共查询到20条相似文献,搜索用时 15 毫秒
1.
Sandeep A. Walujkar Shreyas V. Kumbhare Nachiket P. Marathe Dhrati V. Patangia Parimal S. Lawate Renu S. Bharadwaj Yogesh S. Shouche 《World journal of microbiology & biotechnology》2018,34(6):76
Dysbiosis of intestinal microflora has been postulated in ulcerative colitis (UC), which is characterized by imbalance of mucosal tissue associated bacterial communities. However, the specific changes in mucosal microflora during different stages of UC are still unknown. The aim of the current study was to investigate the changes in mucosal tissue associated microbiota during acute exacerbations and remission stages of UC. The mucosal microbiota associated with colon biopsy of 12 patients suffering from UC (exacerbated stage) and the follow-up samples from the same patients (remission stage) as well as non-IBD subjects was studied using 16S rRNA gene-based sequencing and quantitative PCR. The total bacterial count in patients suffering from exacerbated phase of UC was observed to be two fold lower compared to that of the non-IBD subjects (p?=?0.0049, Wilcox on matched-pairs signed rank tests). Bacterial genera including Stenotrophomonas, Parabacteroides, Elizabethkingia, Pseudomonas, Micrococcus, Ochrobactrum and Achromobacter were significantly higher in abundance during exacerbated phase of UC as compared to remission phase. The alterations in bacterial diversity with an increase in the abnormal microbial communities signify the extent of dysbiosis in mucosal microbiota in patients suffering from UC. Our study helps in identifying the specific genera dominating the microbiota during the disease and thus lays a basis for further investigation of the possible role of these bacteria in pathogenesis of UC. 相似文献
2.
Sandor Z Deng XM Khomenko T Tarnawski AS Szabo S 《Biochemical and biophysical research communications》2006,350(1):147-150
Angiogenesis is an essential component of ulcer healing since it assures delivery of oxygen and nutrients to the healing site. Previous studies demonstrated increased serum and tissue levels of vascular endothelial growth factor (VEGF, the most potent angiogenic growth factor) in patients with active ulcerative colitis (UC) and animal models of UC. However, there is no explanation why the healing of UC-related mucosal injury is impaired despite increased expression of VEGF. Expression of angiogenesis inhibitors, angiostatin and/or endostatin, in UC has not been determined before. We examined expression of VEGF, angiostatin, and endostatin in two models of experimental UC. The results revealed that in addition to increased VEGF, both endostatin and angiostatin levels were markedly (2-3-folds) increased in colonic mucosa at early stage of experimental UC. This is the first demonstration that colitis triggers increase in angiostatin and endostatin levels. The results may explain why mucosal lesions heal slowly despite increased VEGF levels, and may provide a novel and mechanistic insight into UC. 相似文献
3.
Bacterial Interactions in Early Life Stages of Marine Cold Water Fish 总被引:11,自引:0,他引:11
Abstract
The intensive rearing of various fish species in aquaculture has revealed intimate relationships between fish and bacteria
that eventually may affect establishment of a ``normal' mucosal microflora or result in disease epizootics. Interactions
between bacteria and mucosal surfaces play important roles both at the egg and larval stages of marine fish. Bacterial adhesion
and colonization of the egg surface occur within hours after fertilization. The diverse flora which eventually develops on
the egg appears to reflect the bacterial composition and load of the ambient water, but species-specific adhesion at the egg
surface may also play a role in development of the egg epiflora. Proteolytic enzymes produced by members of the adherent epiflora
may cause serious damage to the developing egg and may also affect further adhesion of the epiflora.
Ingestion of bacteria at the yolk sac stage results in establishment of a primary intestinal microflora which seems to persist
beyond first feeding. Establishment of a gut microflora is likely to undergo several stages, resulting in an ``adult' microflora
weeks to months after first feeding. Ingested bacteria may serve as an exogenous supply of nutrients or essential factors
at an early life stage. Early exposure to high bacterial densities is probably important for immune tolerance, and thus for
the establishment of a protective intestinal microflora.
