF\u2010\u03baB (SC\u2010514) increased the ACTH release induced by CRH in the presence or absence of LPS. In co\u2010cultures, CRH and LPS acted synergistically to induce release of both IL\u20106 and ACTH. However, although SC\u2010514 suppressed the release of IL\u20106 evoked by CRH and LPS, it potentiated the concomitant increase in ACTH release. <jats:italic>In vivo<\/jats:italic> both immunological (LPS) and psychological (restraint) stress increased intrapituitary NF\u2010\u03baB, whereas an NF\u2010\u03baB inhibitor (PHA781535E) attenuated the LPS\u2010induced release of ACTH and abolished the HPA response to restraint stress. The results obtained in the present study support the premise that NF\u2010\u03baB plays an important role in mediating LPS signalling in the anterior pituitary gland, particularly in relation to IL\u20106 and ACTH secretion, and provide novel evidence that NF\u2010\u03baB blockade <jats:italic>in vivo<\/jats:italic> compromises stress\u2010induced ACTH release.<\/jats:p>","DOI":"10.1111\/j.1365-2826.2012.02285.x","type":"journal-article","created":{"date-parts":[[2012,1,27]],"date-time":"2012-01-27T22:06:13Z","timestamp":1327701973000},"page":"862-873","source":"Crossref","is-referenced-by-count":9,"title":["Evidence From In Vitro and In Vivo Studies Showing that Nuclear Factor\u2010Kappa B Within the Pituitary Folliculostellate Cells and Corticotrophs Regulates Adrenocorticotrophic Hormone Secretion in Experimental Endotoxaemia"],"prefix":"10.1111","volume":"24","author":[{"given":"D. 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