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1.
《动物营养学报》2021,33(7)
本试验旨在研究植物乳杆菌抑制产肠毒素型大肠杆菌(ETEC)诱发猪肠上皮细胞炎症反应的分子机制。试验利用植物乳杆菌预处理猪肠上皮细胞IPEC-J2 3 h,ETEC刺激细胞1、3、6、12和24 h,收集细胞及其培养上清,采用酶联免疫吸附试验(ELISA)法检测上清液中白细胞介素-1β(IL-1β)、白细胞介素-8(IL-8)和肿瘤坏死因子-α(TNF-α)的含量,采用实时荧光定量PCR检测细胞中Toll样受体2(TLR2)和Toll样受体4(TLR4)以及NOD样受体3(NLRP3)和NOD样受体6(NLRP6)的表达,采用Western blot检测细胞中丝裂原活化蛋白激酶(MAPK)[p38和细胞外信号调节激酶(ERK)]和核转录因子-κB(NF-κB)p65的磷酸化水平以及紧密连接蛋白——闭合小环蛋白-1(zonula occludens-1,ZO-1)和闭锁蛋白(occludin)的表达。分别采用p38 MAPK抑制剂、ERK-MAPK抑制剂和NF-κB p65抑制剂处理IPEC-J2细胞1 h,再用植物乳杆菌预处理细胞3 h,最后用ETEC处理细胞24 h,收集细胞和培养上清,采用ELISA法检测IL-1β、IL-8和TNF-α含量以及乳酸脱氢酶(LDH)活性。结果表明:1)与ETEC处理相比,植物乳杆菌预处理能够极显著降低ETEC感染12～24 h细胞产生IL-1β、IL-8和TNF-α的含量(P0.01),显著或极显著提高ETEC感染3～12 h细胞中TLR2、TLR4、NLRP3和NLRP6的mRNA相对表达量(P0.05或P0.01),极显著降低ETEC感染24 h细胞中TLR2和NLRP3的mRNA相对表达量(P0.01),极显著降低ETEC感染3～6 h细胞中p38 MAPK和NF-κB p65的磷酸化水平(P0.01),显著或极显著提高ETEC感染6～24 h细胞中ZO-1和occludin的表达量(P0.05或P0.01)。2)与ETEC处理相比,抑制剂和植物乳杆菌共同作用能够极显著降低ETEC感染细胞产生IL-1β、IL-8、TNF-α的含量和LDH的活性(P0.01),植物乳杆菌单独作用也可以极显著降低ETEC感染细胞产生LDH的活性(P0.01),并且信号通路抑制剂对植物乳杆菌调控部分促炎性细胞因子的产生有协同作用。综上所述,植物乳杆菌可以通过致弱p38 MAPK磷酸化和阻断NF-κB信号通路的活化而降低炎症相关因子的产生,从而表现出提高猪肠上皮细胞完整性的潜力。 相似文献
2.
《中国畜牧杂志》2019,(4)
本试验旨在研究脂多糖(LPS)刺激后不同时间断奶仔猪肌肉炎症和肌肉蛋白质降解相关基因表达的变化规律。选择42头(7.1±0.9)kg杜×长×大三元杂断奶仔猪,按注射LPS之前(0 h)和注射LPS后1、2、4、8、12、24 h随机分为7个处理,每个处理6头猪。预试14 d后,腹腔注射100μg/kg体重的LPS。按以上时间点将仔猪屠宰,取背最长肌样品待测。结果表明:背最长肌炎性细胞因子肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、IL-6的mRNA表达量在注射LPS 1～2 h后达到峰值;Toll样受体4信号通路关键基因Toll样受体4(TLR4)、骨髓分化因子88(MyD88),核苷酸结合寡聚域信号通路关键基因核苷酸结合寡聚域2(NOD2)、受体互作蛋白激酶2(RIPK2)的mRNA表达量在注射LPS 2～4 h后达到峰值;肌肉蛋白质降解相关基因叉头转录因子-1(FOXO-1)、FOXO-4、肌肉环指蛋白1(MuRF1)、肌萎缩F-box(MAFbx)的mRNA表达量在注射LPS 12 h后达到峰值。可见,LPS刺激诱导肌肉释放大量炎性细胞因子,使TLR4和NOD炎症信号通路关键基因及肌肉蛋白质降解相关基因mRNA显著表达。 相似文献
3.
