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1.
The gastrointestinal epithelium represents a barrier to potentially invasive enteric pathogens, maintains a role in innate immune surveillance, and is a source of both chemokine and cytokine chemotactic mediators in response to bacterial invasion. In the current study, we evaluated cytokine and chemokine mediators known to regulate movement of macrophages (macrophage migration inhibitory factor; MIF), neutrophils (IL8), dendritic cells (CCL20), and epithelial remodeling (osteopontin; OPN) in response to invasive swine enteropathogens Salmonella enterica serovar Typhimurium (ST) or Choleraesuis (SC). For the in vivo experiment, weaned pigs served as uninfected controls (0 h) or were given 3 x 10(9) CFU ST orally. Pigs were sacrificed at 8, 24, 48, and 144 h after inoculation and total RNA was extracted from defined segments of proximal (PI) and distal (DI) ileum. Relative expression of MIF and OPN were not affected by ST. IL8 expression was increased numerically (P = 0.17 for the interaction term) at 24 and 144 h in the PI and these increases accounted for greater expression in the PI relative to the DI (P < 0.05). Relative expression of CCL20 was increased at 24 h after ST (P < 0.05). Next, we evaluated the time course of MIF, IL8, CCL20, and OPN mRNA expression induced by application of lipopolysaccharide (LPS), ST or SC in vitro using pig jejunal epithelial cells (IPEC-J2). Cells were grown to confluency on permeable membranes, and treated apically with LPS (10 ng/mL), ST or SC (10(8)/well). After 1 h, cells were washed to remove LPS or extracellular bacteria, and media containing gentamicin was added to kill remaining extracellular bacteria. Media and RNA were collected at 1.5, 3, and 6 h after treatment. MIF mRNA was not affected by LPS or bacterial treatment. Similarly, IL8 expression was not affected by LPS, but was increased by ST and SC relative to controls at 1.5 and 3 h post exposure (P < 0.05 for all comparisons). Treatment with SC increased CCL20 mRNA relative to controls at 3 h (P < 0.05), while ST increased CCL20 at 1.5, 3, and 6h with maximal expression at 6 h (P < 0.05 for all comparisons). ST and SC increased polarized IL8 secretion. Our data demonstrate that invasive bacterial pathogens in the pig gastrointestinal tract trigger upregulation of selected cytokine and chemokine mediators, but serovars of Salmonella elicited differing patterns of activation in vitro.  相似文献   

2.
Two serovars of Salmonella enterica, namely serovar Typhimurium (ST) and serovar Choleraesuis (SC) account for the vast majority of clinical cases of swine salmonellosis worldwide. These serovars are thought to be transmitted among pigs in production settings mainly through fecal-oral routes. Yet, few studies have evaluated effects of these serovars on expression of innate immune targets when presented to pigs via repeated oral dosing in an attempt to model transmission in production settings. Thus, a primary objective of the current experiments was to evaluate expression of Toll-like receptors (TLR) and selected chemoattractive mediators (interleukin 8, IL8; macrophage migration inhibitory factor, MIF; osteopontin, OPN) in tissues from pigs exposed to ST or SC that had been transformed with kanamycin resistance and green (STG) or red (SCR) fluorescent protein to facilitate isolation from pen fecal samples. In vitro studies confirmed that STG and SCR largely (though not completely) retained their ability to upregulate IL8 and CC chemokine ligand 20 (CCL20) in cultured swine jejunal epithelial cells. Transformed bacteria were then fed to pigs in an in vivo study to determine tissue specific effects on mRNA relative expression. Pigs were fed cookie dough inoculated with bacteria on days 0, 3, 7, and 10 with 10(8)CFU STG (n=8) or SCR (n=8), while control (CTL) pigs (n=8) received dough without bacteria. Animals were sacrificed 14 days from the initial bacterial challenge and samples of tonsil, jejunum, ileum, colon, mesenteric lymph node (MLN), spleen, and liver were removed for subsequent RNA isolation. Expression of mRNA in tissues was determined using real-time quantitative PCR and expressed relative to 18S rRNA. Within CTL pigs, when expressed relative to the content in liver, mRNA for all targets demonstrated substantial tissue effects (P<0.001 for all TLR; MIF, and OPN; P<0.05 for IL8). Feeding STG and SCR resulted in significant (P相似文献   

