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1.
《动物营养（英文）》2021,7(4):997-1008
Selenium (Se) deficiency can seriously affect the small intestine of swine, and cause diarrhea in swine. However, the specific mechanism of Se deficiency-induced swine diarrhea has rarely been reported. Here, to explore the damage of Se deficiency on the calcium homeostasis and autophagy mechanism of swine, in vivo and in vitro models of swine intestinal Se deficiency were established. Twenty-four pure line castrated male Yorkshire pigs (45 d old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into 2 equal groups and fed Se-deficient diet (0.007 mg Se/kg) as the Se-deficiency group, or fed Se-adequate diet (0.3 mg Se/kg) as the control group for 16 weeks. The intestinal porcine enterocyte cell line (IPEC-J2) was divided into 2 groups, and cultured by Se-deficient medium as the Se-deficient group, or cultured by normal medium as the control group. Morphological observations showed that compared with the control group, intestinal cells in the Se-deficiency group were significantly damaged, and autophagosomes increased. Autophagy staining and cytoplasmic calcium staining results showed that in the Se-deficiency group, autophagy increased and calcium homeostasis was destroyed. According to the reactive oxygen species (ROS) staining results, the percentage of ROS in the Se-deficiency group was higher than that in the control group in the in vitro model. Compared with the control group, the protein and mRNA expressions of autophagy-calcium-related genes including Beclin 1, microtubule-associated proteins 1A (LC3-1), microtubule-associated proteins 1B (LC3-2), autophagy-related protein 5 (ATG5), autophagy-related protein 12 (ATG12), autophagy-related protein 16 (ATG16), mammalian target of rapamycin (mTOR), calmodulin-dependent protein kinase kinase β (CAMKK-β), adenosine 5′-monophosphate-activated protein kinase (AMPK), sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA), and calpain in the Se-deficiency group were significantly increased which was consistent in vivo and in vitro (P < 0.05). Altogether, our results indicated that Se deficiency could destroy the calcium homeostasis of the swine small intestine to trigger cell autophagy and oxidative stress, which was helpful to explain the mechanism of Se deficiency-induced diarrhea in swine. 相似文献
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Liqing Huang Peng Yin Fenghua Liu Yilin Liu Yanhan Liu Zhaofei Xia 《Journal of animal physiology and animal nutrition》2020,104(1):385-396
Heat stress (HS) and the associated restricted blood flow to the intestine have been proven to destroy intestinal integrity. Considering the beneficial properties of L-arginine on gut function, we investigated the protective effects of L-arginine on the intestine under HS conditions. In vivo, the serum cortisol level and the rectal temperature increased in response to HS. Under HS, the intestinal damage showed obvious morphological changes. Furthermore, HS decreased the mRNA and protein expression levels of Nurr1, ZO-1, occludin, claudin-6 and E-cadherin, increased the mRNA expression of NF-κB and IL-1β, and increased the protein expression of cleaved caspase-3. In contrast, L-arginine supplementation maintained intestinal integrity and increased the villus/crypt ratio. L-arginine also suppressed the expression of inflammation-related genes and the protein expression of cleaved caspase-3, whereas it upregulated the mRNA and protein expression of tight junction proteins and LC3B protein expression. In vitro, L-arginine attenuated HS-induced apoptosis as demonstrated by flow cytometry and decreased cleaved caspase-3 protein expression. L-arginine induced autophagy, which was demonstrated by decreased expression of p62 and p-mTOR/mTOR, and increased expression of LC3B. The protein expression levels of TJ proteins also enhanced by L-arginine in IEC-6 cells. Taken together, these results suggest that L-arginine can alleviate intestinal damage and protect the intestinal integrity by suppressing local inflammation response, promoting the production of TJs and facilitating autophagy under HS conditions. 相似文献