《中国畜牧兽医》2016,(5)
为探究Toll样受体(TLRs)介导的信号通路在马链球菌马亚种(S.equi)感染小鼠巨噬细胞RAW264.7中的作用,收集S.equi感染后不同时间点的RAW264.7细胞,提取总RNA并反转录成cDNA,利用实时荧光定量PCR技术检测细胞Toll样受体1、2、6(TLR1、TLR2、TLR6)、接头蛋白骨髓分化蛋白88(MyD88)及细胞因子IL-1、IL-6、IL-10、IL-12、TNF-αmRNA的表达情况。结果显示,S.equi感染RAW264.7细胞后6h时,TLR1、TLR2、TLR6与MyD88mRNA水平均较对照组没有显著差异(P0.05);感染后12h时,TLR1、TLR2和TLR6mRNA表达量未出现明显上升(P0.05),而MyD88mRNA水平极显著升高(P0.01);感染后24h时,TLR1、TLR2和TLR6mRNA表达水平出现极显著升高(P0.01),MyD88 mRNA表达没有显著变化(P0.05),且IL-10和IL-12mRNA水平与对照组相比极显著升高(P0.01),IL-1、IL-6和TNF-αmRNA水平均极显著下降(P0.01)。结果表明,TLRs介导的信号通路参与S.equi感染RAW264.7细胞的免疫应答反应。 相似文献
4.
为探究Toll样受体(TLRs)介导的信号通路在马链球菌马亚种(S.equi)感染小鼠巨噬细胞RAW264.7中的作用,收集S.equi感染后不同时间点的RAW264.7细胞,提取总RNA并反转录成cDNA,利用实时荧光定量PCR技术检测细胞Toll样受体1、2、6(TLR1、TLR2、TLR6)、接头蛋白骨髓分化蛋白88(MyD88)及细胞因子IL-1、IL-6、IL-10、IL-12、TNF-αmRNA的表达情况。结果显示,S.equi感染RAW264.7细胞后6h时,TLR1、TLR2、TLR6与MyD88mRNA水平均较对照组没有显著差异(P>0.05);感染后12h时,TLR1、TLR2和TLR6mRNA表达量未出现明显上升(P>0.05),而MyD88mRNA水平极显著升高(P<0.01);感染后24h时,TLR1、TLR2和TLR6mRNA表达水平出现极显著升高(P<0.01),MyD88mRNA表达没有显著变化(P>0.05),且IL-10和IL-12mRNA水平与对照组相比极显著升高(P<0.01),IL-1、IL-6和TNF-αmRNA水平均极显著下降(P<0.01)。结果表明,TLRs介导的信号通路参与S.equi感染RAW264.7细胞的免疫应答反应。 相似文献
5.
取SPF级昆明小鼠进行RT雾化攻毒。攻毒后每隔一段时间通过BCA法测定小鼠支气管灌洗液BALF上清中总蛋白浓度,ELISA法测定小鼠BALF中致炎因子TNF-α、IL-6、IL-1β浓度,利用RT-PCR检测小鼠肺泡巨噬细胞TLR4及其信号通路mRNA的表达情况。结果显示:小鼠吸入1/150LD50剂量雾化RT后,BALF上清总蛋白浓度增加,IL-1β、TNF-α浓度12h时达到最高值,IL-6浓度48h达到最高值。攻毒后12,24h时TLR4表达高于空白组,差异显著(0.01P0.05);12h时MyD88表达高于空白组,差异极显著(P0.01)。12h时IRAK-1、IRAK-4、TRAF6表达高于空白组,差异显著(0.01P0.05)。结果表明:小鼠吸入1/150LD_(50)剂量雾化RT,肺部发生炎症且肺泡组织通透性增加;低浓度蓖麻毒素攻毒后可刺激肺泡巨噬细胞TLR4及其信号转导通路下游MyD88、TRAF6、IRAK-1、IRAK-4等相关因子mRNA的表达,主要通过MyD88途径引起肺部炎症反应。 相似文献
6.