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4.
为了探究猪Toll样受体(Toll-like receptor 5,TLR5) 基因表达水平与F18大肠杆菌抗性的关系,试验通过不同血清型产肠毒素大肠杆菌(F18ab和F18ac)侵染猪小肠上皮细胞(IPEC-J2),同时通过脂多糖(LPS)分别诱导IPEC-J2细胞4和8 h,利用实时荧光定量PCR检测TLR5基因表达水平变化,并利用Western blotting进行蛋白表达分析。结果显示,不同血清型大肠杆菌(F18ab和F18ac)菌体侵染IPEC-J2细胞后,TLR5基因表达水平均极显著上调(P<0.01);LPS诱导IPEC-J2细胞4和8 h后,TLR5基因表达水平均极显著上调(P<0.01),且在LPS诱导IPEC-J2细胞8 h后,TLR5基因表达水平明显高于诱导4 h。与对照组相比,细胞中TLR5蛋白的表达水平极显著上调(P<0.01),与LPS诱导及F18大肠杆菌菌体刺激IPEC-J2细胞后mRNA表达水平结果相一致。本研究在细胞水平上分析了TLR5表达水平和F18大肠杆菌侵染的相关性,进一步证实猪TLR5基因的表达水平在细胞抵抗F18大肠杆菌的侵染过程中发挥了重要的调控作用,为今后关于TLR5基因功能及其在大肠杆菌腹泻遗传育种应用的研究奠定基础。  相似文献   

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本试验旨在探讨不同锌源及锌水平对猪小肠上皮细胞(IPEC-J2)胰高血糖素样肽2(GLP-2)表达的影响。分别以乳酸锌、硫酸锌(锌浓度分别为50、100、150、200 mg/L)作用IPEC-J2细胞,实时荧光定量RT-PCR方法检测GLP-2 mRNA表达,以β-actin mRNA水平作为内参对照。结果表明:在6、12 h检测时间点,不同锌源和水平及其互作对GLP-2 mRNA表达影响极显著(P<0.01);在24 h时不同锌源对其表达影响极显著(P<0.01),锌添加水平对其表达影响显著(P<0.05),不同锌源与锌添加水平交互作用则不显著(P<0.05);乳酸锌、硫酸锌促进GLP-2基因mRNA表达均具有正向浓度效应。乳酸锌和硫酸锌均可上调肠道细胞GLP-2基因mRNA的表达;在同等锌浓度水平下,乳酸锌促进GLP-2基因表达的效果优于硫酸锌。  相似文献   

7.
本试验旨在考察牛膝多糖(ABPS)对脂多糖(LPS)免疫应激下仔猪空肠上皮细胞(IPEC-J2)促炎细胞因子分泌和表达的影响,并探讨ABPS调控IPEC-J2免疫应激可能的作用机制。选用4~5代的IPEC-J2,培养基中分别添加0(对照)、300、600、900、1 200μg/m L ABPS和10μg/m L LPS,每组12个重复,每孔为1个重复。培养72 h后,采用酶联免疫吸附测定(ELISA)方法检测ABPS对促炎细胞因子白细胞介素1(IL-1)、白细胞介素6(IL-6)、白细胞介素8(IL-8)和肿瘤坏死因子α(TNF-α)分泌量的影响,采用实时定量PCR测定Toll样受体4(TLR4)、核转录因子κB(NF-κB)的mRNA表达量,采用Western blot法测定TLR4、NF-κB、磷酸化核转录因子κB(p-NF-κB)蛋白表达量。结果显示:与对照组相比,300、600、900和1 200μg/m L ABPS组能显著减少IL-1、IL-6、IL-8和TNF-α的分泌量(P0.05);300μg/m L ABPS组能显著减少p-NF-κB蛋白的表达量(P0.05),900和1 200μg/m L ABPS组能显著减少TLR4、NF-κB的mRNA和NF-κB蛋白的表达量(P0.05)。由此可见,ABPS通过TLR4/NF-κB信号转导途径来调控促炎细胞因子的分泌,从而缓解免疫应激,低浓度ABPS通过直接抑制NF-κB磷酸化过程来降低免疫应激,高浓度ABPS则是通过抑制TLR4 mRNA、NF-κB mRNA和NF-κB蛋白的表达量来缓解免疫应激。  相似文献   

