Clostridium perfringens (Cp) type A is one of the primary microorganisms responsible for bacterial diarrhoea in weaning piglets. Matrine, a tetracyclic quinolizidine alkaloid, exhibits diverse bioactive properties, including anti-inflammatory and neuroprotective effects. To better understand the anti-inflammatory mechanisms of Matrine on piglets infected with Cp type A (CpA). We investigated its preventive effects against diarrhoea over a 14-days period. Our results showed that 30 mg/kg of Matrine is non-toxic and does not harm the histological structure of organ tissues or alter the haematological indices of piglets. Matrine significantly reduced the abundance of CpA in faecal and intestines, as well as the content of toxin-α. The inflammatory response was mitigated following Matrine treatment, and physiological organ functions were restored, particularly through the repair of intestinal mucosal layer and sIgA level. Matrine also promoted a high abundance of beneficial intestinal microbiota, including Lactobacillus, Bacteroidota, Muribaculaceae, and Oscillospirales. This microbial composition inhibited the abundance of epithelial cells by Cp, thereby further reducing the diarrhoea rate and mortality in piglets. In conclusion, Matrine promotes the abundance of intestinal probiotics, inhibits the colonization of CpA, reduces the inflammatory response as well as restores intestinal tissue hismorphology. It will be used as a therapeutic agent diarrhea of piglets infected with CpA in the furture.

Microbial production of organic acids has been hindered by the poor acid tolerance of microorganisms and the high costs of waste salt reprocessing. The robustness of non-conventional microorganisms in an acidic environment makes it possible to produce organic acids at low pH and greatly simplifies downstream processing. In this review we discuss the environmental adaptability features of non-conventional yeasts, as well as the latest developments in genomic engineering strategies that have facilitated metabolic engineering of these strains. We also use selected examples of three-carbon (C3), C4, and C6 organic acids to illustrate the ongoing efforts and challenges of using non-conventional yeasts for organic acid production. This review provides theoretical guidance for the construction of highly robust organic acid producers.

Porcine reproductive and respiratory syndrome virus (PRRSV) causes abortions, stillbirths, and dummy pregnancies. Previous studies found that PRRSV can promote secondary bacterial infections and elevate bacterial endotoxin levels, further increasing the abortion rate in sows. However, the pathways by which bacterial endotoxins invade the bodies of PRRSV(+) sows and aggravate their clinical symptoms are unknown. In this study, we established a model of PRRSV and lipopolysaccharide (LPS) working together on porcine endometrial epithelial cells (PEECs). We speculate that PRRSV and LPS affect PEECs through viral protein interaction with cytokines and cytokine receptors, natural killer cell-mediated cytotoxicity, and regulation of actin cytoskeleton signaling pathways by analyzing seq-RNA. The PRRSV proteins act on inflammatory factors and their receptors to activate chemokines-5 (CCL5), chemokines-4 (CCL4), and chemokines-8 (CCL8) mRNA expression, causing severe inflammatory reactions. In addition, the elevation of MEK1/2 factors and the integrins acting on NK cells promote the upregulation of VAV1/Tiam1, RAC, and IRSp53, leading to increased expression of Arp2/3 and F-actin in PEECs in the PRRSV + LPS(+) groups. However, the highly expressed cell microfilaments and cytoskeleton disrupt the original network structure, causing changes in the original physiological function of the PEECs. In summary, the PRRSV protein interacts with cytokines and cytokine receptors of PEECs, thereby enhancing virus-mediated chemokine factors and their receptor activity, accelerating bacterial endotoxin entry into the body and the invasion of cells. They destroy the cytoskeletal structure of the cells and increase damage to uterine tissue.

To analysis repair function of mucin-2(MUC2) and glycoprotein particles on the tight junction protein of uterus under bacterial endotoxins. In this experiment, we showed that the thicker mucus layer of the uterus is used to prevent the translocation of endotoxin at 21d postdelivery. When endotoxin acts on the uterus to thin its mucous layer, the cells in the lamina propria of the uterus secrete a large number of glycoprotein particles at 27d postdelivery. Due to a significantly decrease in the expression of glycosyltransferase, the glycoprotein particles are incompletely glycosylation MUC2, which can interact with the cell membrane and are released in large quantities in the form of exocytosis. These glycoprotein particles can significantly repair tight junction proteins in the inter-cellular space and significantly increase the expression of Claudin-1, JAM (Junction adhesion molecule-A), E-cadherin, ZO-1(Zonula occludens-1) and desmosome proteins after endotoxin treatment. The results of the present study show that endotoxins can thin the uterine mucus layer and accelerate the release of incompletely glycosylated MUC2 from lamina propria cells. In inter-cellular spaces, MUC2 can increase its expression levels and distribution area to repair the tight junction structure of cells with larger gaps. Further strengthening of the barrier prevents endotoxin translocation by repairing the tight junction structure of uterine epithelial cells.

