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Mo1757 Probiotic Bacteria and Their Products Can Down-Regulate Leptin-Induced CCR7 Expression on Human DC
AGA Abstracts
enteropathy and ameliorates IBD but its role in T.gondii-induced IBD-like enteritis is less clear. MIF is a proinflammatory cytokine that plays a role in innate and adaptive immunity. Also, MIF is involved in IBD pathogenesis and in T.gondii and S.mansoni mediated immunopathology and disease severity. Our study examines the role of MIF in T.gondii-induced IBD-like enteritis and systemic inflammatory response in mice coinfected with S.mansoni. Methods: Wild type (wt) and MIF knock out (Mif ko) mice were infected by subcutaneous injection with 50 cercaries of BH strain of S.mansoni, and orally with 100 cysts of ME49 strain of T. gondii after 7-9 weeks post S.mansoni infection. Hemogram and alaninetransferase (ALT) levels were determined. Histopathology was analyzed and TNFα, IFNγ and IL-10 levels were measured by ELISA. Results: Histopathologycal analysis of wt mice monoinfected with T.gondii showed intense mononuclear cell infiltration and terminal ileum necrosis, which greatly reduced in the absence of MIF. When analyzing co-infection with S. mansoni, the intestinal mucosa showed a marked attenuation of the inflammation in wt, and an almost complete abrogation of the inflammatory response in Mif ko mice. However, despite profound reduction of inflammatory response in both coinfected groups, they presented increased mortality rates (n=6, Mif ko n=6, wt; p>0.05) though MIF-deficiency was protective in T.gondii single infection when compared to wt mice (n=5, Mif ko, n=5, wt, p<0.01) but not in S.mansoni monoinfection (n=11, Mif ko, n=11, wt, p<0.0001). Nonetheless, increased morbidity was observed in coinfected Mif ko mice which had augmented weight loss (18.6±2.1 x 23.5±3.5g; Mif ko x wt, p<0.05). Systemic response in mono and coinfected wt and Mif ko was determined. Histopathology showed severe liver mononuclear cell infiltration in wt coinfected when compared with monoinfected mice. In contrast, MIF deficiency resulted in amelioration of liver inflammation in mono and coinfected mice. Also, function was more preserved in Mif ko coinfected when compared with wt mice measured by ALT levels (113±13 UI/L x 68±6.3 UI/L; wt x Mif ko, p<0.01). IL-10 plasma levels were lower in coinfected Mif ko compared to wt mice (2.77± 0.67 x 0.56±0.46 ng/ml, wt x Mif ko, p<0.05). Conclusion: Our findings indicate that co-infection regulates MIF-dependent responses at intestinal mucosa but also profoundly affect systemic IL10-dependent and independent protective responses.
subjects was analysed by flow cytometry of PBDC and DC released from fresh colonic biopsies by collagenase treatment. The effect of PRO on LepRb mRNA in monocyte derived DC (MoDC) was determined by RT-PCR and changes in DC migratory capacity were determined by transwell migration of DC towards the chemoattractant, CCL19. Results: Leptin treatment of DC from both colonic biopsies and from blood increased their expression of CCR7 in a concentration-dependent fashion (P<0.01). A significant increase in migration towards CCL19 was also induced. In contrast, PRO decreased the expression of CCR7 on blood and tissue DC after overnight exposure, (p<0.004 and p<0.007 respectively), and down-regulated leptin-induced CCR7 on colonic DC (p<0.04). LepRb mRNA expression in MoDC was also decreased after exposure to PRO. STp also decreased CCR7 expression (p<0.001) and down-regulated leptin-induced CCR7 on colonic DC (p<0.03). Conclusions: Leptin treatment increased migration of both colonic and blood DC towards CCL19 by upregulating CCR7. Probiotic bacteria or their products may have a beneficial anti-inflammatory effect by reducing leptin-induced migration of DC. Mo1758 The Role of the Gut Barrier Function in the Pathophysiology of Viral Liver Cirrhosis Woo Kyu Jeon, Yeowon Choi Background/Aims: Plasma endotoxin levels commonly increase in patients with liver cirrhosis. We purposed to identify change of intestinal permeability and frequency of endotoxemia in patients with viral liver cirrhosis. Additionally, we studied relationship between plasma endotoxin levels and failure of gut barrier function. Methods: Subjects included 27 patients with viral