8.
IgE‐mediated late‐phase reactions can be induced in the skin of normal and atopic dogs by intradermal injections of anti‐IgE antibody. The histology of these reactions is very similar to that of naturally occurring atopic dermatitis. To characterize the cellular, cytokine and chemokine responses in the skin of placebo‐ and prednisolone‐treated dogs, normal beagles received either placebo or 0.5 mg/kg prednisolone twice daily for three days prior to intradermal injection of polyclonal rabbit anti‐canine IgE. Eight‐millimetre punch biopsy skin samples were taken before injection and at the injection sites after 6, 24 and 48 h. Histological and immunohistochemical examination revealed a rapid cellular influx. Eosinophil and neutrophil numbers increased from <1 to 61.4 ± 14.1, and from 7 to 62.2 ± 10.8 cells/mm2, respectively, within 6 h after injection, and remained moderately elevated 48 h later. The numbers of CD1c+, CD3+ and CD4+ mononuclear cells were also increased by 6 h. Taqman analysis demonstrated 2.5‐ to 72‐fold increases in mRNA expression for IL‐13, IL‐5, MCP (CCL2), RANTES (CCL5) and TARC (CCL17). Levels of mRNA for IL‐2, IL‐4, IL‐6, and IFNγ remained negligible. Prednisolone administration suppressed the influx of neutrophils and eosinophils, and the expression of IL‐13, CCL2, CCL5 and CCL17 (33, 97, 58, 86, 73 and 90%, respectively), as well as the influx of CD1c+ and CD3+ cells. These data document the cytokine and chemokine response to anti‐IgE injection and demonstrate the anti‐inflammatory effect of prednisolone. Funding: Schering‐Plough Animal Health.  相似文献   

9.
OBJECTIVE: To evaluate in situ expression of inflammatory cytokine mRNA in lymphoid tissue of swine experimentally infected with Mycobacterium avium serovar 2. ANIMALS: 7 noninfected pigs and 7 pigs infected with M. avium serovar 2. PROCEDURE: Expression of mRNA of inflammatory cytokines such as tumor necrosis factor alpha (TNFalpha), interleukin (IL)-1beta IL-6, and IL-8 in formalin-fixed paraffin-embedded blocks of lymphoid tissue (lymph nodes and tonsil) of swine experimentally infected with M. avium serovar 2 was compared with that of noninfected pigs. Tissues were evaluated by use of morphologic localization of cytokine mRNA, using in situ hybridization at 160 days after inoculation. RESULTS: A noticeable increase in mRNA expression for TNFalpha and mild increases in mRNA expression of IL-8 and IL-1beta were detected in mandibular lymph nodes from infected swine, compared with noninfected swine. Mild increase in mRNA expression for 1L-6 also was observed in tonsils from infected swine. Cytokine mRNA was detected in macrophages and lymphocytes, primarily within cortical follicles and adjacent mantle zones. CONCLUSIONS AND CLINICAL RELEVANCE: Expression of mRNA for inflammatory cytokines was increased in lymphoid tissue of infected swine, possibly resulting from local factors on, or secreted by, M. avium. These results suggest that alterations in cytokine mRNA expression are important in the pathogenesis and clinical course of mycobacteriosis in swine. Modulation of the immune response by vaccines that selectively target cytokine expression and secretion in response to mycobacterial challenge may be effective in prevention of mycobacteriosis in swine.  相似文献   