本试验旨在研究高浓度葡萄糖对牛肺泡巨噬细胞（BAMs）促炎细胞因子IL-1β、IL-6及TNF-α释放的影响及其机制是否与RAGE-TLR4相关信号通路串扰有关。将BAMs随机分为正常糖组（NG）、高糖组（HG）、高糖+RAGE抑制剂组（H+F）、高糖+TLR4抑制剂组（H+T）及DMSO组,处理12 h后收集上清及下层细胞。采用qRT-PCR和Western blot检测细胞RAGE、TLR4、MyD88、NF-κB p65的mRNA及蛋白表达情况,ELISA检测上清TNF-α、IL-1β、IL-6浓度。结果表明,高糖极显著上调RAGE、TLR4、MyD88和NF-κB p65基因、蛋白表达水平以及上清液中IL-1β、IL-6、TNF-α浓度（P<0.01）;RAGE抑制剂与TLR4抑制剂均极显著抑制高糖引起的RAGE、TLR4、MyD88和NF-κB p65基因、蛋白表达水平上调以及IL-1β、IL-6、TNF-α释放（P<0.01）,即RAGE与TLR4均在激活RAGE/TLR4/MyD88/NF-κB炎症信号通路中发挥调控作用。综上所述,高糖能够通过RAGE-TLR4串扰引起牛肺泡巨噬细胞释放促炎细胞因子IL-1β、IL-6及TNF-α,进一步阐明了高糖促进牛肺泡巨噬细胞炎症反应的分子机制。 相似文献
7.
本试验旨在研究富马酸（FA）与肉桂醛（CA）联用调节产肠毒素型大肠杆菌（ETEC）K88诱导猪肠上皮细胞IPEC-J2氧化应激的分子机制。试验选用IPEC-J2细胞建立氧化损伤模型,用不同浓度FA和CA处理IPEC-J2细胞12和24 h,并用CCK-8法检测细胞活力,确定最佳处理浓度和时间;以最佳处理浓度的FA和CA预处理细胞,ETEC K88感染细胞3、6、12和24 h,检测其活菌黏附率,采用酶联免疫吸附测定（ELISA）检测细胞因子含量和抗氧化指标,并用实时荧光定量PCR(RT-qPCR)测定热休克蛋白70(Hsp70)和核因子-κB(NF-κB)信号通路相关基因mRNA相对表达量。结果表明：1) FA和CA的最佳处理浓度分别为1.00 mg/mL和1.00μL/mL,最适培养时间为12 h。2）添加FA和CA可有效抑制ETEC K88黏附IPEC-J2细胞,当ETEC K88感染细胞3 h时其黏附率显著下降（P<0.05）,6、12和24 h时极显著下降（P<0.01）。3）添加FA和CA可极显著降低ETEC K88感染细胞中促炎性细胞因子白细胞介素-8(IL-8... 相似文献
8.
《中国兽医学报》2016,(6):964-970
本研究模拟体内肺泡的气液相环境,采用肺脏上皮细胞与巨噬细胞的气液相共培养模型,探讨肺脏上皮细胞对巨噬细胞抗结核分枝杆菌感染的免疫调节作用。建立人肺泡上皮细胞A549与人单核细胞U937分化而来的巨噬细胞的气液相共培养模型,利用人结核分枝杆菌H37Rv株分别感染A549细胞、U937细胞和共感染A549/U937细胞,然后利用定量反转录PCR(qRT-PCR)、ELISA和Western blot检测巨噬细胞U937中的Toll样受体(TLR)信号分子及其下游炎症因子的表达变化。结果显示,H37Rv分别感染共培养模型中的A549细胞和U937细胞都能明显上调U937巨噬细胞中TLR信号分子TLR2、TLR4、TLR6、TLR8、MyD88和TRAF6,及其下游炎症因子NFκB、TNFα、IL-1α、IL-2、IL-6、IL-10和IL-12α的表达;但当H37Rv共感染上皮细胞和巨噬细胞,H37Rv诱导的U937巨噬细胞的上述因子表达较单独其感染的巨噬细胞显著下降。结果表明,在上皮细胞和巨噬细胞共培养体系中,结核分枝杆菌H37Rv分别感染人A549上皮细胞和U937巨噬细胞都能激发巨噬细胞的TLR信号及其下游的炎症反应,但2种细胞共感染H37Rv,上皮细胞感染后能够降低巨噬细胞的TLR信号活性,并减轻后者的炎症反应。由此可见,肺泡内上皮细胞与巨噬细胞之间可能存在某种相互调控机制,避免抗感染过程中的过度炎症反应以保持肺泡内细胞的组织及其功能的稳态。 相似文献
9.