liver cirrhosis(LC) and 45 volunteers as healthy control(HC). Intestinal permeability index were determined by level of urinary excretion of polyethylene-glycol after oral administration and plasma endotoxin levels by using quantitative Limulus assay. Grades of liver dysfunction were categorized by Child-Pugh classification and MELD score. Results: Intestinal permeability indexes were higher in LC than in HC(1.48±0.56%, n=27 vs. 0.93±0.50%, n= 45, P=0.019). Plasma endotoxin levels were higher in LC than in HC(0.35±0.17EU/ml vs. 0.11±0.14EU/ml, P<0.001). In LC, plasma endotoxin levels progressively increased in relation to severity of liver dysfunction(Child-Pugh class A/B/C=0.31±0.17/0.37±0.14/0.42±0.23EU/ ml, P=0.013, MELD category 1/2/3/4=0.27±0.14/ 0.39±0.17/0.32±0.21/0.47±0.28EU/ml, P= 0.043). LC with/without portal hypertension (1.47±0.55%, P<0.01/1.29±0.59%, P<0.05) had higher intestinal permeability indexes than HC(0.93±0.50%). Conclusions: Severity of liver dysfunction was associated with endotoxemia. Although gut barrier function did not show a significant relationship with endotoxemia, increased intestinal permeability may be a significant finding that at least in part is associated with the pathophysiology of viral liver cirrhosis.
Mo1756 CD4+ T Cells Regulate the Multifactorial Gastrointestinal Inflammation Induced Following Colonization With Bacterial Provocateurs Amanda E. Ramer-Tait, Anne-Marie C. Overstreet, Jesse M. Hostetter, Albert Jergens, Michael J. Wannemuehler Aberrant mucosal immune responses to the resident microbiota are a significant cofactor in the pathogenesis of inflammatory bowel diseases (IBD). It is estimated that 1 to 1.5 million Americans suffer with IBD and its consequences, with total IBD-associated treatment costs in the United States exceeding $6.2 billion in 2008. An overarching question is: How much of IBD derives from genetics and how much from environmental factors such as the microbiota? Our laboratory has demonstrated that prior colonization of mice harboring only the highly simplified altered Schaedler flora (DM mice) with Helicobacter bilis increases host susceptibility to the onset of colitis following a subsequent inflammatory insult with a very low dose (1.5%) of the inflammatory trigger, dextran sulfate sodium (DSS). This dose of DSS alone is not sufficient to elicit colitis. In addition, prior colonization with non-pathogenic Escherichia coli SWW33 failed to affect disease severity. Our most intriguing finding is that both H. bilis- and E. coli-colonized mice treated with DSS upregulate mucosal expression of IL-17A mRNA. However, expression is higher in E. coli-colonized mice compared to H. biliscolonized mice at 3 weeks post-infection. This pattern reverses at 12 weeks post-infection and antigen-specific IL-17A protein production by CD4+ T cells follows a similar pattern. Although the induction of IL-17 was demonstrable in mice colonized with either provocateur, only mice colonized with H. bilis were found to be more susceptible to low-dose DSSinduced colitis. The objective of our present study was to understand how H. bilis and E. coli differentially induce pathogenic or beneficial mucosal immune responses to antigens arising from the resident microbiota. Specifically, we hypothesized that the dichotomous immune responses induced following colonization with these bacterial provocateurs would be reflected in the differential functional capacity of the antigen-specific CD4+ T cells. Following colonization with either H. bilis or E. coli for 3 weeks, DM mice were administered either a monoclonal antibody to deplete CD4+ T cells or an isotype control antibody. Mice then received an inflammatory insult in the form of 1.5% DSS. Unexpectedly, depletion of CD4+ T cells in H. bilis-colonized mice prior to the DSS treatment period exacerbated disease as evidenced by marked clinical signs of disease as well as severe colonic shortening, cecal atrophy, edema and luminal blood. Depletion of CD4+ T cells from E. coli-colonized mice caused only a minor increase in disease severity. Together, these findings indicate that colonization with distinct bacterial provocateurs alters the mucosal environment to promote either pathogenic or beneficial CD4+ T cell responses following a multifactorial inflammatory insult.