10.
Recent studies associate obesity and insulin resistance in horses with development of abnormal reproductive function and debilitating laminitis. The factors contributing to insulin resistance in obese horses are unknown. However, human studies provide evidence that elevated inflammatory cytokines such as tumor necrosis factor alpha (TNFalpha), IL1, and IL6 play direct roles in development of obesity-associated insulin resistance. Thus, inflammation may be a key link between obesity and insulin resistance in horses. The aim of the current investigation was to examine possible relationships between obesity, inflammatory cytokines, and insulin sensitivity (IS) in the horse. Age was recorded and BCS and percent body fat (% FAT) were determined as measures of obesity in 60 mares. In addition, blood mRNA expression of IL1, IL6, and TNFalpha and circulating concentrations of TNFalpha protein (TNFp) were determined in each mare. Finally, fasted concentrations of insulin were determined, and IS was determined using the hyperinsulinemic, euglycemic clamp. Significant correlations between several variables provided evidence for the design of 4 population regression models to estimate relationships between measures of obesity, inflammatory factors, and IS in the sample population. The results of these analyses revealed that IS decreased as BCS and % FAT increased (P < 0.001) in the sample population. Additionally, increased IL1 (P < 0.05) and TNFp (P < 0.01) were associated with decreased IS. However, increased TNFalpha (P < 0.001) was associated with decreased IS only in mares 20 yr of age and older. Increased BCS and % FAT were associated with increased expression of TNFalpha (P = 0.053) and IL1 (P < 0.05), and increased TNFp (P < 0.05). Surprisingly, increased BCS and % FAT were associated with decreased IL6 expression (P = 0.05) in mares <20 yr of age. Finally, evaluation of the influence of obesity and inflammatory cytokines on IS within the same model suggested that BCS and % FAT (P < 0.001) with TNFalpha [mRNA (P = 0.07) and protein (P < 0.05)] are inversely associated with IS independently of one another. Combined, these results provide the first evidence associating obesity with increased inflammatory factors in the horse. Furthermore, the results suggest that an interrelationship exists among obesity, inflammatory cytokines, and IS in the horse and emphasize the need for further studies to elucidate the nature of these relationships.  相似文献   

11.
The objective of this study was to determine cytokine and chemokine mRNA expression profiles in tracheobronchial lymph nodes from pigs singularly infected with porcine circovirus type 2 (PCV2), Mycoplasma hyopneumoniae (MHYO), or coinfected with both. Twenty-eight pigs were randomly assigned to one of four groups: (1) negative controls (NEG), (2) inoculated with MHYO (IMHYO), (3) inoculated with MHYO and PCV2 (CoI), and (4) inoculated with PCV2 (IPCV2). MHYO infection significantly (P<0.05) stimulated innate cytokines, IL1B and IL8. PCV2 infection significantly stimulated expression of IFNG, IL8, NOS2A and chemokines CCL2, CCL5, and CXCL10. IFNB, IL1B and IL12 were slightly increased with PCV2 infection and IFNA and IL4 were significantly downregulated. Compared to NEG pigs, coinfection resulted in a significant increase in expression of IFNG, IL1B, IL8, CCL5, CXCL10, and weak stimulation of IFNB, IL6 and IL10; IL13 and IFNA were significantly downregulated. Overall MHYO potentiated PCV2 infection by increasing IFNG and IL10 mRNA expression levels. The increase of IFNG and chemokines and decrease of IFNA in IPCV2 and CoI pigs were correlated with increased severity of lymphoid lesions and the presence of PCV2 antigen. In summary, this work provided evidence that the increased severity of lesions in PCV2 and MHYO coinfected pigs was associated mainly with the presence of PCV2 antigen and alterations of cytokine mRNA expression profiles.  相似文献   

12.
本试验以猪空肠上皮细胞(IPEC-J2)为模型细胞,探讨T-2毒素诱导IPEC-J2炎性反应的影响及相关作用机制.通过四甲基偶氮唑盐(MTT)方法测定细胞活力,选择适宜的T-2毒素和N-乙酰-L-半胱氨酸(NAC)浓度.试验分为4个组,分别为对照组、NAC组(4.0 mmol/L NAC)、T-2组(4.0 ng/mL...  相似文献   

