Lipopolysaccharide (LPS), an important component in the outer membrane of the cell wall of Gram-negative bacteria, can induce a systemic inflammatory response and play an important role in bacterial infection and disease evolution. The thick layer of mucus covering the small intestinal villus acts primarily to the first barrier from damage by toxic substances. We aimed to study the effects of LPS on the intestinal mucus layer barrier. The results showed that the thickness of the mucus layer was significantly increased by a low dose of LPS. Further, LPS can cross this barrier into the blood, put the body in a state of chronic low-grade inflammation, and activate the body's immune response. However, after a long-term high dose of LPS exposure, a large number of lysosomes in goblet cells caused a loss of function, and mucus layer thickness was significantly decreased. A large amount of LPS stuck to the mucus, leading to normal LPS and inflammatory cytokines level of plasma. The intestinal tissue morphology was damaged, and many immune cells died through necrosis in the intestine. Collectively, the function of the goblet cell was normal, a low dose of LPS cannot be stuck to the mucus layer. However, a high dose of LPS stuck to the mucus when goblet cells caused a loss of function, which can be directly linked to the severity of the immunosuppression in the body.

脂多糖（LPS）是革兰氏阴性细菌细胞壁外膜中的重要成分，可诱导全身性炎症反应，并在细菌感染和疾病演变中发挥重要作用。覆盖小肠绒毛的粘液层很厚，主要作用是防止有毒物质损坏的第一道屏障。我们旨在研究LPS对肠粘液层屏障的影响。结果表明，低剂量的LPS显着增加了粘液层的厚度。此外，LPS可以穿过该屏障进入血液，使人体处于慢性低度炎症状态，并激活人体的免疫反应。但是，长期高剂量的LPS暴露后，杯状细胞中的大量溶酶体导致功能丧失，粘液层厚度明显减少。大量的LPS粘在粘液上，导致正常的LPS和血浆炎症细胞因子水平。肠道组织形态受损，许多免疫细胞因肠道坏死而死亡。总的来说，杯状细胞的功能正常，不能将低剂量的LPS粘在粘液层上。但是，当杯状细胞导致功能丧失时，高剂量的LPS会粘在粘液上，这可能与体内免疫抑制的严重程度直接相关。低剂量的LPS不会粘在粘液层上。但是，当杯状细胞导致功能丧失时，高剂量的LPS会粘在粘液上，这可能与体内免疫抑制的严重程度直接相关。低剂量的LPS不会粘在粘液层上。但是，当杯状细胞导致功能丧失时，高剂量的LPS会粘在粘液上，这可能与体内免疫抑制的严重程度直接相关。