To analysis fuction of mucin-2 on the tight junction structure of uterus under dacterial endotoxins. Endotoxins are produced by lipopolysaccharides (LPS) components in the outer membrane of gram-negative bacteria, which cause great harm to humans and animals. A vast number of mucin-2 (MUC2) forms a mucus layer covering endometrial epithelial cells. The mucus layer and tight junction structure of epithelial cells can resist damage from foreign bacteria and their toxins in the uterus. However, the interaction between MUC2 and tight junction proteins is not clear. In this experiment, we used endotoxin to treat uterine tissue pre- and postweaning in female mice and observed the effect of endotoxin-induced MUC2 on the tight junction structure of epithelial cells in the uterus. The results showed that a large amount of endotoxin accumulated in the uterus after 21 days of postdelivery weaning. The thicker mucus layer of the uterus is used to prevent the translocation of endotoxin at 21d postdelivery. When endotoxin acts on the uterus to thin its mucous layer, the cells in the lamina propria of the uterus secrete a large number of glycoprotein particles at 27d postdelivery. The glycoprotein particles are incompletely glycosylation-modified MUC2, which can interact with the cell membrane and are released in large quantities in the form of exocytosis. These glycoprotein particles can significantly repair tight junction structures in the intercellular space and significantly increase the expression of claudin-1, JAM, E-cadherin, ZO-1 and desmosome proteins after endotoxin treatment. The results of the present work showed that endotoxins can thin the uterine mucus layer and accelerate the release of incompletely glycosylated MUC2 from lamina propria cells. In intercellular spaces, MUC2 can increase its expression levels and distribution area to repair the tight junction structure of cells with larger gaps. Further strengthening of the barrier prevents endotoxin translocation by repairing the tight junction structure of uterine epithelial cells.

The function of endometrial epithelial cells is to secrete various substances that are rich in growth factors and nutrients. These substances support both embryo implantation and its subsequent development into a fetus. A vast number of mucins are expressed in endometrial epithelial cells, and they play an important role in regulating the processes of embryo implantation, pregnancy, and parturition. Previous studies have shown that mucin forms a mucus layer covering endometrial epithelial cells, which helps resist damage from foreign bacteria and their toxins. Therefore, this article aims to investigate the location of mucins in the endometrium, the mechanism of mucin secretion by the endometrium, and the regulation of mucins in the uterine epithelium by reproductive hormones, as well as the role of mucins in the protection of the epithelium’s structure. This research aims to provide a foundational understanding for future studies on the role and mechanism of endometrial mucins throughout the pregnancy cycle.

Enterotoxigenic Escherichia coli (ETEC) is a common diarrheal pathogen in humans and animals. To prevent and treat ETEC induced diarrhea, we synthesized mannan oligosaccharide selenium (MOSS) and studied its beneficial effect on ETEC-induced diarrhea. A total of 32 healthy weaned piglets (6.69 ± 0.01 kg) were randomly divided into four groups: NC group (Basal diet), MOSS group (0.4 mg/kg MOSS supplemented diet), MOET group (0.4 mg/kg MOSS supplemented diet + ETEC treatment), ETEC group (ETEC treatment). NC and ETEC group fed with basal diet, MOSS and MOET group fed with the MOSS supplemented diet. On the 8th and 15th day of the experiment, MOET and ETEC group were gavaged with ETEC, and NC and MOSS group were gavaged with stroke-physiological saline solution. Our data showed that dietary MOSS supplementation increased average daily gain (ADG) and average daily feed intake (ADFI) and significantly decreased diarrhea index and frequency in ETEC-treated piglets. MOSS did not affect the α diversity and β diversity of ileal microbial community, but it significantly decreased the proportion of lipopolysaccharide biosynthesis in ileal microbial community. MOSS supplementation regulated colonic microbiota community composition, which significantly increased carbohydrate metabolism, and inhibited lipopolysaccharide biosynthesis pathway in colonic microbial community. Moreover, MOSS significantly decreased inflammatory stress, and oxidative stress in ETEC treated piglets. Furthermore, dietary MOSS supplementation significantly decreased intestinal barrier permeability, and alleviated ETEC induced intestinal mucosa barrier irritation. In conclusion, our study showed that dietary MOSS supplementation ameliorated intestinal mucosa barrier, and regulated intestinal microbiota to prevent ETEC induced diarrhea in weaned piglets.

