(J Am Coll Cardiol Intv 2009;2:655-62) (C) 2009 by the American C

(J Am Coll Cardiol Intv 2009;2:655-62) (C) 2009 by the American College of Cardiology Foundation”
“Trichomonas vaginalis commonly causes vaginitis and perhaps cervicitis in women and urethritis in men and women. Macrophages are important immune cells in response to T. vaginalis infection. In this study, we investigated whether human macrophages could be involved in inflammation induced by T. vaginalis. Human monocyte-derived macrophages

( HMDM) were co-cultured with T. vaginalis. Live, opsonized-live trichomonads, and T. vaginalis lysates increased proinflammatory cytokines, such as TNF-alpha, IL-1 beta, and IL-6 by HMDM. The involvement of nuclear factor (NF)-kappa B signaling pathway in cytokine production induced by T. vaginalis BMS-777607 cost was confirmed by phosphorylation and nuclear translocation of p65 NF-kappa B. In addition, stimulation with live T. vaginalis induced marked augmentation of nitric oxide ( NO) production and expression of inducible NO synthase ( iNOS) levels in HMDM. However, trichomonad-induced

NF-kappa B activation and TNF-alpha production in macrophages were significantly inhibited by inhibition of iNOS levels with L-NMMA ( NO synthase inhibitor). Moreover, pretreatment with NF-kappa B inhibitors ( PDTC or Bay11-7082) caused human macrophages to produce less TNF-alpha. These results suggest that T. vaginalis stimulates human macrophages to produce proinflammatory cytokines, such as IL-1, IL-6, and TNF-alpha, and NCT-501 concentration NO. In particular, we showed that T. vaginalis induced TNF-alpha production in macrophages through NO-dependent activation of NF-kappa B, which might be closely involved in inflammation caused by T. vaginalis.”
“In immune responses, activated

T cells migrate to B-cell follicles and develop into follicular T-helper (T-FH) cells, a recently identified subset of BI6727 CD4(+) T cells specialized in providing help to B lymphocytes in the induction of germinal centres(1,2). Although Bcl6 has been shown to be essential in T-FH-cell function, it may not regulate the initial migration of T cells(3) or the induction of the T-FH program, as exemplified by C-X-C chemokine receptor type 5 (CXCR5) upregulation(4). Here we show that expression of achaete-scute homologue 2 (Ascl2)-a basic helix-loop-helix (bHLH) transcription factor(5)-is ;selectively upregulated in T-FH cells. Ectopic expression of Ascl2 upregulates CXCR5 but not Bcl6, and downregulates C-C chemokine receptor 7 (CCR7) expression in T cells in vitro, as well as accelerating T-cell migration to the follicles and T-FH-cell development in vivo in mice. Genome-wide analysis indicates that Ascl2 directly regulates T-FH-related genes whereas it inhibits expression of T-helper cell 1 (T(H)1) and T(H)17 signature genes.

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