Successful rearing of early life stages of several marine fish species depends on knowledge of the complex interactions among
the cultured organisms and the bacterial communities which develop at the mucosal surfaces and in the ambient water and rearing
systems. The routine use of antibiotics during rearing of fish larvae is not advisable, since it may increase the risk of
promoting antibiotic resistance and adversely affect the indigenous microflora of the larvae. The use of probiotics has proven
advantageous in domestic animal production, and the search for effective probiotics may have a great potential in aquaculture
of marine organisms. Bacteria with antagonistic effects against fish pathogens have been successfully administered to several
fish species, resulting in decreased mortality or increased growth rate.
Received: 14 December 1998; Accepted: 7 April 1999 相似文献
4.
溃疡性结肠炎(Ulcerative colitis,UC)的发病被认为是宿主遗传易感性、黏膜免疫与肠道菌群共同作用的结果。许多临床研究显示,与正常人相比,UC患者存在不同程度的菌群失调。艰难梭菌、致病性大肠埃希菌等致病微生物被怀疑与UC的发病相关,但目前还未找到充分证据证明它们与UC患者肠道炎症间的因果关系。就UC患者肠道菌群分布的研究现状、肠道菌群检测方法及未来研究进展进行了阐述。 相似文献
5.
Ulcerative colitis (UC) is a chronic inflammatory bowel disease with mucosal inflammation and ulceration of the colon. There seems to be no single etiological factor responsible for the onset of the disease. Autoimmunity has been emphasized in the pathogenesis of UC. Perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) are common in UC, and recently two major species of proteins immunoreactive to pANCA were detected in bacteria from the anaerobic libraries. This implicates colonic bacterial protein as a possible trigger for the disease-associated immune response. Autoantibodies and T-cell response against human tropomyosin isoform 5 (hTM5), an isoform predominantly expressed in colon epithelial cells, were demonstrated in patients with UC but not in Crohn's colitis. We identified two bacterial protein sequences in NCBI database that have regions of significant sequence homology with hTM5. Our hypothesis is that molecular mimicry may be responsible for the pathogenesis of UC. 相似文献
6.
Onderdonk AB 《Anaerobe》2005,11(4):189-195
Animal models simulating human disease have played an important role in our understanding of the pathogenesis and treatment of infections caused by obligately anaerobic bacteria. These models helped document the primary source of such infections as the host's own normal microflora. In addition, the polymicrobial nature of anaerobic infections was documented by using animal models for intraabdominal sepsis. Subsequent studies using animal models have led to an understanding of the nature of the host immune response to abscess causing agents and have been instrumental in defining the molecular basis for the virulence and protection provided by the polysaccharide capsule of Bacteroides fragilis. Animal models have also been important components for studies of toxigenic clostridial diseases, such as antibiotic associated colitis and ulcerative colitis. A discussion of some of these models is provided in this review. 相似文献
7.
Xiaohan Wu Shuchun Wei Meilin Chen Jinting Li Yuping Wei Jixiang Zhang Weiguo Dong 《International journal of biological sciences》2022,18(13):5056
The pathogenesis of ulcerative colitis (UC) is unclear, while genetic factors have been confirmed to play an important role in its development. P2RY13 is a G protein-coupled receptor (GPCRs), which are involved in the pathogenesis of inflammation and immune disorders. According to GEO database analysis, we first observed that the expression of P2Y13 was increased in UC patients. Therefore, we sought to determine the role of P2Y13 in the development of colitis. Our data showed that P2RY13 was highly expressed in the inflamed intestinal tissues of UC patients. In mice, pharmacological antagonism of P2Y13 can significantly attenuate the intestinal mucosal barrier disruption. In LPS-induced NCM460 cell, knockdown or pharmacological inhibition of P2RY13 increased the expression of intestinal tight junction protein and reduced apoptosis. In addition, we found that the effect of P2Y13 on colitis is related to the activation of the IL-6/STAT3 pathway. Activation of P2Y13 increases IL-6 expression and promotes STAT3 phosphorylation and nuclear transport. Deletion of the STAT3 gene in the intestinal epithelial cells of mice significantly mitigated the exacerbation of colitis due to P2Y13 activation. Thus, P2Y13 can aggravate intestinal mucosal barrier destruction by activating the IL-6/STAT3 pathway. P2Y13 might be a potential drug target for UC. 相似文献
8.