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《动物营养（英文）》2020,6(1):98-106
As major fuels for the small intestinal mucosa, dietary amino acids (AA) are catabolized in the mitochondria and serve as sources of energy production. The present study was conducted to investigate AA metabolism that supply cell energy and the underlying signaling pathways in porcine enterocytes. Intestinal porcine epithelial cells (IPEC-J2) were treated with different concentrations of AA, inhibitor, or agonist of mammalian target of rapamycin complex 1 (mTORC1) and adenosine monophosphate activated protein kinase (AMPK), and mitochondrial respiration was monitored. The results showed that AA treatments resulted in enhanced mitochondrial respiration, increased intracellular content of pyruvic acid and lactic acid, and increased hormone-sensitive lipase mRNA expression. Meanwhile, decreased citrate synthase, isocitrate dehydrogenase alpha, and carnitine palmitoyltransferase 1 mRNA expression were also observed. We found that AA treatments increased the protein levels of phosphorylated mammalian target of rapamycin (p-mTOR), phosphorylated-p70 ribosomal protein S6 kinase, and phosphorylated-4E-binding protein 1. What is more, the protein levels of phosphorylated AMPK α (p-AMPKα) and nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-1 (SIRT1) were decreased by AA treatments in a time depending manner. Mitochondrial bioenergetics and the production of tricarboxylic acid cycle intermediates were decreased upon inhibition of mTORC1 or AMPK. Moreover, AMPK activation could up-regulate the mRNA expressions of inhibitor of nuclear factor kappa-B kinase subunit beta (Ikbkβ), integrin-linked protein kinase (ILK), unconventional myosin-Ic (Myo1c), ribosomal protein S6 kinase beta-2 (RPS6Kβ2), and vascular endothelial growth factor (VEGF)-β, which are downstream effectors of mammalian target of rapamycin (mTOR). The mRNA expressions of phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit delta isoform (PIK3CD) and 5′-AMP-activated protein kinase subunit gamma-1 (PRKAG1), which are upstream regulators of mTOR, were also up-regulated by AMPK activation. On the other hand, AMPK activation also down-regulated FK506-binding protein 1A (FKBP1A), serine/threonine-protein phosphatase 2A 55 kDa regulatory subunit B beta isoform, phosphatase and tensin homolog (PTEN), and unc-51 like autophagy activating kinase 1 (Ulk1), which are up-stream regulators of mTORC1. Taken together, these data indicated that AA regulated cellular energy metabolism through mTOR and AMPK pathway in porcine enterocytes. These results demonstrated interactions of AMPK and mTORC1 pathways in AA catabolism and energy metabolism in intestinal mucosa cells of piglets, and also provided reference for using AA to remedy human intestinal diseases. 相似文献
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Mansour ABOELENAIN Manabu KAWAHARA Ahmed Zaky BALBOULA Abd El-monem MONTASSER Samy Mowaed ZAABEL Kiyoshi OKUDA Masashi TAKAHASHI 《The Journal of reproduction and development》2015,61(3):229-236