本试验以IPEC-1细胞为材料,探究解淀粉芽孢杆菌SC06(以下简称SC06)与肠毒性大肠杆菌K88(以下简称K88)对肠上皮屏障功能相关基因表达的影响。将IPEC-1细胞分为4个组并作不同处理:CK组为空白对照,不作处理; SC06组和SC06+K88组用含有108CFU/mL SC06的DM EM/F12培养基先预处理6 h,之后K88组和SC06+K88组加入含有108CFU/mL K88的DM EM/F12培养基处理3 h;乳酸脱氢酶(LDH)活性测定另设以含1%Trinton X-100的DM EM/F12培养基处理的Trinton组为阳性对照。各组细胞均培养9 h。结果表明:1)与CK组相比,K88和SC06单独处理均显著降低了葡萄糖转运载体2 (GLUT2)和小肽转运载体1(PepT1)基因的相对表达量(P<0.05),SC06单独处理显著增加了丙氨酸/丝氨酸/半胱氨酸/苏氨酸转运载体2(ASCT2)和兴奋性氨基酸转运载体1(EAAC1)基因的相对表达量(P<0.05);与K88单独处理相比,SC06预处理显著抑制了K88诱导的LDH活性和EAAC1基因相对表达量的增加(P<0.05)。2)与CK组相比,K88单独处理显著上调了闭锁小带蛋白-1(ZO-1)、闭合蛋白(occludin)基因的表达(P <0.05),显著下调了密封蛋白(claudin)-3、claudin-4和黏蛋白-1(MUC1)基因的表达(P <0.05); SC06单独处理显著上调了ZO-1、claudin-4基因的表达(P <0.05); K88和SC06单独处理均显著促进了天冬氨酸蛋白水解酶-3(caspase-3)、凋亡相关因子(Fas)及B淋巴细胞瘤-2(Bcl-2)基因的表达(P<0.05),显著抑制了天冬氨酸蛋白水解酶-9(caspase-9)与Bcl-2相关X蛋白(Bax)基因的表达(P<0.05),且K88单独处理还显著降低了天冬氨酸蛋白水解酶-8(caspase-8)基因的表达(P<0.05)。与K88单独处理相比,SC06预处理显著阻止了由K88诱导的ZO-1、caspase-3和Bcl-2基因相对表达量的增加(P<0.05)及claudin-3、claudin-4、MUC1、caspase-9和Bax基因相对表达量的降低(P <0.05)。3)与CK组相比,K88单独处理显著上调了肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-8(IL-8)及转化生长因子β(TGF-β)基因的表达(P<0.05),并显著上调了核转录因子-κB-p50(NF-κB-p50)、肿瘤坏死因子受体相关因子-6(TRAF-6)、髓样分化因子88(MyD88)、核苷酸结合寡聚域1(NOD-1)及Toll样受体-4(TLR4)基因的表达(P <0. 05); SC06单独处理显著降低了IL-6、NOD1与Toll样受体-6(TLR6)基因的表达(P<0.05),显著上调了TG F-β和MyD88基因的表达(P<0.05)。与K88单独处理相比,SC06预处理显著抑制了由K88导致的MyD88、NOD-1及TLR4基因相对表达量的增加(P<0.05)。综上所述,K88诱导IPEC-1细胞发生炎症反应,破坏肠上皮细胞的完整性,SC06在一定程度上有缓解作用。 相似文献
10.
为探究马链球菌马亚种(Streptococcus equi subsp.equi,S.equi)对小鼠骨髓源树突状细胞(bone marrow derived dendritic cells,BMDCs)TLR1、TLR2、TLR6、MyD88、IL-1、IL-6、IL-10、IL-12、TNF-αmRNA表达的影响,用GM-CSF、IL-4细胞因子刺激小鼠骨髓细胞使其诱导分化成未成熟的BMDCs,感染S.equi后16、20、26h,采用SYBR GreenⅠ实时荧光定量PCR检测感染组及未感染组细胞TLRs、MyD88和细胞因子mRNA的表达情况。结果显示,S.equi感染BMDCs后16、20、26h,TLR1、TLR2、TLR6、MyD88mRNA的表达量均显著或极显著的高于未感染组(P0.05或P0.01)。S.equi感染DCs后16、26h,IL-1的分泌量较未感染组没有变化(P0.05),IL-10、TNF-α的分泌量显著或极显著增加(P0.05或P0.01)。IL-6在S.equi感染DCs后16h的分泌量显著增加(P0.05),但感染后26h无显著变化(P0.05)。IL-12在S.equi感染DCs后16h的表达没有变化(P0.05),但感染后26h分泌量有所增加(P0.05)。说明S.equi具有调节DCs TLRs、MyD88和细胞因子表达的能力,从而介导机体的免疫应答反应。 相似文献
11.