Yalan Dong Heng Fan Zhe Zhang Feng Jiang Mingyue Li Haifeng Zhou Weina Guo Zili Zhang Zhenyu Kang Yang Gui Zhexing Shou Junyi Li Rui Zhu Yu Fu Alexey Sarapultsev Huafang Wang Shanshan Luo Ge Zhang Desheng Hu 《International journal of biological sciences》2022,18(4):1381
Ulcerative colitis (UC) is an idiopathic, chronic inflammatory disorder of the colon, and it has become one of the world-recognized medical problems as it is recurrent and refractory. Berberine (BBR) is an effective drug for UC treatment. However, the underlying mechanism and targets remain obscure. In this study, we systematically investigated the therapeutic effect and its mechanism of BBR in ameliorating DSS-induced mouse colitis. Expectedly, the colon inflammation was significantly relieved by BBR, and microbiota depletion by antibiotic cocktail significantly reversed the therapeutic effect. Further studies showed that BBR can regulate the abundance and component of bacteria, reestablish the broken chemical and epithelial barriers. Meanwhile, BBR administration dramatically decreased ILC1 and Th17 cells, and increased Tregs as well as ILC3 in colonic tissue of DSS-induced mice, and it was able to regulate the expression of various immune factors at the mRNA level. Moreover, a proteomic study revealed that Wnt/β-catenin pathway was remarkably enhanced in colonic tissue of BBR-treated mice, and the therapeutic effect of BBR was disappeared after the intervention of Wnt pathway inhibitor FH535. These results substantially revealed that BBR restores DSS-induced colon inflammation in a microbiota-dependent manner, and BBR performs its protective roles in colon by maintaining the structure and function of the intestinal mucosal barrier, regulating the intestinal mucosal immune homeostasis and it works through the Wnt/β-catenin pathway. Importantly, these findings also provided the proof that BBR serves as a potential gut microbiota modulator and mucosal barrier protector for UC prevention and therapy. 相似文献
9.
10.
Arezo Judaki Mohamadreza Hafeziahmadi Atefe Yousefi Mohamad Reza Havasian Jafar Panahi Koroush Sayehmiri Sajjad Alizadeh 《Bioinformation》2014,10(11):693-696
The intestine is the largest mucosal organ of the body and also the first line immune homeostasis. Inflammatory bowel disease or
IBD is divided into ulcerative colitis and Crohn''s disease. One of the problems that can occur with UC is dietary allergy to some
foods. This study aimed to evaluated the dairy allergy among patients with ulcerative colitis. This study is a Case - control study,
that studied 72 patients with Ulcerative Colitis, after recording history of the disease, colonoscopy and confirmed by biopsy and 72
person without history of colitis. In this study, in order to investigate of food allergy, used of the EUROMMUM kit with an
international code number DP3420-1601-11E. We used chi-square and Monte Carlo method for analysis of data. Among UC
patients, 30.6% mild, 52.8% moderate and 16.6% of cases were in sever stage. 9.7% of them reported a history of abdominal surgery
due to disease. According to the chi-square and Monte Carlo methods, dairy allergy (including: cow milk, cow milk UHT and
casein) in UC group was significant (P=0.00). This study indicated that there is significant relationship between UC and cow milk,
cow milk UHT and casein. UC patients who are allergic to dairy products and the use of dairy products can increase the severity of
UC. 相似文献
11.