The objective of this study was to investigate the effects of exposure to endotoxin on the reproductive performance of humans and animals in pregnancy and delivery period. Mucin is considered to play a critical role in protecting the tissue epithelium. At pregnancy period, the MUC2 expression of uterus in the High LPS group was significantly higher than that in the Control group. The glycosaminoglycans of gland cells were secreted into the uterine cavity to protect the uterus. Then, the MUC2 layer became thinner, and LPS entered the lamina propria of the uterus. The mRNA expression of tight junction proteins showed a marked drop, and morphological damage of the uterus occurred. Subsequently, the glycosaminoglycans of gland cells in the High LPS and Low LPS groups increased with the increasing LPS dose, and the damage to the endometrial epithelium was repaired in female mice at Day 5 postdelivery. A low dose of LPS activated the PI3K/AKT signaling pathways to increase the glycosaminoglycans particles, while a high dose of LPS inhibited the PI3K/AKT signaling pathway to decrease the glycosaminoglycans particles. Taken together, our results suggest that gland cells secreted glycosaminoglycans particles into the uterine cavity by exocytosis to increase the thickness of the mucus layer to protect the uterus and that this process was regulated by PI3K/AKT signaling pathways.

醉马芨芨草(Achnatherum inebrians)是我国西北、华北地区严重危害草地畜牧业和生态安全的主要毒害草之一,但其在药用、造纸、脱毒后饲用等方面有一定利用价值.本研究利用优化的MaxEnt模型预测了当前(1970—2000年)条件下和未来(2050 s和2070 s)4种气候变化情景下的醉马芨芨草潜在分布.结果显示:影响当前醉马芨芨草分布的关键环境变量与其适生阈值为12月平均最高气温(—7.5～7.9℃)、海拔(1053.8～4590.9m)、最冷季降水量(1.6～24.6 mm)和降水量变异系数(25.5～111.5);当前醉马芨芨草主要分布于新疆、西藏、四川、青海、甘肃、内蒙古、宁夏、陕西和山西等省区;在未来4种气候情景下,醉马芨芨草适生区面积均会增加,并向高纬度和高海拔地区迁移.研究为醉马芨芨草的防治和资源利用、草地生态学研究和草地放牧管理提供了理论依据和参考.

探讨苦豆子生物碱对小鼠溃疡性结肠炎的治疗作用,从而明确其抗炎活性.试验分为对照组、模型组、苦豆子总碱治疗组(60、30、15 mg/kg).小鼠自由饮用40 mg/mL葡聚糖硫酸钠溶液(DSS)7 d建立溃疡性结肠炎(UC)模型,同时采用苦豆子总碱进行治疗.试验期结束后处死小鼠,观察各组小鼠结肠充血水肿程度以及结肠长度的变化,用HE染色观察小鼠结肠组织病理变化,用ELISA检测小鼠结肠组织炎症因子TNF-α和IL-1β的水平.结果显示,治疗组与模型组相比,小鼠疾病指数评分降低、结肠长度缩短改善、结肠黏膜充血水肿程度减轻以及炎症因子TNF-α和IL-1β的水平降低.结果表明,苦豆子生物碱对UC有较好的治疗作用.

Endotoxins are toxic substances that widely exist in the environment and can enter the intestine with food and other substances. Intestinal epithelial cells are protected by a mucus layer that contains MUC2 as its main structural component. However, a detailed understanding of the mechanisms involved in the function of the mucus barrier in endotoxin penetration is lacking. Here, we established the most suitable proportion of Caco-2/HT-29 co-culture cells as a powerful tool to evaluate the intestinal mucus layer. Our findings significantly advance current knowledge as focal adhesion and ECM-receptor interaction were identified as the two most significantly implicated pathways in MUC2 small interfering RNA (siRNA)-transfected Caco-2/HT-29 co-culture cells after 24 h of LPS stimulation. When the mucus layer was not intact, LPS was found to damage the tight junctions of Caco-2/HT29 co-cultured cells. Furthermore, LPS was demonstrated to inhibit the integrin-mediated focal adhesion structure and damage the matrix network structure of the extracellular and actin microfilament skeletons. Ultimately, LPS inhibited the interactive communication between the extracellular matrix and the cytoskeleton for 24 h in the siMUC2 group compared with the LPS(+) and LPS(-) groups. Overall, we recognized the potential of MUC2 as a tool for barrier function in several intestinal bacterial diseases.