Mo1759 Pathology Associated With Okadaella Gastrococcus Infection Among the Younger Generation Takayuki Okada, Kazutoshi Hori, Graham F. Adkins, Hiroto Miwa Background: There is an increasing incidence of H. pylori-negative and NSAIDs-negative gastritis in many countries, and gastric cancer may be found among the younger generation. Recently, we have reported the intracellular presence of the Gram-negative coccoid bacterium Okadaella gastrococcus (Og; ATCC BAA-2258, NBRC 107862, GenBank HQ699465) in the classic cancer cascades. It is not known whether the younger generation who are H. pylorinegative and NSAIDs-negative suffer from Og infection, and related pathology. The investigation was aimed to see what types of pathology could be found among the Og-positive, H. pylori-negative and NSAIDs-negative dyspeptic younger generation. Methods: 30 H. pylori-negative and NSAIDs-negative Japanese patients (age: 18-29, male: female =15:15) with dyspeptic symptoms who were found to be Og-positive under electron microscopy, were subjected to investigation. No patients had previous H. pylori eradication treatments. All targeted biopsy specimens obtained at the time of esophago-gastro-duodenoscopy (EGD) were examined for culture, urease, histology (H&E, WSS, AYTB stains), and transmission electron microscopy. Some specimens were examined by scanning electron microscopy. Results: Culture was only successful for nine (30%) cases. Histological findings of the stomach (n=30) were active chronic gastritis 5 (16.6%), mild chronic gastritis 19 (63.3%), gastric congestion and edema 2 (6.6%), and unremarkable gastric mucosa 4 (13.3%). Intestinal metaplasia was found in four cases (13.3%). Focal small gastric erosions 18 (60%) and gastric hemorrhage with/without free gastric blood clots 15 (50%) were seen at the time of EGD. Histological findings of the gastroesophageal junction (GEJ, n=25) were severe 1 (4%), moderate 1 (4%) and mild inflammation of GEJ 23(92%). All patients with unremarkable gastric mucosa had mild inflammation of GEJ. Conclusions: Og was found to be associated with various H. pylori -negative and NSAIDs-negative gastritis and inflammation of GEJ among the younger generation with dyspeptic symptoms. Macroscopic and microscopic appearances of the stomach and GEJ were subtle with mild inflammation in the majority of cases, though intestinal metaplasia could be present. It is recommended to take biopsy specimens from the stomach and GEJ to examine for Og related pathology.
Mo1757 Probiotic Bacteria and Their Products Can Down-Regulate Leptin-Induced CCR7 Expression on Human DC Hafid O. Al-Hassi, David Bernardo Ordiz, Borja Sánchez, Elizabeth R. Mann, Aravinth U. Murugananthan, Cheng T. Tee, Nicholas R. English, Ailsa Hart, Alex I. Blakemore, Abelardo Margolles, Andrew J. Stagg, Stella C. Knight
Mo1760
Background: Dendritic cells (DC) migrate to lymph nodes on expression of CCR7, and control immune activity. CCR7 on blood DC increases in response to the pro-inflammatory adipokine, leptin. Increased mesenteric fat and leptin occur early in Crohn's disease (CD) and ongoing production of the signaling isoform of leptin receptor (LepRb) is significantly higher in colonic DC from CD tissue than in DC from normal colon. Moreover, leptin induces functional CCR7 on peripheral blood DC (PBDC) and colonic DC (Al-hassi et al., 2011) suggesting leptin-mediated change in intestinal CCR7 expression on DC as a proinflammatory mechanism. We assessed changes in migration of blood and colonic DC in response to leptin, and their modulation by anti-inflammatory probiotioc bactetria (PRO; a combination of B. longum and B.breve) and by a proteolysis-resistant ‘anti-inflammatory' peptide derived from gut lactobacilli (STp). Methods: Expression of CCR7 by health human
AGA Abstracts
High-Throughput 454 Pyrosequencing Analysis Reveals Dysbiosis of the Mucosa-Associated Microbiota in Dogs With Inflammatory Bowel Disease Jan Suchodolski, Scot E. Dowd, Joerg M. Steiner, Albert Jergens Background: Canine inflammatory bowel disease (IBD) is an immune-mediated enteropathy likely triggered by environmental and immunoregulatory factors in genetically susceptible dogs. The underlying mechanisms that initiate and drive intestinal inflammation are only partially understood but suggest a pivotal role for gut bacteria in disease pathogenesis, similar to human IBD. New molecular tools, such as 454-pyrosequencing, can be used for in-depth phylogenetic analysis of the intestinal microbiota to identify imbalances in microbial diversity and composition associated with chronic intestinal inflammation. Aim: To use a