Suárez J Romero-Zerbo Y Márquez L Rivera P Iglesias M Bermúdez-Silva FJ Andreu M Rodríguez de Fonseca F 《PloS one》2012,7(5):e37729
Studies in animal models and humans suggest anti-inflammatory roles on the N-acylethanolamide (NAE)-peroxisome proliferators activated receptor alpha (PPARα) system in inflammatory bowel diseases. However, the presence and function of NAE-PPARα signaling system in the ulcerative colitis (UC) of humans remain unknown as well as its response to active anti-inflammatory therapies such as 5-aminosalicylic acid (5-ASA) and glucocorticoids. Expression of PPARα receptor and PPARα ligands-biosynthetic (NAPE-PLD) and -degrading (FAAH and NAAA) enzymes were analyzed in untreated active and 5-ASA/glucocorticoids/immunomodulators-treated quiescent UC patients compared to healthy human colonic tissue by RT-PCR and immunohistochemical analyses. PPARα, NAAA, NAPE-PLD and FAAH showed differential distributions in the colonic epithelium, lamina propria, smooth muscle and enteric plexus. Gene expression analysis indicated a decrease of PPARα, PPARγ and NAAA, and an increase of FAAH and iNOS in the active colitis mucosa. Immunohistochemical expression in active colitis epithelium confirmed a PPARα decrease, but showed a sharp NAAA increase and a NAPE-PLD decrease, which were partially restored to control levels after treatment. We also characterized the immune cells of the UC mucosa infiltrate. We detected a decreased number of NAAA-positive and an increased number of FAAH-positive immune cells in active UC, which were partially restored to control levels after treatment. NAE-PPARα signaling system is impaired during active UC and 5-ASA/glucocorticoids treatment restored its normal expression. Since 5-ASA actions may work through PPARα and glucocorticoids through NAE-producing/degrading enzymes, the use of PPARα agonists or FAAH/NAAA blockers that increases endogenous PPARα ligands may yield similar therapeutics advantages. 相似文献
12.
Karla G. Sifroni Carlos R. Damiani Cristhopher Stoffel Mariane R. Cardoso Gabriela K. Ferreira Isabela C. Jeremias Gislaine T. Rezin Giselli Scaini Patricia F. Schuck Felipe Dal-Pizzol Emilio L. Streck 《Molecular and cellular biochemistry》2010,342(1-2):111-115
Ulcerative colitis (UC) is a chronic inflammatory disease of the large bowel. Its pathogenesis remains unclear, but it appears to result from a deregulated immune response, with infiltration of leukocytes into the mucosal interstitium. Several studies link oxidative stress and mitochondrial dysfunction to the pathogenesis of UC. Thus, the aim of this study was to evaluate the activities of mitochondrial respiratory chain complexes in the colonic mucosal of UC patients. Colonic biopsies were obtained from UC patients (n = 13). The control specimens were taken from patients without any history of inflammatory bowel disease (n = 8). Colon mucosal was removed by colonoscopy and homogenized. Mitochondrial respiratory chain complexes activities were then measured. Our results showed that the activity of complex I was not altered in UC patients, when compared to the control group. On the other hand, complexes II, III, and IV were decreased around 50–60% in the colonic mucosal of UC patients. Based on the present findings, we hypothesize that mitochondrial dysfunction may play a role in pathogenesis of UC. 相似文献
13.
F Souza-Fonseca-Guimaraes Y Krasnova T Putoczki K Miles K P MacDonald L Town W Shi G C Gobe L McDade L A Mielke H Tye S L Masters G T Belz N D Huntington G Radford-Smith M J Smyth 《Cell death & disease》2016,7(7):e2302
Inflammatory bowel disease (IBD) is an immunoregulatory disorder, associated with a chronic and inappropriate mucosal immune response to commensal bacteria, underlying disease states such as ulcerative colitis (UC) and Crohn''s disease (CD) in humans. Granzyme M (GrzM) is a serine protease expressed by cytotoxic lymphocytes, in particular natural killer (NK) cells. Granzymes are thought to be involved in triggering cell death in eukaryotic target cells; however, some evidence supports their role in inflammation. The role of GrzM in the innate immune response to mucosal inflammation has never been examined. Here, we discover that patients with UC, unlike patients with CD, display high levels of GrzM mRNA expression in the inflamed colon. By taking advantage of well-established models of experimental UC, we revealed that GrzM-deficient mice have greater levels of inflammatory indicators during dextran sulfate sodium (DSS)-induced IBD, including increased weight loss, greater colon length reduction and more severe intestinal histopathology. The absence of GrzM expression also had effects on gut permeability, tissue cytokine/chemokine dynamics, and neutrophil infiltration during disease. These findings demonstrate, for the first time, that GrzM has a critical role during early stages of inflammation in UC, and that in its absence colonic inflammation is enhanced.Inflammatory bowel disease (IBD) is a gut-associated inflammatory disorder, which stems from a dysfunctional