苦豆子(Sophora alopecuroides)为豆科槐属多年生草本植物,分布于我国西北地区荒漠、半荒漠草地,在陕西的分布主要在陕西北部毛乌素沙地边缘,其分布面积广,蕴藏量大.苦豆子主要化学成分有生物碱和黄酮等,具有明显的抗炎、抗心律失常、抗癌、镇痛和抗变态反应等作用.溃疡性结肠炎是一种表现为长期或间歇性的腹泻、血便、黏液便和里急后重等临床症状的慢性非特异性炎症疾病.西医药物治疗溃疡性结肠炎,长期使用往往会引起多种副作用.因此,本文对苦豆子的分布、苦豆子生物碱的药理作用和苦豆子对结肠炎的治疗机制进行综述,为苦豆子的药用植物资源开发和生态保护提供新的思路和研究方向.

试验以雌性小鼠为试验模型,经脂多糖(LPS)灌胃检测母鼠妊娠后不同组织中LPS、sIgA、E2、P4、LH和FSH的含量.结果表明,母鼠经LPS灌胃,分娩后5 d对照组结肠、回肠和子宫的LPS和sIgA含量与染毒组无显著性差异(P>0.05);染毒组仔鼠肠道的LPS含量显著高于对照组(P<0.05).分娩后15 d,对照组母鼠结肠、回肠和子宫中的LPS含量显著高于染毒组(P<0.05);染毒组仔鼠肠道LPS含量显著高于对照组(P<0.05).分娩后15 d,对照组母鼠结肠和回肠的sIgA含量与染毒组无显著性差异;对照组母鼠子宫的sIgA含量显著高于染毒组(P<0.05);染毒组仔鼠肠道的sIgA含量显著高于对照组(P<0.05).随后记录母鼠的繁殖性能指标,染毒组母鼠平均产仔数与对照组无显著性差异;但染毒组母鼠出生后5 d和15 d仔鼠存活率显著低于对照组;同时检测的生殖激素水平发现,染毒组母鼠血液FSH与LH的含量显著低于对照组.说明内毒素干预妊娠母鼠后,母鼠回肠、结肠和子宫组织中的内毒素可经胎盘屏障传递至胎儿体内,使母鼠繁殖性能指标下降,仔鼠体内内毒素含量增高,抑制仔鼠免疫抗体的水平.

天然草地是草地畜牧业发展的物质基础,也是重要的绿色生态屏障,对维护生态安全和食物安全,保护人类生存环境具有重要意义.长期以来,由于草地干旱、超载过牧、盲目开垦等自然和人为因素的影响,导致草地大面积沙化和毒草化.含吡咯里西啶生物碱(Pyrrolizidine alkaloids,PAs)有毒植物具有种类多、分布广等特点,已成为天然草地主要毒害草之一,给草地畜牧业造成严重经济损失.目前,国内外对PAs的研究主要集中在代谢方式及毒理学研究,对于含PAs有毒植物的资源分布、危害程度及科学利用等情况的调查尚不系统.因此,本文就含PAs有毒植物种类和地理分布、在天然草地中的毒性灾害状况以及PAs结构与代谢方式、毒性毒理、药理作用、综合利用等内容进行了综述,对认识含PAs有毒植物在天然草地中的生态作用及科学利用具有重要的指导意义.

