Enterocyte apoptosis and barrier function are modulated by SIgA after exposure to bacteria and hypoxia/reoxygenation
Enterocyte apoptosis and barrier function are modulated by SIgA after exposure to bacteria and hypoxia/reoxygenation
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DOI：
10.1016/s0039-6060(03)00302-7
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发表时间：
2003-10-01
期刊：
影响因子：
3.8
通讯作者：
Brown, WJ
中科院分区：
文献类型：
--
作者：
Diebel, LN;Liberati, DM;Brown, WJ
背景。分泌性免疫球蛋白 A (SIgA) 是肠道粘膜表面针对管腔病原体的主要免疫防御。它还具有抗炎活性，这对于维持粘膜表面完整性可能很重要。在受到侵入性细菌攻击和缺血再灌注损伤后，肠细胞凋亡（Apo）增加。 Apo 增加还与肠道屏障功能受损有关。然而，在共生菌攻击和缺血再灌注后，SIgA 对肠细胞凋亡和粘膜屏障完整性的影响尚不清楚。方法。将 Caco2 肠上皮细胞单层置于 21% O-2（对照）或 95% N-2/15% CO2（缺氧）条件下 90 分钟，然后加入 21% O-2。大肠杆菌和 SIgA 被添加到子集中。 Caco2 细胞 Apo 通过流式细胞术和以葡聚糖-异硫氰酸荧光素渗透性为指标的屏障功能进行鉴定。结果。与对照组相比，暴露于细菌或缺氧复氧后 Apo Caco2 细胞的百分比没有差异。在细菌/缺氧-复氧联合挑战后，Apo 显着增加。 SIgA 在这种联合攻击后消除了 Apo 反应并保留了屏障功能。结论。 SIgA 对肠上皮细胞 Apo 的调节可能有助于维持肠道屏障功能，从而减少与肠道缺血再灌注损伤相关的临床状况后的全身炎症反应。
Background. Secretory immunoglobulin A (SIgA) is the principal immune defense against luminal pathogens at gut mucosal surfaces. It also has anti-inflammatory activities that may be important for the maintenance Of mucosal surface integrity. Enterocyte apoptosis (Apo) is increased after challenge with invasive bacteria and ischemia-reperfusion insults. Increased Apo also has been associated with impaired intestinal barrier function. However, the impact of SIgA on enterocyte apoptosis and mucosal barrier integrity after challenge with commensal bacteria and ischemia-reperfusion is unknown.Methods. Caco2 intestinal epithelial cell monolayers were subjected to 21% O-2 (control) or 95% N-2/ 15% CO2 (hypoxic) conditions for 90 minutes, followed by 21% O-2. Escherichia coli and SIgA were added in subsets. Caco2 cell Apo was identified by flow cytometry and barrier function indexed by permeability to dextran-fluorescein isothiocyanate.Results. There were no differences in the percentage of Apo Caco2 cells after exposure to either bacteria or hypoxic-reoxygenation versus control. There was a significant increase in Apo after the combined bacteria/hypoxia-reoxygenation challenge. SIgA abrogated the Apo response and preserved barrier function after this combined challenge.Conclusion. Modulation of enterocyte Apo by SIgA may serve to maintain intestinal barrier function and thereby decrease the systemic inflammatory response after clinical conditions associated with gut ischemia-reperfusion insults.