mucosal immune response to commensal bacteria.1 As a multifactorial disease, IBD is the consequence of a complex interplay between environmental triggers, genetic susceptibility, and immunoregulatory defects, resulting in a pathogenesis that is still poorly understood.2 These interactions result in the inability of an individual to control the normal inflammatory response to pathogens in the gut, leading to a chronic state of sustained and inappropriate inflammation. IBD underlies disease states such as ulcerative colitis (UC) and Crohn''s disease (CD), with symptoms including weight loss, abdominal pain, diarrhea, and rectal bleeding which often require intensive medical therapy and resective surgery.3 The pathogenesis of IBD, characterized by a defective mucosal immune response to microbial exposure in the gastrointestinal tract, is thought to be caused by a dysfunctional immune response to host microbiota, infection by specific pathogens, and/or a defective mucosal barrier to luminal pathogens.1, 2 IBD patients also have a high risk of developing colitis-associated colon cancer (CAC).4 Additionally, histological assessment of inflamed ileal and colonic segments from IBD patients typically shows increased infiltration of immune cells, particularly neutrophils, as well as crypt abscesses, mucin depletion, and ulcers—all correlating with the severity of small bowel and colonic tissue damage.5Cytotoxic pathways mediated by lymphocytes directly trigger cell death in target cells.6 These cytotoxic pathways are mediated by proteins such as perforin, which mediates pore formation in the target cell surface and allows granzyme (Grz)s to enter the intracellular compartment and induce cell death.7 To date, five different Grzs have been identified in humans (GrzA, GrzB, GrzH, GrzK, and GrzM), whereas mice express eleven Grzs (GrzA, GrzB, GrzC, GrzD, GrzE, GrzF, GrzG, GrzK, GrzL, GrzM, and GrzN).8, 9 Walch et al.10 recently demonstrated that Grzs (GrzA and GrzB) directly kill bacteria through granulysin-mediated delivery, suggesting that Grzs act as microbial modulating factors. Moreover, recently GrzA was shown to be increased in the colon biopsies of UC patients undergoing treatment with Etrolizumab, a monoclonal antibody targeting the β7 integrin subunit. Higher levels of GrzA could predict which patients were more likely to benefit from the therapy; however, the precise mechanism of action of GrzA in UC remains to be addressed.11 GrzM was initially described as being constitutively expressed by natural killer (NK) cells,12, 13 and specifically associated with inflammation.14 This enzyme has been shown to preferentially cleave methionine and leucine residues in target cells, mediating direct, non-specific cell death.15, 16 More recently, GrzM was also shown to be an important mediator for the release of MIP-1α from NK cells, inducing NK cell and neutrophil recruitment during early microbial infection.17 We now observe that GrzM expression is increased in inflamed colon tissue samples from UC, but not CD patients. Further, GrzM-deficient (GrzM−/−) mice are more sensitive to a mouse model of IBD and IBD-induced colorectal cancer (CRC). These findings demonstrate, for the first time, that GrzM has a critical role in mediating the early stages of the gut mucosal immune response. 相似文献
14.
Jacob Tveiten Bjerrum Yulan Wang Jingtao Zhang Lene Buhl Riis Ole Haagen Nielsen Jakob Benedict Seidelin 《International journal of biological sciences》2022,18(5):1813
Improving the long-term prognosis of ulcerative colitis (UC) requires sustained deep mucosal colonic healing with histologic remission, making the study of colonic tissue regeneration essential. In experimental colitis models, lipid metabolites are recognized as pivotal components of this process. This study aimed to describe the kinetics of wound healing and lipid metabolites engaged in regeneration in the normal colonic mucosa and how they are affected in UC to reveal new therapeutic targets. Experimental colonic wounds were created endoscopically in quiescent UC (n=21) and controls (n=9), and the healing process was surveilled by serial endoscopies and cross-sectional wound biopsies post-wounding. Biopsies were analyzed by liquid chromatography coupled with mass spectrometry. Endoscopic wound scores were significantly higher in UC at day two (p=0.001) and seven (p<0.0001) post-wounding, demonstrating a prolonged wound healing process. The wound scores were correlated with lipid mediators crucial for normal regeneration and sustained UC-specific changes in key phospholipids and eicosanoids, i.e., lysophosphatidylcholine, phosphatidylcholine, lysophosphatidic acid, phosphatidylglycerol, phosphatidylinositol, prostaglandin D2, and prostaglandin E1, were observed. A prolonged wound healing process is identified in quiescent UC with altered disease specific lipidomic trajectories providing potential novel therapeutic avenues for stimulating mucosal regeneration as an add-on to the traditional immune suppression treatment. 相似文献
15.
