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首页> 外文期刊>Infection and immunity >Critical Role for Interleukin-1β (IL-1β) during Chlamydia muridarum Genital Infection and Bacterial Replication-Independent Secretion of IL-1β in Mouse Macrophages
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Critical Role for Interleukin-1β (IL-1β) during Chlamydia muridarum Genital Infection and Bacterial Replication-Independent Secretion of IL-1β in Mouse Macrophages

机译：白细胞介素1β（IL-1β）在鼠衣原体生殖器感染和小鼠巨噬细胞中细菌复制非依赖性分泌IL-1β的过程中的关键作用

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Recent findings have implicated interleukin-1β (IL-1β) as an important mediator of the inflammatory response in the female genital tract during chlamydial infection. But how IL-1β is produced and its specific role in infection and pathology are unclear. Therefore, our goal was to determine the functional consequences and cellular sources of IL-1β expression during a chlamydial genital infection. In the present study, IL-1β?/? mice exhibited delayed chlamydial clearance and decreased frequency of hydrosalpinx compared to wild-type (WT) mice, implying an important role for IL-1β both in the clearance of infection and in the mediation of oviduct pathology. At the peak of IL-1β secretion in WT mice, the major producers of IL-1β in vivo are F4/80+ macrophages and GR-1+ neutrophils, but not CD45? epithelial cells. Although elicited mouse macrophages infected with Chlamydia muridarum in vitro secrete minimal IL-1β, in vitro prestimulation of macrophages by Toll-like receptor (TLR) ligands such as lipopolysaccharide (LPS) purified from Escherichia coli or C. trachomatis L2 prior to infection greatly enhanced secretion of IL-1β from these cells. By using LPS-primed macrophages as a model system, it was determined that IL-1β secretion was dependent on caspase-1, potassium efflux, and the activity of serine proteases. Significantly, chlamydia-induced IL-1β secretion in macrophages required bacterial viability but not growth. Our findings demonstrate that IL-1β secreted by macrophages and neutrophils has important effects in vivo during chlamydial infection. Additionally, prestimulation of macrophages by chlamydial TLR ligands may account for the elevated levels of pro-IL-1β mRNA observed in vivo in this cell type.
机译：最近的发现暗示白细胞介素-1β（IL-1β）是衣原体感染期间女性生殖道炎症反应的重要介体。但是尚不清楚IL-1β的产生方式及其在感染和病理学中的特殊作用。因此，我们的目标是确定衣原体生殖器感染期间IL-1β表达的功能后果和细胞来源。在本研究中，与野生型（WT）小鼠相比，IL-1β？/？小鼠的衣原体清除延迟，输卵管积水的频率降低，这暗示IL-1β在清除中均具有重要作用感染和输卵管病理的介导。在WT小鼠的IL-1β分泌高峰期，体内IL-1β的主要产生者是F4 / 80 + 巨噬细胞和GR-1 + 中性粒细胞，但不是CD45 ？上皮细胞。尽管在体外感染了 C 衣原体 muridarum 的小鼠巨噬细胞分泌的IL-1β极少，但Toll样受体（TLR）在体外对巨噬细胞的预刺激）配体，例如从 E 沙门氏菌 大肠杆菌或 C纯化的脂多糖（LPS）。感染前沙眼L2大大增强了这些细胞中IL-1β的分泌。通过使用LPS引发的巨噬细胞作为模型系统，可以确定IL-1β的分泌取决于caspase-1，钾的流出和丝氨酸蛋白酶的活性。值得注意的是，衣原体诱导的巨噬细胞IL-1β分泌需要细菌生存力，但不需要生长。我们的发现表明巨噬细胞和中性粒细胞分泌的IL-1β在衣原体感染期间在体内具有重要作用。另外，衣原体TLR配体对巨噬细胞的预刺激可能解释了这种细胞类型在体内观察到的pro-IL-1βmRNA水平升高。

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