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enteropathy and ameliorates IBD but its role in T.gondii-induced IBD-like enteritis is less clear. MIF is a proinflammatory cytokine that plays a role in innate and adaptive immunity. Also, MIF is involved in IBD pathogenesis and in T.gondii and S.mansoni mediated immunopathology and disease severity. Our study examines the role of MIF in T.gondii-induced IBD-like enteritis and systemic inflammatory response in mice coinfected with S.mansoni. Methods: Wild type (wt) and MIF knock out (Mif ko) mice were infected by subcutaneous injection with 50 cercaries of BH strain of S.mansoni, and orally with 100 cysts of ME49 strain of T. gondii after 7-9 weeks post S.mansoni infection. Hemogram and alaninetransferase (ALT) levels were determined. Histopathology was analyzed and TNFα, IFNγ and IL-10 levels were measured by ELISA. Results: Histopathologycal analysis of wt mice monoinfected with T.gondii showed intense mononuclear cell infiltration and terminal ileum necrosis, which greatly reduced in the absence of MIF. When analyzing co-infection with S. mansoni, the intestinal mucosa showed a marked attenuation of the inflammation in wt, and an almost complete abrogation of the inflammatory response in Mif ko mice. However, despite profound reduction of inflammatory response in both coinfected groups, they presented increased mortality rates (n=6, Mif ko n=6, wt; p>0.05) though MIF-deficiency was protective in T.gondii single infection when compared to wt mice (n=5, Mif ko, n=5, wt, p<0.01) but not in S.mansoni monoinfection (n=11, Mif ko, n=11, wt, p<0.0001). Nonetheless, increased morbidity was observed in coinfected Mif ko mice which had augmented weight loss (18.6±2.1 x 23.5±3.5g; Mif ko x wt, p<0.05). Systemic response in mono and coinfected wt and Mif ko was determined. Histopathology showed severe liver mononuclear cell infiltration in wt coinfected when compared with monoinfected mice. In contrast, MIF deficiency resulted in amelioration of liver inflammation in mono and coinfected mice. Also, function was more preserved in Mif ko coinfected when compared with wt mice measured by ALT levels (113±13 UI/L x 68±6.3 UI/L; wt x Mif ko, p<0.01). IL-10 plasma levels were lower in coinfected Mif ko compared to wt mice (2.77± 0.67 x 0.56±0.46 ng/ml, wt x Mif ko, p<0.05). Conclusion: Our findings indicate that co-infection regulates MIF-dependent responses at intestinal mucosa but also profoundly affect systemic IL10-dependent and independent protective responses.
subjects was analysed by flow cytometry of PBDC and DC released from fresh colonic biopsies by collagenase treatment. The effect of PRO on LepRb mRNA in monocyte derived DC (MoDC) was determined by RT-PCR and changes in DC migratory capacity were determined by transwell migration of DC towards the chemoattractant, CCL19. Results: Leptin treatment of DC from both colonic biopsies and from blood increased their expression of CCR7 in a concentration-dependent fashion (P<0.01). A significant increase in migration towards CCL19 was also induced. In contrast, PRO decreased the expression of CCR7 on blood and tissue DC after overnight exposure, (p<0.004 and p<0.007 respectively), and down-regulated leptin-induced CCR7 on colonic DC (p<0.04). LepRb mRNA expression in MoDC was also decreased after exposure to PRO. STp also decreased CCR7 expression (p<0.001) and down-regulated leptin-induced CCR7 on colonic DC (p<0.03). Conclusions: Leptin treatment increased migration of both colonic and blood DC towards CCL19 by upregulating CCR7. Probiotic bacteria or their products may have a beneficial anti-inflammatory effect by reducing leptin-induced migration of DC. Mo1758 The Role of the Gut Barrier Function in the Pathophysiology of Viral Liver Cirrhosis Woo Kyu Jeon, Yeowon Choi Background/Aims: Plasma endotoxin levels commonly increase in patients with liver cirrhosis. We purposed to identify change of intestinal permeability and frequency of endotoxemia in patients with viral liver cirrhosis. Additionally, we studied relationship between plasma endotoxin levels and failure of gut barrier function. Methods: Subjects included 27 patients with viral liver cirrhosis(LC) and 45 volunteers as healthy control(HC). Intestinal permeability index were determined by level of urinary excretion of polyethylene-glycol after oral administration and plasma endotoxin levels by using quantitative Limulus assay. Grades of liver dysfunction were categorized by Child-Pugh classification and MELD score. Results: Intestinal permeability indexes were higher in LC than in HC(1.48±0.56%, n=27 vs. 0.93±0.50%, n= 45, P=0.019). Plasma endotoxin levels were higher in LC than in HC(0.35±0.17EU/ml vs. 0.11±0.14EU/ml, P<0.001). In LC, plasma endotoxin levels progressively increased in relation to severity of liver dysfunction(Child-Pugh class A/B/C=0.31±0.17/0.37±0.14/0.42±0.23EU/ ml, P=0.013, MELD category 1/2/3/4=0.27±0.14/ 0.39±0.17/0.32±0.21/0.47±0.28EU/ml, P= 0.043). LC with/without portal hypertension (1.47±0.55%, P<0.01/1.29±0.59%, P<0.05) had higher intestinal permeability indexes than HC(0.93±0.50%). Conclusions: Severity of liver dysfunction was associated with endotoxemia. Although gut barrier function did not show a significant relationship with endotoxemia, increased intestinal permeability may be a significant finding that at least in part is associated with the pathophysiology of viral liver cirrhosis.