了解溃疡性结肠炎(UC)小鼠肠道黏膜菌群的构成及其与盲肠内容物菌群的差异, 探讨肠道菌群在UC小鼠发病中的作用。
12只C57BL/6N雄性小鼠随机分为正常组、治疗组和模型组, 每组4只。采用葡聚糖硫酸钠盐(DSS)进行造模, 采用柳氮磺胺吡啶灌胃进行治疗, 造模第8天处死全部小鼠。采用16S rRNA基因高通量测序法对肠道黏膜和盲肠内容物菌群进行测序分析。
UC小鼠肠道黏膜菌群与盲肠内容物菌群相比, OTU数量和多样性均降低; Beta多样性分析显示其黏膜和盲肠内容物菌群差异较正常小鼠更大。在门和属的分类水平上, UC小鼠黏膜菌群中变形菌门、疣微菌门、魏斯菌属和肠球菌属丰度较正常小鼠升高, 厚壁菌门和拟杆菌门丰度降低; 阿克曼菌属在UC小鼠黏膜和盲肠内容物菌群中增多, 颤螺菌属在治疗组小鼠黏膜和盲肠内容物菌群中均减少。此外, 黏膜菌群中脱铁杆菌门
UC小鼠黏膜菌群与盲肠内容物菌群在群落组成、多样性、优势菌群等方面存在明显差异, 黏膜菌群在UC发病机制中可能发挥着主要的作用。
16.
溃疡性结肠炎(UC)是一种肠道非特异性炎症性疾病,迁延不愈,严重影响患者的生活质量。目前认为,肠道菌群的改变是诱发和维持结肠炎症的主要原因。临床上应用益生菌制剂作为UC患者的辅助治疗,可平衡患者肠道菌群,减轻炎症反应。UC患者免疫调节功能紊乱,TLR4及其信号传导通路是UC发病的重要环节。易感人群肠道中的菌群突破肠上皮屏障,免疫系统被各种微生物抗原激活,炎症细胞活化从而导致结肠黏膜组织产生炎症反应,该过程可由TLR4-NF-κB信号传导通路介导。本研究就益生菌基于TLR4-NF-κB信号通路对溃疡性结肠炎的治疗进行综述。 相似文献
17.
Tomasello G Sciumé C Rappa F Rodolico V Zerilli M Martorana A Cicero G De Luca R Damiani P Accardo FM Romeo M Farina F Bonaventura G Modica G Zummo G Conway de Macario E Macario AJ Cappello F 《European journal of histochemistry : EJH》2011,55(4):e38
Ulcerative colitis (UC) is a form of inflammatory bowel disease (IBD) characterized by damage of large bowel mucosa and frequent extra-intestinal autoimmune comorbidities. The role played in IBD pathogenesis by molecular chaperones known to interact with components of the immune system involved in inflammation is unclear. We previously demonstrated that mucosal Hsp60 decreases in UC patients treated with conventional therapies (mesalazine, probiotics), suggesting that this chaperonin could be a reliable biomarker useful for monitoring response to treatment, and that it might play a role in pathogenesis. In the present work we investigated three other heat shock protein/molecular chaperones: Hsp10, Hsp70, and Hsp90. We found that the levels of these proteins are increased in UC patients at the time of diagnosis and decrease after therapy, supporting the notion that these proteins deserve attention in the study of the mechanisms that promote the development and maintenance of IBD, and as biomarkers of this disease (e.g., to monitor response to treatment at the histological level). 相似文献
18.
