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首页> 外文期刊>Infection and immunity >Expansion of Paneth Cell Population in Response to Enteric Salmonella enterica Serovar Typhimurium Infection
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Expansion of Paneth Cell Population in Response to Enteric Salmonella enterica Serovar Typhimurium Infection

机译：响应肠道小肠沙门氏菌血清型鼠伤寒感染潘氏细胞群的扩大。

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Paneth cells residing at the base of the small intestinal crypts contribute to the mucosal intestinal first line defense by secreting granules filled with antimicrobial polypeptides including lysozyme. These cells derive from the columnar intestinal stem cell located at position 0 and the transit amplifying cell located at position +4 in the crypts. We have previously shown that Salmonella enterica serovar Typhimurium (ST), a leading cause of gastrointestinal infections in humans, effects an overall reduction of lysozyme in the small intestine. To extend this work, we examined small-intestinal tissue sections at various time points after ST infection to quantify and localize expression of lysozyme and assess Paneth cell abundance, apoptosis, and the expression of Paneth cell differentiation markers. In response to infection with ST, the intestinal Paneth cell-specific lysozyme content, the number of lysozyme-positive Paneth cells, and the number of granules per Paneth cell decreased. However, this was accompanied by increases in the total number of Paneth cells and the frequency of mitotic events in crypts, by increased staining for the proliferation marker PCNA, primarily at the crypt side walls where the transit amplifying cell resides and not at the crypt base, and by apoptotic events in villi. Furthermore, we found a time-dependent upregulation of first β-catenin, followed by EphB3, and lastly Sox9 in response to ST, which was not observed after infection with a Salmonella pathogenicity island 1 mutant deficient in type III secretion. Our data strongly suggest that, in response to ST infection, a Paneth cell differentiation program is initiated that leads to an expansion of the Paneth cell population and that the transit amplifying cell is likely the main progenitor responder. Infection-induced expansion of the Paneth cell population may represent an acute intestinal inflammatory response similar to neutrophilia in systemic infection.
机译：驻留在小肠隐窝底部的Paneth细胞通过分泌填充有包括溶菌酶在内的抗菌多肽的颗粒来促进粘膜小肠一线防御。这些细胞来自隐窝中位于位置0的柱状肠干细胞和位于位置+4的转运扩增细胞。先前我们已经表明，肠炎沙门氏菌血清型鼠伤寒沙门氏菌（ST）是人类胃肠道感染的主要原因，它会导致小肠溶菌酶的总体减少。为了扩展这项工作，我们检查了ST感染后各个时间点的小肠组织切片，以量化和定位溶菌酶的表达，并评估Paneth细胞的丰度，凋亡和Paneth细胞分化标志物的表达。响应ST感染，肠道Paneth细胞特有的溶菌酶含量，溶菌酶阳性Paneth细胞的数量以及每个Paneth细胞的颗粒数均减少。但是，这伴随着Paneth细胞总数的增加和隐窝中有丝分裂事件的发生率的增加，主要是通过增殖标记PCNA染色的增加，主要是在转运放大细胞所在的隐窝侧壁而不是隐窝底部以及绒毛中的凋亡事件。此外，我们发现第一个β-catenin，EphB3，最后是Sox9对ST的响应呈时间依赖性上调，但感染III型分泌缺陷的沙门氏菌致病岛1突变体后未观察到。我们的数据强烈表明，响应ST感染，启动了Paneth细胞分化程序，该程序导致Paneth细胞群体的扩大，而转运扩增细胞很可能是主要的祖细胞应答者。感染引起的Paneth细胞群扩增可能代表与全身感染中的中性粒细胞相似的急性肠道炎症反应。

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