Mo1756 CD4+ T Cells Regulate the Multifactorial Gastrointestinal Inflammation Induced Following Colonization With Bacterial Provocateurs Amanda E. Ramer-Tait, Anne-Marie C. Overstreet, Jesse M. Hostetter, Albert Jergens, Michael J. Wannemuehler Aberrant mucosal immune responses to the resident microbiota are a significant cofactor in the pathogenesis of inflammatory bowel diseases (IBD). It is estimated that 1 to 1.5 million Americans suffer with IBD and its consequences, with total IBD-associated treatment costs in the United States exceeding $6.2 billion in 2008. An overarching question is: How much of IBD derives from genetics and how much from environmental factors such as the microbiota? Our laboratory has demonstrated that prior colonization of mice harboring only the highly simplified altered Schaedler flora (DM mice) with Helicobacter bilis increases host susceptibility to the onset of colitis following a subsequent inflammatory insult with a very low dose (1.5%) of the inflammatory trigger, dextran sulfate sodium (DSS). This dose of DSS alone is not sufficient to elicit colitis. In addition, prior colonization with non-pathogenic Escherichia coli SWW33 failed to affect disease severity. Our most intriguing finding is that both H. bilis- and E. coli-colonized mice treated with DSS upregulate mucosal expression of IL-17A mRNA. However, expression is higher in E. coli-colonized mice compared to H. biliscolonized mice at 3 weeks post-infection. This pattern reverses at 12 weeks post-infection and antigen-specific IL-17A protein production by CD4+ T cells follows a similar pattern. Although the induction of IL-17 was demonstrable in mice colonized with either provocateur, only mice colonized with H. bilis were found to be more susceptible to low-dose DSSinduced colitis. The objective of our present study was to understand how H. bilis and E. coli differentially induce pathogenic or beneficial mucosal immune responses to antigens arising from the resident microbiota. Specifically, we hypothesized that the dichotomous immune responses induced following colonization with these bacterial provocateurs would be reflected in the differential functional capacity of the antigen-specific CD4+ T cells. Following colonization with either H. bilis or E. coli for 3 weeks, DM mice were administered either a monoclonal antibody to deplete CD4+ T cells or an isotype control antibody. Mice then received an inflammatory insult in the form of 1.5% DSS. Unexpectedly, depletion of CD4+ T cells in H. bilis-colonized mice prior to the DSS treatment period exacerbated disease as evidenced by marked clinical signs of disease as well as severe colonic shortening, cecal atrophy, edema and luminal blood. Depletion of CD4+ T cells from E. coli-colonized mice caused only a minor increase in disease severity. Together, these findings indicate that colonization with distinct bacterial provocateurs alters the mucosal environment to promote either pathogenic or beneficial CD4+ T cell responses following a multifactorial inflammatory insult.