LI Hai-hua ZHU Qi WANG Shi-qiong YANG Chun-lei ZHAO Xiang-hua QIAO Jia-yun WANG Wen-jie 《中国畜牧兽医》2017,44(1):262-267
To investigate the molecular mechanism of the inflammatory response in the piglets infected with enterotoxigenic E. coli (ETEC) K88, piglets were infected with ETEC K88,the IL-8 content in serum of piglets were assayed by ELISA,and the mRNA relative expression levels of TLR2/4 and its signal transduction pathway related genes (MyD88,Tollip and Bcl3) in mesenteric lymph nodes were detected by quantitative Real-time PCR. The results showed that compared with control group,the content of IL-8 in serum and the expressions of TLR2/4 in lymph nodes were all extremely significantly or significantly increased at 6 and 24 h after infection (P<0.01;P<0.05),and the IL-8 content and TLR2/4 mRNA expression at 24 h after infection were all significantly lower than those at 6 h after infection (P<0.05).In addition,the expressions of MyD88,Tollip and Bcl3 in lymph nodes were all extremely significantly increased at 24 h after infection compared with control group (P<0.01), but there was no significant difference between experimental group and control group at 6 h after infection (P>0.05). In conclusion,ETEC K88 infected piglets might produce inflammatory cytokines IL-8 through the TLR2/4-MyD88 signaling pathway,which could promote the inflammatory reaction in piglets. This inflammatory response might be regulated by Tollip and Bcl3,which could weak the inflammatory intensity in piglets. 相似文献
12.
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
13.
Three- to four-week-old, just-weaned piglets were infected with transmissible gastroenteritis (TGE) virus and the next day with K88ac+ enterotoxigenic Escherichia coli (ETEC). Histological examination of caudal jejunum and ileum of piglets killed 2-3 days after virus challenge (1-2 days after ETEC infection) revealed severe villus atrophy especially in the jejunum compared with controls (P less than 0.05). Four-5 days after TGE virus infection villus length increased and after 7 days it was near normal. Villi scraped from jejunal and ileal mucosa of the piglets were incubated in vitro with K88ac+ E. coli and the number of bacteria adhering to 250 micron villus brush border was counted. Attachment of bacteria to villi of piglets killed 2-3 days after TGE virus infection was significantly decreased in comparison with adhesion to villi of non-infected piglets or of piglets killed 7 days after the virus infection. Correlation between in vitro adhesion and villus height was 0.6649 (P less than 0.001). The results suggest that the experimentally-induced villus atrophy was attended with a temporarily diminished susceptibility of villus enterocytes to adhesion of K88ac+ E. coli. 相似文献
14.
F.O. Opapeju M. Rademacher R.L. Payne D.O. Krause C.M. Nyachoti 《Livestock Science》2010,131(1):58-64
Forty piglets (average body weight = 5.32 kg) were used to investigate the effect of dietary crude protein (CP) content on immunological responses following a challenge with enterotoxigenic Escherichia coli (ETEC) K88. Pigs, housed 4 per pen, were randomly allotted to 2 diets: 1) a high, 225 g/kg CP diet (HCP) or 2) a low, 176 g/kg CP diet (LCP) supplemented with crystalline amino acids. Pigs were orally challenged with 6 mL of an ETEC K88 suspension containing 1010 cfu/mL on d 8 after weaning. Blood samples were collected from 10 pigs (1 pig/pen) on d 7 (at weaning), −24 h, 8 h, 72 h and 7 d after the challenge for determination of plasma urea N (PUN) and serum concentrations of tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) and haptoglobin (Hp). Tumor necrosis factor alpha, IL-1β and Hp were measured as indicators of inflammatory responses. The concentrations of serum TNF-α at 8 h, 72 h and 7 d after challenge were similar to the level observed at 24 h before challenge but higher (P < 0.05) than the weaning level. Pigs fed the LCP diet had lower (P = 0.032) concentrations of IL-1β (72 vs. 116 pg/mL) at 8 h post-challenge compared with those fed the HCP diet. Likewise, pigs fed the LCP diet tended to have lower (P = 0.088) concentration of Hp (9 vs. 25 mg/dL) compared with those fed the HCP diet at 8 h post-challenge. Compared with the weaning concentration, PUN concentration at 72 h after ETEC challenge was higher (P < 0.05) in pigs fed the HCP diet. The results indicate that the LCP diet supplemented with crystalline amino acids reduced inflammatory responses, as indicated by serum IL-1β, in piglets infected with ETEC K88. 相似文献
15.