13.
本研究旨在探讨姜黄素对猪轮状病毒(PRV)感染猪肠上皮细胞(IPEC-J2细胞)的抗病毒作用。以IPEC-J2细胞为试验对象,分别设置阴性对照组、感染PRV(感染复数=0.1)组和感染PRV后姜黄素(20μmol/L)处理组。在感染PRV后观察细胞病变,利用流式细胞术检测细胞内活性氧(ROS)含量,并通过实时荧光定量PCR(qRT-PCR)技术和病毒滴度测定法检测PRV在IPEC-J2细胞内的复制与增殖。结果表明:与阴性对照组相比,1)PRV感染导致IPEC-J2细胞病变,显著降低细胞活力(P<0.05),极显著上调细胞内ROS含量(P<0.01);2)姜黄素可显著抑制PRV在细胞内的复制与增殖(P<0.05);3)在PRV吸附细胞阶段添加姜黄素显著抑制了病毒的复制与增殖(P<0.05);4)姜黄素在感染前与PRV直接孵育能显著降低感染后病毒的滴度(P<0.05);5)PRV感染显著提高了细胞内黑色素瘤分化相关基因5、干扰素诱导蛋白44样蛋白抗体和干扰素β的mRNA相对表达量(P<0.05),显著降低了细胞内Toll样受体适配器分子1、线粒体抗病毒信...  相似文献   

14.
本研究采用荧光定量PCR方法,检测了IPEC-J2细胞不同时间点紧密连接蛋白3(claudin 3,CLDN-3)、细胞角蛋白8(cytokeratin 8,KRT8)、黏蛋白1(mucin 1,MUC1)3种蛋白mRNA的表达量变化。本试验将猪传染性胃肠炎病毒(TGEV)感染IPEC-J2细胞,探索食淀粉乳杆菌代谢产物是否通过维持或改善CLDN-3、KRT8、MUC1蛋白mRNA表达来增强细胞的屏障功能,是否对IPEC-J2细胞感染TGEV后的屏障功能产生影响。试验结果发现,正常细胞对照组MUC1、CLDN-3及KRT8蛋白mRNA表达量随时间没有显著变化(P> 0.05),MRS培养基对照组与正常细胞对照组相比没有显著变化(P> 0.05),食淀粉乳杆菌代谢产物单独处理组对细胞MUC1、CLDN-3及KRT8蛋白mRNA表达量呈显著上调作用(P< 0.05);食淀粉乳杆菌代谢产物+TGEV试验组与病毒对照组相比,处理24、36和48 h,MUC1、CLDN-3及KRT8蛋白的表达显著升高(P< 0.05)。结果表明,食淀粉乳杆菌代谢产物不仅能提高MUC1、CLDN-3及KRT8在IPEC-J2细胞上的表达,还能负调节TGEV诱导的MUC1、CLDN-3及KRT8在IPEC-J2细胞上的表达,从而加强IPEC-J2细胞对TGEV感染的屏障功能。  相似文献   

15.
This study used Real-time PCR to detect the changes of expression quantity of claudin 3 (CLDN-3), cytokeratin 8 (KRT8) and mucin 1 (MUC1) three proteins mRNA in IPEC-J2 cells at three different time points.IPEC-J2 cells were infected by TGEV, we explored whether Lactobacillus amylovorus metabolites could enhance cell barrier function by maintaining or improving mRNA expression of CLDN-3, KRT8 and MUC1, whether had effects on the barrier function of IPEC-J2 infected by TGEV.The results showed that mRNA expressions of MUC1, CLDN-3 and KRT8 in the normal cell control group did not change significantly with time (P> 0.05); MRS medium culture group did not change significantly compared to the normal cell control group(P> 0.05); Gene expressions of MUC1, CLDN-3 and KRT8 proteins in Lactobacillus amylovorus metabolites alone treatment group showed significant time-dependent effect (P< 0.05).After being treated 24, 36 and 48 h, gene expressions of MUC1, CLDN-3 and KRT8 proteins in Lactobacillus amylovorus metabolites+TGEV experiment group was significantly higher than virus control group (P< 0.05).Lactobacillus amylovorus metabolites could improve MUC1, CLDN-3 and KRT8 expressions in IPEC-J2 cells, while being able to negatively regulate MUC1, CLDN-3 and KRT8 expressions that TGEV induced in IPEC-J2 cells, thereby inhencing the barrier function of IPEC-J2 cell against TGEV.  相似文献   