为调查猪场免疫程序的合理性及猪群的免疫成效,论文对陕西省某规模化猪场的猪瘟(CSF)、猪繁殖与呼吸综合征(PRRS)和猪伪狂犬病(PR)3种传染病进行血清学系统检测,并对检测结果进行分析.检测结果显示,22周龄后备母猪CSF抗体阳性率(30％)低于其他阶段猪群,哺乳母猪CSF抗体阳性率(96％)高于其他阶段猪群,整体猪群CSF抗体阳性率为80％;12日龄仔猪PRRS抗体阳性率(67％)低于其他阶段猪群,75 d妊娠母猪PRRS抗体阳性率(100％)高于其他阶段猪群,整体猪群PRRS抗体阳性率为90％;22周龄后备母猪PR抗体阳性率(40％)低于其他阶段猪群,妊娠母猪、仔猪及保育猪的PR抗体阳性率(100％)高于其他阶段猪群,整体猪群PR抗体阳性率为91％.结果表明,猪群整体免疫效果较好,3种疫病的抗体阳性率在80％ 以上,但个别猪群的免疫状况须引起注意,22周龄后备母猪的CSF及PR的抗体阳性率偏低,12日龄仔猪的PRRS抗体阳性率偏低.笔者认为应结合免疫程序及抗体检测结果实时调整免疫程序,及时完善猪群免疫漏洞.

The intestine is the most extensive storage organ of bacteria and endotoxins, and the mucosal immune system is the first barrier of the intestine. Mucin-2 (MUC2) is the major component of the mucus layers. In this study, we explored whether MUC2 plays a role in how lipopolysaccharide (LPS) invades the fetus from the gut to the uterus in pregnant mice. The results showed that the LPS levels of the ileum, colon, and uterus were significantly increased, and the content of secretory IgA (sIgA) in the ileum, colon, and uterus tissues was significantly decreased in the LPS(+) group on the 35th day after LPS treatment. On the 16th day of pregnancy, compared with the LPS(-) group, the level of ileum LPS was significantly decreased, and the content of LPS in the fetus was significantly increased in the LPS(+) group. The sIgA content in the fetus was significantly decreased in the uterus and placenta. The expression of MUC2 in the uterus, ileum, and colon was increased significantly in the LPS(+) group, especially in the uterus. It is suggested that endotoxins accumulate in the uterus during non-pregnancy. The high expression of MUC2 in the uterus can prevent LPS from translocating into uterine tissue. After pregnancy, MUC2 still protects uterine tissue, allowing a large amount of LPS to enter the fetal body through blood circulation. Therefore, the level of sIgA significantly decreased, resulting in a decline in fetal innate immune function.

应用酶联免疫吸附试验(ELISA)对2017年-2019年采自陕西省陕南、陕北及关中地区的部分规模化养殖场和散养户的2658份血清分别进行猪瘟(CSF)、猪繁殖与呼吸综合征(PRRS)及猪伪狂犬病(PR)抗体检测.结果表明,CSF、PRRS及PR的免疫情况较好,抗体阳性率均超过农业农村部规定的70％标准;CSF抗体阳性率为81％,PRRS抗体阳性率为73％,PR(PR-gB)抗体阳性率为91％,PRRS和PR(PR-gE)抗体呈逐年上升趋势;关中地区PRRS抗体阳性率最高为81％,陕北地区PR(PR-gE)抗体阳性率最高为25％;3个地区猪瘟抗体阳性率差别不大,抗体阳性率为77％～91％;规模化猪场的CSF、PRRS及PR(PR-gB)平均抗体水平高于散养户.说明陕西省CSF、PRRS及PR免疫效果较好,符合国家的规定标准.但PR野毒感染情况呈年度上升趋势,应净化猪群,建立PR阴性猪场来提高陕西省猪群疫病的防控水平.

The main toxic component of endotoxins released from the death or dissolution of Gram-negative bacteria is lipopolysaccharide (LPS), which exists widely in the natural environment, and a large amount of endotoxin can significantly inhibit the reproductive performance of animals. A previous study showed that endotoxins mainly damaged the physiological function of mucins in the endometrium, but the mechanism is not clear. In this study, the PI3K/Akt signaling pathway was not activated, and the NF-κB signaling pathway was inhibited by LPS treatment; the expression of occludin and E-cadherin proteins were decreased and ZO-1 protein expression was increased, because LPS can lead to the mucous layer becoming thinner, so that the embryonic survival rate is significantly reduced in early pregnancy. In middle and late pregnancy, LPS translocated to the epithelial cells of the uterus and the expression of claudin-1, JAMA, and E-cadherin proteins were decreased; at this time, a large number of glycosaminoglycan particles were secreted by endometrial gland cells through the PI3K/Akt/NF-κB signaling pathway that was activated after LPS treatment, However, there was no significant difference between the survival rates of fetal mice in the LPS (+) and LPS (-) groups. Glycosaminoglycan particles and mucins are secreted by gland cells, which can protect and maintain the pregnancy in the middle and late gestational periods.