Experimental colibacillosis in gnotobiotic piglets exposed to 3 enterotoxigenic serotypes 总被引：1，自引：0，他引：1
Three strains of enterotoxigenic Escherichia coli (ETEC) (064:KSNT, K88ac; 020:KSNT, K88ac and 08:K85ab, K99) originally cultured from outbreaks of diarrhoea in piglets a few hours old, were administered orally to gnotobiotic piglets. There was a marked age-related difference in the clinical response to infection between the 3 strains although they all produced heat-stable toxin. All 3 strains produced severe clinical signs of depression, anorexia, vomiting, diarrhoea, followed by dehydration and death in one-day-old piglets. In piglets infected at 3 days of age the two K88+ ETEC caused diarrhoea and death but the K99+ ETEC induced moderate diarrhoea only. In piglets infected at 7 days of age, the 064 strain produced severe diarrhoea and death, and 020 strain caused mild diarrhoea in 3 of 6 piglets with one death while the 08 strain caused no illness. Pathological changes in the intestinal tract associated with these infections were minimal, or absent. Immunofluorescent staining with homologous hyperimmune sera demonstrated adherence of the 3 ETEC strains to the brush border of small intestinal epithelial cells. Fluorescing organisms were observed in all infected piglets irrespective of the severity of clinical signs but the degree and extent of colonisation varied with the age of the piglets and the infecting strain. This may explain the difference in clinical response between the 3 strains. 相似文献
16.
本试验旨在研究亚麻籽油对脂多糖(LPS)刺激仔猪肝脏Toll样受体4(TLR4)和核苷酸结合寡聚化结构域(NOD)信号通路关键基因表达的影响。选取24头断奶仔猪,按体重相近原则随机分为4个组,分别为对照组、LPS组、2.5%亚麻籽油组(2.5%亚麻籽油+LPS)、5.0%亚麻籽油组(5.0%亚麻籽油+LPS),每组6个重复,每个重复1头猪,试验期21 d。试验组注射100μg/kg体重的LPS,对照组注射等量的生理盐水。注射LPS或生理盐水4 h后屠宰仔猪,取肝脏,测定TLR4和NOD信号通路关键基因及相关炎性介质的mRNA表达水平。结果表明:1)LPS刺激显著提高了肝脏肿瘤坏死因子-α(TNF-α)、环氧酶2(COX2)、热休克蛋白70(HSP70)的mRNA相对表达量(P0.05),2.5%亚麻籽油可显著降低COX2、TNF-α的mRNA相对表达量(P0.05),5.0%亚麻籽油可显著降低TNF-α的mRNA相对表达量(P0.05)。2)LPS刺激显著提高了肝脏TLR4、髓样分化因子88(My D88)、白细胞介素-1受体相关激酶1(IRAK1)、NOD1、NOD2、受体互作蛋白2(RIPK2)、核因子-κB(NF-κB)的mRNA相对表达量(P0.05);2.5%亚麻籽油可显著降低NOD1、NOD2的mRNA相对表达量(P0.05),有降低RIPK2 mRNA相对表达量的趋势(0.05≤P0.10);5.0%亚麻籽油可显著降低NOD2的mRNA相对表达量(P0.05)。这表明LPS刺激导致仔猪发生炎症反应,亚麻籽油可能通过抑制NOD信号通路进而缓解肝脏炎症反应。 相似文献