Corpus luteum (CL) regression is required during the estrous cycle. During CL regression, luteal cells stop producing progesterone and are degraded by apoptosis. However, the detailed mechanism of CL regression in cattle has not been fully elucidated. The aim of this study was to evaluate autophagy, lysosome activity, and apoptosis during CL regression in cattle. The expression of autophagy-related genes (LC3α, LC3β, Atg3, and Atg7) and the protein LC3-II was significantly higher in the late CL than in the mid CL. In addition, autophagy activity was significantly increased in the late CL. Moreover, gene expression of the autophagy inhibitor mammalian target of rapamycin (mTOR) was significantly lower in the late CL than in the mid CL. Lysosome activation and expression of cathepsin-related genes (CTSB, CTSD, and CTSZ) showed significant increases in the late CL and were associated with an
increase in cathepsin B protein. In addition, mRNA expression and activity of caspase 3 (CASP3), an apoptotic enzyme, were significantly higher in the late CL than in the mid CL. These results suggest simultaneous upregulation of autophagy-related factors, lysosomal enzymes and apoptotic mediators, which are involved in regression of the bovine CL. 相似文献
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《动物营养（英文）》2021,7(4):1061-1069
As the first line of defence against pathogens and endotoxins crossing the intestine-blood barrier, the intestinal epithelial barrier plays a determinant role in pigs' health and growth. 4-Phenylbutyric acid (4-PBA), an aromatic fatty acid, was reported to benefit homeostasis of endoplasmic reticulum and protein synthesis. However, whether 4-PBA affects intestinal epithelial barrier function in pigs is unknown. This study aimed to explore the effects of 4-PBA on the intestinal barrier function, using in vitro models of well-differentiated intestinal porcine epithelial cell (IPEC-J2) monolayers in the transwell plates. Cell monolayers with or without 4-PBA (1.0 mmol/L) treatment were challenged with physical scratch, deoxynivalenol (DON, 2.0 μg/mL, 48 h), and lipopolysaccharide (LPS, 5.0 μg/mL, 48 h), respectively. Transepithelial electrical resistance (TEER) and fluorescein isothiocyanate-dextran (FD-4) permeability were measured to indicate barrier integrity and permeability. Real-time PCR and Western blot were conducted to determine relative gene and protein expressions of tight junction proteins. As expected, physical scratch, DON, and LPS challenges decreased TEER and increased FD-4 permeability. 4-PBA treatment accelerated cell mitigation and rehabilitation of the physical scratch-damaged intestinal epithelial barrier but did not alleviate DON or LPS induced barrier damage. However, once 48-h DON and LPS challenges were removed, rehabilitation of the epithelial barrier function of IPEC-J2 monolayer was accelerated by the 4-PBA treatment. Also, the relative gene and protein expressions of zonula occludens-1 (ZO-1), occludin, and claudin-1 were further upregulated by the 4-PBA treatment during the barrier rehabilitation. Taken together, 4-PBA accelerated the IPEC-J2 cell monolayer barrier recovering from physical scratch, DON-, and LPS-induced damage, via enhancing cell mitigation and expressions of tight junction proteins. 相似文献
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l-proline (Pro) is a precursor of ornithine, which is converted into polyamines via ornithine decarboxylase (ODC). Polyamines plays a key role in the proliferation of intestinal epithelial cells. The study investigated the effect of Pro on polyamine metabolism and cell proliferation on porcine enterocytes in vivo and in vitro. Twenty-four Huanjiang mini-pigs were randomly assigned into 1 of 3 groups and fed a basal diet that contained 0.77% alanine (Ala, iso-nitrogenous control), 1% Pro or 1% Pro + 0.0167% α-difluoromethylornithine (DFMO) from d 15 to 70 of gestation. The fetal body weight and number of fetuses per litter were determined, and the small and large