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柠檬醛缓解了肽聚糖诱导的猪肠上皮细胞炎症和屏障功能障碍。

Citral alleviates peptidoglycan-induced inflammation and disruption of barrier functions in porcine intestinal epithelial cells.

机构信息

College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.

Department of Animal Science, University of Manitoba, Winnipeg, Manitoba, Canada.

出版信息

J Cell Physiol. 2022 Mar;237(3):1768-1779. doi: 10.1002/jcp.30640. Epub 2021 Nov 18.

DOI:10.1002/jcp.30640
PMID:34791644
Abstract

Peptidoglycan (PGN) is a major polymer in bacterial cell walls and may constrain gut functionality and lower intestinal efficiencies in livestock. Citral has been reported to exhibit antibacterial and anti-inflammatory biological activities, improving the gastrointestinal function of swine. However, the protective effect of citral against PGN-elicited cellular responses and possible underlying mechanisms are unknown. In this study, the porcine jejunal epithelial cell line (IPEC-J2) was challenged with PGN from Staphylococcus aureus (S. aureus) or Bacillus subtilis (B. subtilis) to explore PGN-induced inflammatory responses. Our data showed that the inflammatory response stimulated by PGN from harmful bacteria (S. aureus) was more potent than that from commensal bacteria (B. subtilis) in IPEC-J2 cells. Based on the inflammatory model by PGN from S. aureus, it was demonstrated that PGN could significantly induce inflammatory cytokine production and influence nutrient absorption and barrier function in a dose-dependent manner. However, the PGN-mediated immune responses were remarkably suppressed by citral. In addition, citral significantly attenuated the effect of PGN on the intestine nutrient absorption and barrier function. The expression of TLR2 was strongly induced by PGN stimulation, which was suppressed by citral. All data nominated that citral downregulated PGN-induced inflammation via TLR2-mediated activation of the NF-κB signaling pathway in IPEC-J2 cells. Furthermore, the results also indicate that the PGN degradation through the inclusion of enzymes (e.g., muramidase) as well as the inclusion of citral for attenuating inflammation may improve pig gut health and functionality.

摘要

肽聚糖(PGN)是细菌细胞壁的主要聚合物,可能会限制肠道功能并降低家畜的肠道效率。柠檬醛已被报道具有抗菌和抗炎的生物活性,可改善猪的胃肠道功能。然而,柠檬醛对 PGN 引发的细胞反应的保护作用及其潜在机制尚不清楚。在这项研究中,用金黄色葡萄球菌(S. aureus)或枯草芽孢杆菌(B. subtilis)的 PGN 刺激猪空肠上皮细胞系(IPEC-J2),以探讨 PGN 诱导的炎症反应。我们的数据表明,有害细菌(金黄色葡萄球菌)的 PGN 刺激引起的炎症反应比共生细菌(枯草芽孢杆菌)更强。基于金黄色葡萄球菌 PGN 引起的炎症模型,证明 PGN 可显著诱导炎症细胞因子的产生,并以剂量依赖的方式影响营养物质的吸收和屏障功能。然而,柠檬醛显著抑制了 PGN 介导的免疫反应。此外,柠檬醛显著抑制了 PGN 对肠道营养吸收和屏障功能的影响。TLR2 的表达在 PGN 刺激下被强烈诱导,而柠檬醛抑制了这一作用。所有数据都表明,柠檬醛通过 TLR2 介导的 NF-κB 信号通路的激活,下调了 IPEC-J2 细胞中 PGN 诱导的炎症。此外,研究结果还表明,通过包含酶(如溶菌酶)降解 PGN 以及包含柠檬醛来减轻炎症可能会改善猪的肠道健康和功能。

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