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17.

Background

Feline idiopathic cystitis (FIC) is a common lower urinary tract disorder of domestic cats that resembles interstitial cystitis/painful bladder syndrome (IC/PBS) in humans. Diagnosis of FIC is based on clinical signs and exclusion of other disorders because of a lack of specific pathologic findings or other objective biomarkers. Cytokines are potential noninvasive biomarkers to define the presence, severity, and progression of disease, and response to treatment.

Objectives

The objective of this pilot study was to determine concentrations of selected cytokines in serum from healthy cats and cats with acute FIC.

Animals

Serum samples from 13 healthy cats and from 12 cats with nonobstructive acute FIC were utilized.

Methods

Multiplex analysis of 19 cytokines (CCL2, CCL5, CXCL1, CXCL12, CXCL8, Flt3L, GM‐CSF, IFN‐γ, IL‐12 (p40), IL‐13, IL‐18, IL‐1β, IL‐2, IL‐4, IL‐6, PDGF‐BB, SCF, sFas, and TNF‐α) was performed with a commercially available feline‐specific multiplex bead‐based assay.

Results

Mean serum concentrations of IL‐12 (p40; P < 0.0001), CXCL12 (P = 0.002), IL‐18 (P = 0.032), and Flt3L (P = 0.0024) were significantly increased in FIC cats compared to healthy cats. GM‐CSF, IL‐1b, IL‐2, and PDGF‐BB were undetectable or detected in an insufficient number of cats to allow meaningful comparisons.

Conclusions and Clinical Importance

We have identified increased serum concentrations of pro‐inflammatory cytokines and chemokines CXCL12, IL‐12, IL‐18, and Flt3L in FIC‐affected cats. These findings suggest potential candidates for noninvasive biomarkers for diagnosis, staging, and therapeutic outcome monitoring of affected cats and provide additional insight into the etiopathogenesis of FIC.  相似文献   

18.
试验旨在探索革兰氏阴性菌大肠杆菌(Escherichia coli,E.coli)及其表面分子脂多糖(LPS)诱导胰腺再生蛋白Ⅲγ(RegⅢγ)表达调控的机制。首先,用不同浓度灭活E.coli(109、108、107、106、105、104 CFU/mL)和LPS (0.01、0.1、1、5、10、20、40、80 μg/mL)诱导猪肠黏膜上皮细胞(IPEC-JⅡ),用MTT法测D490 nm值,检测E.coli和LPS对IPEC-JⅡ细胞活力的影响;其次,用不同浓度灭活E.coli(107、106、105 CFU/mL)和LPS (0.01、0.1、1、5 μg/mL)处理IPEC-JⅡ细胞24 h,用实时荧光定量PCR和Western blotting检测RegⅢγ mRNA和蛋白的表达;最后,用1 μg/mL LPS处理IPEC-JⅡ细胞24 h,用实时荧光定量PCR和Western blotting检测p65、p38、JNK、ERK mRNA和蛋白表达及磷酸化水平。结果显示,除0.01 μg/mL LPS不抑制IPEC-JⅡ细胞活力外,其他浓度的灭活E.coli和LPS均可抑制IPEC-JⅡ细胞活力,且109、108 CFU/mL E.coli和10、20、40、80 μg/mL LPS组细胞活力极显著下降(P<0.01);与对照组相比,107、106和105 CFU/mL E.coli均能诱导RegⅢγ表达增加,且105 CFU/mL E.coli组RegⅢγ mRNA表达量极显著高于对照组(P<0.01),蛋白表达量显著高于对照组(P<0.05);0.01、0.1、1和10 μg/mL LPS均能诱导RegⅢγ表达增加,且0.1和1 μg/mL LPS组RegⅢγ mRNA表达量极显著高于对照组(P<0.01),RegⅢγ蛋白表达虽有增加趋势,但差异不显著(P>0.05);与对照组相比,1 μg/mL LPS组p65、p38 mRNA表达量极显著增加(P<0.01),JNK、ERK mRNA表达量显著增加(P<0.05);同时,p38、JNK蛋白表达量和磷酸化水平均极显著增加(P<0.01),p65蛋白磷酸化水平显著增加(P<0.05),ERK蛋白和磷酸化水平均增加,但差异不显著(P>0.05)。以上结果表明,灭活E.coli和LPS均可诱导RegⅢγ表达,1 μg/mL LPS可增加p65、p38和JNK蛋白的磷酸化水平。  相似文献   

