scholarly journals Interleukin-1β-induced Expression of IL-6 and Production of Human Chorionic Gonadotropin in Human Trophoblast Cells via Nuclear Factor-κB Activation

2004 ◽  
Vol 52 (3) ◽  
pp. 218-223 ◽  
Author(s):  
Satoru Tsukihara ◽  
Tasuku Harada ◽  
Imari Deura ◽  
Masahiro Mitsunari ◽  
Souichi Yoshida ◽  
...  
PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e39441 ◽  
Author(s):  
Ignacio Caballero ◽  
Sumiah Al Ghareeb ◽  
Shaghayegh Basatvat ◽  
Javier A. Sánchez-López ◽  
Mehrnaz Montazeri ◽  
...  

2002 ◽  
Vol 87 (11) ◽  
pp. 5199-5208 ◽  
Author(s):  
Kenzo Kosaka ◽  
Hiroshi Fujiwara ◽  
Keiji Tatsumi ◽  
Shinya Yoshioka ◽  
Yukiyasu Sato ◽  
...  

Abstract To investigate immune-endocrine interactions between the embryo and the mother early in pregnancy, we examined the effects of human chorionic gonadotropin (HCG) on IL-8 production by peripheral blood mononuclear cells (PBMC). Recombinant HCG promoted IL-8 secretion by PBMC derived from nonpregnant women. The induction of IL-8 mRNA expression was observed after 30 min of HCG stimulation. Adsorption of the HCG with anti-HCG antibodies confirmed the specificity of this effect. The translocation of nuclear factor κB into the nucleus and subsequent IL-8 production were observed mainly in monocytes, and IL-8 production was reduced when a proteasome inhibitor was added to inactivate nuclear factor κB. Although fluorescein isothiocyanate-labeled HCG was bound to the majority of monocytes, cell surface expression of HCG receptor was hardly detected. IL-8 production by HCG was not affected by inhibitors of protein kinases A and C. In contrast, this stimulation was attenuated by d-mannose, which inhibits binding to C-type lectins. The basal IL-8 production by PBMC from women early in pregnancy was significantly elevated, compared with that from nonpregnant women. This study showed that human monocytes respond to HCG and secrete IL-8 through a pathway different from the HCG receptor system, suggesting that this glycoprotein hormone can react with not only endocrine cells but also immune cells early in pregnancy, probably via primitive systems such as C-type lectins.


2007 ◽  
Vol 197 (6) ◽  
pp. S172
Author(s):  
Kathryn Drennan ◽  
Adrian Platts ◽  
Amelia Linneman ◽  
Graham Johnson ◽  
Stephen Krawetz

2004 ◽  
Vol 68 (2) ◽  
pp. 313-321 ◽  
Author(s):  
Fumie Hashimoto ◽  
Yoshinobu Oguchi ◽  
Mieko Morita ◽  
Kikumi Matsuoka ◽  
Satoru Takeda ◽  
...  

2001 ◽  
Vol 280 (6) ◽  
pp. G1296-G1304 ◽  
Author(s):  
Satoru Takahashi ◽  
Takuya Fujita ◽  
Akira Yamamoto

We investigated the role of nuclear factor-κB (NF-κB) in gastric ulcer healing in rats. NF-κB was activated in ulcerated tissue but not in normal mucosa, and the level of the activation was decreased with ulcer healing. NF-κB activation was observed in fibroblasts, monocytes/macrophages, and neutrophils. Treatment of gastric fibroblasts, isolated from the ulcer base, with interleukin-1β activated NF-κB and the subsequently induced cyclooxygenase-2 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) mRNA expression. Inhibition of activated NF-κB action resulted in suppression of both their mRNA expression and increases in PGE2 and CINC-1 levels induced by interleukin-1β. Persistent prevention of NF-κB activation caused an impairment of ulcer healing in rats. Gene expression of interleukin-1β, CINC-1, cyclooxygenase-2, and inducible nitric oxide synthase in ulcerated tissue had been inhibited before the delay in ulcer healing became manifest. The increased levels of cyclooxygenase-2 protein and PGE2 production were also reduced. These results demonstrate that NF-κB, activated in ulcerated tissue, might upregulate the expression of healing-promoting factors responsible for gastric ulcer healing in rats.


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