Mo1759 Pathology Associated With Okadaella Gastrococcus Infection Among the Younger Generation Takayuki Okada, Kazutoshi Hori, Graham F. Adkins, Hiroto Miwa Background: There is an increasing incidence of H. pylori-negative and NSAIDs-negative gastritis in many countries, and gastric cancer may be found among the younger generation. Recently, we have reported the intracellular presence of the Gram-negative coccoid bacterium Okadaella gastrococcus (Og; ATCC BAA-2258, NBRC 107862, GenBank HQ699465) in the classic cancer cascades. It is not known whether the younger generation who are H. pylorinegative and NSAIDs-negative suffer from Og infection, and related pathology. The investigation was aimed to see what types of pathology could be found among the Og-positive, H. pylori-negative and NSAIDs-negative dyspeptic younger generation. Methods: 30 H. pylori-negative and NSAIDs-negative Japanese patients (age: 18-29, male: female =15:15) with dyspeptic symptoms who were found to be Og-positive under electron microscopy, were subjected to investigation. No patients had previous H. pylori eradication treatments. All targeted biopsy specimens obtained at the time of esophago-gastro-duodenoscopy (EGD) were examined for culture, urease, histology (H&E, WSS, AYTB stains), and transmission electron microscopy. Some specimens were examined by scanning electron microscopy. Results: Culture was only successful for nine (30%) cases. Histological findings of the stomach (n=30) were active chronic gastritis 5 (16.6%), mild chronic gastritis 19 (63.3%), gastric congestion and edema 2 (6.6%), and unremarkable gastric mucosa 4 (13.3%). Intestinal metaplasia was found in four cases (13.3%). Focal small gastric erosions 18 (60%) and gastric hemorrhage with/without free gastric blood clots 15 (50%) were seen at the time of EGD. Histological findings of the gastroesophageal junction (GEJ, n=25) were severe 1 (4%), moderate 1 (4%) and mild inflammation of GEJ 23(92%). All patients with unremarkable gastric mucosa had mild inflammation of GEJ. Conclusions: Og was found to be associated with various H. pylori -negative and NSAIDs-negative gastritis and inflammation of GEJ among the younger generation with dyspeptic symptoms. Macroscopic and microscopic appearances of the stomach and GEJ were subtle with mild inflammation in the majority of cases, though intestinal metaplasia could be present. It is recommended to take biopsy specimens from the stomach and GEJ to examine for Og related pathology.
Mo1757 Probiotic Bacteria and Their Products Can Down-Regulate Leptin-Induced CCR7 Expression on Human DC Hafid O. Al-Hassi, David Bernardo Ordiz, Borja Sánchez, Elizabeth R. Mann, Aravinth U. Murugananthan, Cheng T. Tee, Nicholas R. English, Ailsa Hart, Alex I. Blakemore, Abelardo Margolles, Andrew J. Stagg, Stella C. Knight
Mo1760
Background: Dendritic cells (DC) migrate to lymph nodes on expression of CCR7, and control immune activity. CCR7 on blood DC increases in response to the pro-inflammatory adipokine, leptin. Increased mesenteric fat and leptin occur early in Crohn's disease (CD) and ongoing production of the signaling isoform of leptin receptor (LepRb) is significantly higher in colonic DC from CD tissue than in DC from normal colon. Moreover, leptin induces functional CCR7 on peripheral blood DC (PBDC) and colonic DC (Al-hassi et al., 2011) suggesting leptin-mediated change in intestinal CCR7 expression on DC as a proinflammatory mechanism. We assessed changes in migration of blood and colonic DC in response to leptin, and their modulation by anti-inflammatory probiotioc bactetria (PRO; a combination of B. longum and B.breve) and by a proteolysis-resistant ‘anti-inflammatory' peptide derived from gut lactobacilli (STp). Methods: Expression of CCR7 by health human
AGA Abstracts
High-Throughput 454 Pyrosequencing Analysis Reveals Dysbiosis of the Mucosa-Associated Microbiota in Dogs With Inflammatory Bowel Disease Jan Suchodolski, Scot E. Dowd, Joerg M. Steiner, Albert Jergens Background: Canine inflammatory bowel disease (IBD) is an immune-mediated enteropathy likely triggered by environmental and immunoregulatory factors in genetically susceptible dogs. The underlying mechanisms that initiate and drive intestinal inflammation are only partially understood but suggest a pivotal role for gut bacteria in disease pathogenesis, similar to human IBD. New molecular tools, such as 454-pyrosequencing, can be used for in-depth phylogenetic analysis of the intestinal microbiota to identify imbalances in microbial diversity and composition associated with chronic intestinal inflammation. Aim: To use a
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