19.

Background

The hypothalamic‐pituitary‐adrenal (HPA) is influenced by the proinflammatory cytokines IL‐6, IL‐1β, and TNF‐α in critically ill humans. Information about the association of cytokines with the HPA axis in neonatal foals is lacking.

Hypothesis/Objectives

The objectives were to describe for hospitalized septic and nonseptic foals (1) temporal changes in blood concentrations of ACTH, and cortisol, and leukocyte cytokine gene expression, and (2) coassociation of these HPA axis hormones with blood leukocyte cytokine gene expression.

Animals

Hospitalized septic foals (N = 15) and hospitalized nonseptic foals (N = 11).

Methods

Blood samples, obtained from study foals at admission (T = 0), and 24 (T = 1), 48 (T = 2), 72 (T = 3), and 96 (T = 4) hours after admission, were processed to isolate RNA from leukocytes and to harvest plasma and serum for hormone assays. Plasma ACTH and serum cortisol concentrations were determined by radioimmunoassay. Leukocyte mRNA expression of IL‐1β IL‐6, IL‐8, IL‐10, and TNF‐α was determined using RT‐PCR.

Results

Cortisol concentrations were greater (P < .05) in foals at admission than at other time points. The expressions of IL‐8 and IL‐10 mRNA were lower (P < .05) at each time point in septic than in nonseptic foals. Among septic foals, ACTH was positively associated (P = .0026) with IL‐6 mRNA expression.

Conclusions

Sepsis influences secretion of the HPA axis hormones and expression of cytokines in foals. A positive association with the HPA axis and IL‐6 expression was detected. The clinical importance of these findings requires additional study.  相似文献   

20.
Tumor Necrosis Factor-alpha (TNFalpha) is a pleiotrophic cytokine, affects either normal or tumor cells, and influences cellular differentiation. TNFalpha role in female reproduction has been proven to be mediated through an influence on prostaglandin (PGs) synthesis and output. To evaluate the possible role of TNFalpha in an auto-/paracrine regulation in the cat uterus, mRNA expression coding for TNFalpha and its receptors (TNFR1 and TNFR2), and TNFalpha protein content at different stages of the estrous cycle were investigated. Additionally, TNFalpha involvement in PG secretion at different stages of the estrous cycle was investigated by in vitro tissue culture. Gene expressions coding for TNFalpha and TNFR1 were the highest at diestrus (P < 0.05). TNFalpha protein expression was the lowest at interestrus (P < 0.05). Nevertheless, TNFR2 was not affected by the estrous stage. TNFalpha at a dose of 1 ng/ml significantly increased PGF2alpha secretion at estrus (P < 0.01) and PGE2 secretion at diestrus (P < 0.001) after 12h incubation. Overall findings indicate that TNFalpha locally produced in the cat's uterus, stimulates PG secretion in an estrous cycle-related manner.  相似文献   

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