intestines were obtained on d 70 ± 1.78 of gestation. The in vitro study was performed in intestinal porcine epithelial (IPEC-J2) cells cultured in Dulbecco''s modified Eagle medium-high glucose (DMEM-H) containing 0 μmol/L Pro, 400 μmol/L Pro, or 400 μmol/L Pro + 10 mmol/L DFMO for 4 d. The results showed that maternal dietary supplementation with 1% Pro increased fetal weight; the protein and DNA concentrations of the fetal small intestine; and mRNA levels for potassium voltage-gated channel, shaker-related subfamily, member 1 (Kv1.1) in the fetal small and large intestines (P < 0.05). Supplementing Pro to either gilts or IPEC-J2 cells increased ODC protein abundances and polyamine concentrations in the fetal intestines and IPEC-J2 cells (P < 0.05). In comparison with the Pro group, the combined administration of Pro and DFMO reduced the expression of ODC protein and spermine concentration in the fetal intestine, as well as the concentrations of putrescine, spermidine and spermine in IPEC-J2 cells (P < 0.05). Meanwhile, the percentage of cells in the S-phase and the mRNA levels of proto-oncogenes c-fos and c-myc were increased in response to Pro supplementation, whereas depletion of cellular polyamines with DFMO increased tumor protein p53 (p53) mRNA levels (P < 0.05). Taken together, dietary supplementation with Pro improved fetal pig growth and intestinal epithelial cell proliferation via enhancing polyamine synthesis. 相似文献
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Dongsheng Che Bao Zhao Yueli Fan Rui Han Chun Zhang Guixin Qin Seidu Adams Hailong Jiang 《Journal of animal physiology and animal nutrition》2019,103(4):1174-1184
Eleutheroside B (EB) is a phenylpropanoid glycoside with anti‐inflammatory properties, neuroprotective abilities, immunomodulatory effects, antinociceptive effects, and regulation of blood glucose. The aim of this study was to investigate the effects of EB on the barrier function in the intestinal porcine epithelial cells J2 (IPEC‐J2). The IPEC‐J2 cells were inoculated into 96‐well plates at a density of 5 × 103 cells per well for 100% confluence. The cells were cultured in the presence of EB at concentrations of 0, 0.05, 0.10, and 0.20 mg/ml for 48 hr. Then, 0.10 mg/ml was selected as the suitable concentration for the estimation of transepithelial electric resistance (TEER) value, alkaline phosphatase activity, proinflammatory cytokines mRNA expression, tight junction mRNA and protein expression. The results of this study indicated that the supplementation of EB in IPEC‐J2 cells decreased cellular membrane permeability and mRNA expression of proinflammatory cytokines, including interleukin‐6 (IL‐6), interferon‐γ (INF‐γ), and tumour necrosis factor‐α (TNF‐α). The supplementation of EB in IPEC‐J2 cells increased tight junction protein expression and anti‐inflammatory cytokines, interleukin 10 (IL‐10) and transforming growth factor beta (TGF‐β). In addition, the western blotting and real‐time quantitative polymerase chain reaction (RT‐qPCR) results indicated that EB significantly (p < 0.05) increased the mRNA and protein expression of intestinal tight junction proteins, Claudin‐3, Occludin, and Zonula Occludins protein‐1 (ZO‐1). Therefore, dietary supplementation of EB may increase intestinal barrier function, tight junction protein expression, anti‐inflammatory cytokines, and decrease proinflammatory cytokines synthesis in IPEC‐J2 cells. 相似文献
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Guangmang Liu Xiaomei Xu Caimei Wu Gang Jia Hua Zhao Xiaoling Chen Gang Tian Jingyi Cai Jing Wang 《动物营养（英文）》2022,8(1):135
