期刊
CLINICAL AND EXPERIMENTAL IMMUNOLOGY
卷 149, 期 1, 页码 155-161出版社
WILEY
DOI: 10.1111/j.1365-2249.2007.03376.x
关键词
chemotaxis; lactoferrin; LPS; neutrophil; TGF-beta
类别
资金
- NIAID NIH HHS [T32 AI007363, 1 P01 AI/NS 51877, P01 AI051877, AI07363] Funding Source: Medline
Neutrophils enter tissues including the uterus and are found in the endometrium in increased numbers prior to menses. In this environment, they are exposed to transforming growth factor (TGF)-beta 1 produced by endometrial stromal and epithelial cells. We observed that incubation of neutrophils in vitro with TGF-beta 1 at 1 pg/ml significantly reduced their secretion of lactoferrin in response to lipopolysaccharide (LPS). This effect was achieved with as little as 15 min of pretreatment with TGF-beta 1. Inhibition of lactoferrin release by TGF-beta 1 was observed irrespective of whether neutrophils were stimulated by ligands for Toll-like receptor (TLR)-2, TLR-4 or FPR, the G protein-coupled receptor for formylated peptides. Inhibition by TGF-beta 1 was negated by SB-431542, a small molecule inhibitor that specifically blocks the kinase activity of the type I TGF-beta receptor (ALK5) In contrast to lactoferrin release, another important neutrophil function, interleukin (IL)-8 driven chemotaxis, was not affected by TGF-beta 1 at 1 pg/ml or 100 pg/ml. We conclude that in tissues of the female reproductive tract, TGF-beta 1 inhibition of neutrophil degranulation may prevent these cells from initiating an inflammatory response or releasing degradative enzymes that could potentially damage the oocyte or fetus.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据