目的:通过检测白细胞介素23受体(1L-23R)及白细胞介素17A(IL-17A)在炎症性肠病(IBD)患者肠黏膜及血清中的表达水平,探讨其在IBD发病过程中的作用及意义。方法:收集32例克罗恩病(CD)患者、29例溃疡性结肠炎(UC)患者及27例对照者的内镜肠黏膜活检标本,采用荧光定量PCR技术检测肠黏膜内IL-23R、IL-17AmRNA的表达情况,免疫组化技术分析IL-23R、IL-17A在肠黏膜中的原位表达。结果:与健康对照组相比,CD及UC患者肠黏膜组织内IL-23RmRNA表达显著增高(P〈0.05),CD及UC组间的表达量差异无统计学意义(P〉0.05)。CD及UC患者肠黏膜组织内IL-17AmRNA表达显著增高(P〈0.05),CD组肠黏膜组织内IL.17AmRNA表达显著高于uc组(P〈0.05)。免疫组化分析显示IL-23R阳性细胞在CD与uc肠黏膜固有层内有较多表达,较正常黏膜内的肠上皮细胞相比,CD及UC患者肠黏膜IL-23R蛋白表达量最著增高(P〈0.05),UC及CD组间的表达量差异无统计学意义(P〉0.05)。IL-17A阳性细胞在CD与UC肠黏膜固有层内有较多表达,较正常黏膜内的肠上皮细胞相比,CD及UC患者肠黏膜IL-17A蛋白表达量最著增高(P〈0.05)。结论:IL.23R及IL-17A在IBD患者肠黏膜中表达显著增高,提示IL-23R及IL-17A表达异常与IBD的发生发展密切相关,有可能成为IBD治疗的新靶点。 相似文献
19.
Ince MN Elliott DE Setiawan T Blum A Metwali A Wang Y Urban JF Weinstock JV 《Journal of immunology (Baltimore, Md. : 1950)》2006,176(2):726-729
Helminths are immune modulators that down-regulate colitis in inflammatory bowel disease. In animal models, intestinal bacteria drive colitis and in humans certain alleles of the LPS receptor protein TLR4 increase inflammatory bowel disease susceptibility. To understand helminthic immune modulation in the gut, we studied the influence of intestinal Heligmosomoides polygyrus colonization on LPS-induced lamina propria mononuclear cell (LPMC) cytokine responses in mice. LPS did not stimulate TGFbeta production from LPMC of uninfected mice. LPS strongly induced LPMC from worm-infected animals to secrete TGFbeta, but not TNF-alpha or IL-12. The TGFbeta derived from mucosal T cells. Helminth infection up-regulated TLR4 expression only in lamina propria T cells. LPMC from worm-infected TLR4 mutant animals did not respond to LPS, suggesting that LPS required TLR4 to stimulate TGFbeta secretion. Thus, during helminth infection, LPS challenge induces mucosal T cells to make TGFbeta through a TLR4-dependent process without promoting synthesis of proinflammatory cytokines. 相似文献
20.
Antibiotics as growth promotants: mode of action 总被引:5,自引:0,他引:5
Recent concerns about the use of growth-promoting antibiotics in pig diets have renewed interest in the immunologic and growth-regulating functions of the gastrointestinal (GI) tract. The numerically dense and metabolically active microbiota ofthe pig GI tract represents a key focal point for such questions. The intestinal microbiota is viewed typically as a beneficial entity for the host. Intestinal bacteria provide both nutritional and defensive functions for their host. However, the host animal invests substantially in defensive efforts to first sequester gut microbes away from the epithelial surface, and second to quickly mount immune responses against those organisms that breach epithelial defenses. The impact of host responses to gut bacteria and their metabolic activities require special consideration when viewed in the context of pig production in which efficiency of animal growth is a primary objective. Here, we summarize the working hypothesis that antibiotics improve the efficiency of animal growth via their inhibition of the normal microbiota, leading to increased nutrient utilization and a reduction in the maintenance costs ofthe GI system. In addition, novel molecular ecology techniques are described that can serve as tools to uncover the relationship between intestinal microbiology and growth efficiency. 相似文献