Weaning stress can cause tight junctions damage and intestinal permeability enhancement, which leads to intestinal imbalance and growth retardation, thereby causing damage to piglet growth and development. Spermine can reduce stress. However, the mechanism of spermine modulating the intestinal integrity in pigs remains largely unknown. This study aims to examine whether spermine protects the intestinal barrier integrity of piglets through ras-related C3 botulinum toxin substrate 1 (Rac1)/phospholipase C-γ1 (PLC-γ1) signaling pathway. In vivo, 80 piglets were categorised into 4 control groups and 4 spermine groups (10 piglets per group). The piglets were fed with normal saline or spermine at 0.4 mmol/kg BW for 7 h and 3, 6 and 9 d. In vitro, we investigated whether spermine protects the intestinal barrier after a tumor necrosis factor α (TNF-α) challenge through Rac1/PLC-γ1 signaling pathway. The in vivo study found that spermine supplementation increased tight junction protein mRNA levels and Rac1/PLC-γ1 signaling pathway gene expression in the jejunum of piglets. The serum D-lactate content was significantly decreased after spermine supplementation (P < 0.05). The in vitro study found that 0.1 μmol/L spermine increased the levels of tight junction protein expression, Rac1/PLC-γ1 signaling pathway and transepithelial electrical resistance, and decreased paracellular permeability (P < 0.05). Further experiments demonstrated that spermine supplementation enhanced the levels of tight junction protein expression, Rac1/PLC-γ1 signaling pathway and transepithelial electrical resistance, and decreased paracellular permeability compared with the NSC-23766 and U73122 treatment with spermine after TNF-α challenge (P < 0.05). Collectively, spermine protects intestinal barrier integrity through Rac1/PLC-γ1 signaling pathway in piglets. 相似文献
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I-Ting Tsai Ying-Hsin Chen Yau-Hung Chen Yun-Hsin Wang 《Journal of toxicologic pathology》2013,26(1):79-82
Despite its medical use, little is known about the mechanisms underlying amikacin-induced embryotoxicity, including fin reduction, in zebrafish. In this study, we examined the expression of well-known autophagy markers mTOR (target of rapamycin), atg10 (autophagy-related gene), atg12 and LC3 (mammalian homolog of Atg8) in amikacin-treated zebrafish embryos. Our results indicated that the mRNA expression level of atg12 in the amikacin-treated group was significantly increased by 1.5-fold (p<0.05) compared with the corresponding mock control group, while the expression levels of atg10 and mTOR were significantly decreased by 0.74-fold (p<0.05) and 0.58-fold (p<0.05), respectively. Western blot analysis revealed that LC3 protein expression was induced by amikacin. Taken together, these data suggest that amikacin-induced fin reduction is mediated by fin cell autophagy. 相似文献
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Luca Lo Verso Kristina Dumont Martin Lessard Karoline Lauzon Chantale Provost Carl A Gagnon Younes Chorfi Frdric Guay 《Journal of animal science》2021,99(9)
This study aimed to evaluate the impact of grading levels of deoxynivalenol (DON) in the diet of weaned pigs, as well as the effects of a supplementation with antioxidants (AOX), hydrated sodium calcium aluminosilicates (HSCAS), and their combination on the growth, AOX status, and immune and vaccine responses against the porcine reproductive and respiratory syndrome virus (PRRSV) and porcine circovirus type 2 (PCV2). At weaning, 336 piglets were allocated to six dietary treatments according to a randomized complete block design. Treatments were as follows: basal diet (CTRL); basal diet containing DON at 1.2 mg/kg (DON1.2); basal diet containing DON at 2.4 mg/kg (DON2.4); DON2.4 diet + a mix of AOX which included vitamins A and E at 20,000 IU and 200 IU/kg feed respectively, selenized yeast at 0.3 mg/kg, and a grape seed extracts at 100 mg/kg feed (DON2.4 + AOX); DON2.4 diet + the mix of AOX and the modified HSCAS mentioned above (DON2.4 + AOX + HSCAS); DON2.4 + AOX + HSCAS. Pigs were vaccinated against PRRSV and PCV2 at 7 d; on 0, 14, and 35 d, growth performance was recorded, and blood samples were collected in order to evaluate the oxidative status, inflammatory blood markers, lymphocyte blastogenic response, and vaccine antibody response. Increasing intake of DON resulted in a quadratic effect at 35 d in the lymphocyte proliferative response to concanavalin A and PCV2 as well as in the anti-PRRSV antibody response, whereas the catalase activity decreased in DON2.4 pigs compared with the CTRL and DON1.2 groups (P ≤ 0.05). Compared with the DON2.4 diet, the AOX supplementation slightly reduced gain to feed ratio (P = 0.026) and increased the ferric reducing ability of plasma as well as α-tocopherol concentration (P < 0.05), whereas the association of AOX + HSCAS increased the anti-PRRSV IgG (P < 0.05). Furthermore, the HSCAS supplement reduced haptoglobin levels in serum at 14 d compared with the DON2.4 group; however, its concentration decreased in all the experimental treatments from 14 to 35 d and particularly in the DON2.4 + AOX pigs, whereas a different trend was evidenced in the DON2.4 + HSCAS group, where over the same period haptoglobin concentration increased (P < 0.05). Overall, our results show that the addition of AOX and HSCAS in the diet may alleviate the negative effects due to DON contamination on the AOX status and immune response of vaccinated weanling pigs. 相似文献
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细胞自噬对犬骨髓间充质干细胞干性的影响 总被引：1，自引：0，他引：1
本研究旨在探讨细胞自噬对犬骨髓间充质干细胞（cBMSCs）干性的影响。分离培养cBMSCs，将其分为对照组、使用雷帕霉素促进细胞自噬的雷帕霉素组、使用3-MA抑制细胞自噬的3-MA组，于药物处理12、24、48 h后收集细胞，利用间接细胞免疫荧光法检测自噬微管相关蛋白1轻链3 Ⅱ（LC 3Ⅱ）的蛋白表达水平；荧光定量PCR检测自噬相关基因LC 3、Beclin 1、自噬相关基因7（Atg 7）以及干性相关基因性别决定基因相关转录因子2（Sox 2）、特异AT序列结合蛋白2（Satb 2）mRNA转录水平；通过茜素红染色检测经成骨诱导的cBMSCs的成骨分化能力，通过油红O染色检测经成脂诱导的cBMSCs的成脂分化能力。结果显示：雷帕霉素组的LC 3Ⅱ蛋白表达量上调，3-MA组则为下调。雷帕霉素组干性相关基因与自噬相关基因在不同时间点的表达水平均有不同程度的上调，且随感染时间的延长呈上调趋势；3-MA组干性相关基因与自噬相关基因的mRNA转录水平在不同时间点不同程度降低，且随感染时间延长呈下调趋势。成骨诱导试验中雷帕霉素组cBMSCs形态变化最明显，且矿化面积较大，3-MA组细胞矿化面积小；成脂诱导试验中雷帕霉素组脂滴数量少，3-MA组脂滴数量多且聚集程度高。在一定程度上促进cBMSCs自噬水平可以更好地维护其干性并提高成骨分化能力，为优化治疗中cBMSCs的质量提供理论基础和技术支持。 相似文献
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Yulong He Zhan Sang Yisha Zhuo Xueyi Wang Zeheng Guo Lihua He Cuiping Zeng Hanchuan Dai 《Journal of animal physiology and animal nutrition》2019,103(5):1521-1529
Pig transportation is associated with intestinal oxidative stress and results in destruction of intestinal integrity. Autophagy has been contributed to maintain cell homeostasis under stresses. The purpose of this study was to evaluate the effects of transport stress on morphology, intestinal mucosal barrier and autophagy/mitophagy levels in pig jejunum. A total of 16 finishing pigs were randomly divided into two groups. The control group was directly transported to the slaughterhouse and rested for 24 hr. The experimental groups were transported for 5 hr and slaughtered immediately. The results showed that transportation induced obvious stress responses with morphological and histological damage in jejunum accompanying with an elevated level of malondialdehyde (MDA; p < .05), endotoxin (LPS; p < .05), lactic dehydrogenase (LDH; p < .05) and a decreased level of serum superoxide dismutase (SOD; p < .05). Also, hemeoxy genase 1 (HO‐1; p < .01) as well as tight junction protein (claudin‐1 [p < .001], occludin [p < .05] and zonula occludens 1 [ZO‐1; p < 0.05]) levels were attenuated in jejunum tissue, and NADPH oxidase 1 (NOX1; p < .01) mRNA expression was up‐regulated. Further research indicated that transport stress could induce autophagy through increasing microtubule‐associated protein light chain 3 (LC3; p < .05) and autophagy‐related gene 5 (ATG5; p < .01) levels and suppressing p62 expression. Additionally, transport stress increased the protein levels of PTEN‐induced putative kinase 1 (PINK1; p < .05) and Parkin (p < .05) which was associated with mitophagy. In conclusions, transport stress could induce the destruction of intestinal integrity and involve in the intestinal mucosal barrier oxidative damage, and also contribute to activation of autophagy/mitophagy. 相似文献
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Awad WA Aschenbach JR Zentek J 《Journal of animal physiology and animal nutrition》2012,96(4):709-716
The digestive tract is a target for the Fusarium toxin deoxynivalenol (DON), a major cereal grain contaminant of animal and public health concern. Toxic effects of DON range from diarrhoea, vomiting and gastrointestinal inflammation to necrosis of several tissues. Following ingestion of contaminated food or feed, intestinal epithelial cells are exposed to a high concentration of ingested DON, potentially affecting intestinal functions. Pigs are considered to be the species most sensitive to DON toxicity. However, only few studies directly evaluated DON effects on porcine intestinal epithelial cells. Therefore, we used the porcine intestinal cell line (IPEC-J2) to assess short-term effects of DON on functional characteristics of the intestinal epithelial cells. The cytotoxic effect of DON on IPEC-J2 cells was evaluated by measuring the count of living cells and the activity of lactate dehydrogenase (LDH) released in the culture media at a DON concentration range from 0, 0.5, 2.5 and 10 μm. We demonstrated that DON at concentrations of 2.5 and 10 μm decreased significantly (p < 0.001) the cell count in a dose-dependent manner. At a concentration of 10 μm, DON caused cell damage, including rounding of cells, autolysis and cell loss from the monolayer. The mycotoxin, DON, increased LDH release into the culture medium compared with the control value. The alterations of LDH showed a good agreement with the decrease in cell count. Deoxynivalenol decreased the l-lactate concentration in the fluid supernatant of IPEC-J2 cells at 2.5 μm (p < 0.05) with a maximal effect at 10 μm of DON. To determine whether the altered lactate production may be linked to alterations of energy balance, we measured cellular ATP levels in IPEC-J2 cells. A significant decrease in ATP levels was seen at 48 h in a dose-dependent manner. It could be demonstrated that DON has a distinct cytotoxic effect on IPEC-J2 cells. 相似文献
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Kuanmin M Yang Cui Zhu Li Wang Shuting T Cao Xuefen F Yang Kaiguo G Gao Zongyong Y Jiang 《Journal of animal science》2021,99(6)
This study was conducted to investigate the effects of early supplementation during 4 to 18 d of age with Lactobacillus plantarum (LP) in liquid diets on intestinal innate immune response in young piglets infected with enterotoxigenic Escherichia coli (ETEC) K88. Seventy-two barrow piglets at 4 d old were assigned to basal or LP-supplemented liquid diet (5 × 1010 CFU·kg−1). On day 15, piglets from each group were orally challenged with either ETEC K88 (1 × 108 CFU·kg−1) or the same amount of phosphate-buffered saline. The intestinal mucosa, mesenteric lymph node (MLN), and spleen samples were collected on day 18. Here, we found that LP pretreatment significantly decreased the mRNA relative expression of inflammatory cytokines (interleukin [IL]-1β, IL-8, and tumor necrosis factor-α), porcine β-defensin 2 (pBD-2), and mucins (MUC1 and MUC4) in the jejunal mucosa in piglets challenged with ETEC K88 (P < 0.05). Moreover, LP significantly decreased the ileal mucosa mRNA relative expression of IL-8 and MUC4 in young piglets challenged with ETEC K88 (P < 0.05). Furthermore, the piglets of the LP + ETEC K88 group had lower protein levels of IL-8, secretory immunoglobulin A, pBD-2, and MUC4 in the jejunal mucosa than those challenged with ETEC K88 (P < 0.05). Besides, LP supplementation reduced the percentage of gamma/delta T cells receptor (γδTCR) and CD172a+ (SWC3+) cells in MLN and the percentage of γδTCR cells in the spleen of young piglets after the ETEC K88 challenge. Supplementation with LP in liquid diets prevented the upregulated protein abundance of toll-like receptor (TLR) 4, phosphorylation-p38, and phosphorylation-extracellular signal-regulated protein kinases in the jejunal mucosa induced by ETEC K88 (P < 0.05). In conclusion, LP supplementation in liquid diet possesses anti-inflammatory activity and modulates the intestinal innate immunity during the early life of young piglets challenged with ETEC K88, which might be attributed to the suppression of TLR4-mediated mitogen-activated protein kinase signaling pathways. Early supplementation with LP in liquid diets regulates the innate immune response, representing a promising immunoregulation strategy for maintaining intestinal health in weaned piglets. 相似文献
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The combination of deoxynivalenol and zearalenone at permitted feed concentrations causes serious physiological effects in young pigs 总被引：1，自引：0，他引：1
Feng Chen Yulin Ma Chunyi Xue Jingyun Ma Qingmei Xie Genhu Wang Yingzuo Bi Yongchang Cao 《Journal of veterinary science (Suw?n-si, Korea)》2008,9(1):39-44
This study was to investigate the effects of the combination of deoxynivalenol (DON) and zearalenone (ZON) on pigs. Twenty-four weaning piglets were divided into a control group fed a diet free of mycotoxins and a toxin group fed a diet containing 1 mg/kg DON and 250 µg/kg ZON. The results showed that supplementation of DON and ZON in diets had extensive effects on pigs. More specifically, DON and ZON caused levels of total protein, albumin, and globulin in sera to decrease (p < 0.05) by 14.5%, 6.5% and 11.3%, respectively, and at the same time increased (p < 0.05) the serum enzyme activities of γ-glutamyltransferase, aspartate aminotransferase and alanine aminotransferase by 72.0%, 32.6% and 36.6%, respectively. In addition, DON and ZON decreased (p < 0.05) the level of anti-classical swine fever antibody titers by 14.8%. Real-time PCR showed that DON and ZON caused the mRNA expression levels of IFN-γ, TNF-α, IL-2, to decrease (p < 0.05) by 36.0%, 29.0% and 35.4%, respectively. Histopathological studies demonstrated that DON and ZON caused abnormalities in the liver, spleen, lymph nodes, uterus, and kidney. The concentrations of DON and ZON used in this study are in line with the published critical values permitted by BML. Our study clearly put the standard and adequacy of safety measures for these toxins into question. The authors suggest that with the increasing availability of cellular and molecular technologies, it is time to revisit the safety standards for toxins in feeds so as to make feeds safer, providing consumers with safer products. 相似文献
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本试验旨在研究脱氧雪腐镰刀菌烯醇（DON）与T-2毒素对热应激蛋鸡肠道屏障功能及内质网应激和炎症反应的影响。选择36周龄体重相近的京红1号蛋鸡96只，随机分成4组，每组8个重复，每个重复3只鸡。对照组（CON组）饲喂基础饲粮，DON组、T-2组、DON+T-2组分别在基础饲粮中添加3.00 mg/kg DON、 0.50 mg/kg T-2毒素、 1.50 mg/kg DON+0.25 mg/kg T-2毒素。预试期3 d，正试期28 d。试验期间白天平均温湿指数为84.87。结果表明：1）与CON组相比，T-2组十二指肠、空肠隐窝深度显著升高（P<0.05）,DON+T-2组空肠隐窝深度显著升高（P<0.05）,DON、T-2、DON+T-2组十二指肠绒毛高度/隐窝深度（V/C）值显著降低（P<0.05）,T-2、DON+T-2组空肠V/C值显著降低（P<0.05）,DON组回肠隐窝深度显著升高（P<0.05）。2）与CON组相比，DON、T-2、DON+T-2组血清脂多糖（LPS）含量显著升高（P<0.05）,DON+T-2组血清二胺氧化酶（DA... 相似文献