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James G Fox - One of the best experts on this subject based on the ideXlab platform.
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effects of colonization of gnotobiotic swiss webster mice with Helicobacter Bilis
Comparative Medicine, 2020Co-Authors: Mark T Whary, Yan Feng, Catherine Ruff, Mallory J Divincenzo, C Labriola, Vasu Bakthavatchalu, Suresh Muthupalani, Bruce H Horwitz, Chuanwu Wang, James G FoxAbstract:Helicobacter Bilis (Hb) causes hepatitis in some strains of inbred mice. The current study confirmed that Hb directly causes portal hepatitis in outbred gnotobiotic Swiss Webster (SW) mice, as we previously reported for conventional SW mice. Hbmonoassociated SW mice also developed mild enterocolitis, expanded gut-associated lymphoid tissue (GALT), and tertiary lymphoid tissue in the lower bowel. At 1 and 10 mo after infection, Hb-induced GALT hyperplasia exhibited well-organized, ectopic germinal centers with increased mononuclear cell apoptosis, MHC class II antigen presentation, and pronounced endothelial venule formation, consistent with features of tertiary lymphoid tissue. In the lower bowel, Hb induced mainly B220+ cells as well as CD4+ IL17+, CD4+ IFNγ+, and CD4+ FoxP3+ regulatory T cells and significantly increased IL10 mRNA expression. This gnotobiotic model confirmed that Hb causes portal hepatitis in outbred SW mice but stimulated GALT with an antiinflammatory bias. Because Hb had both anti- and proinflammatory effects on GALT, it should be considered a 'pathosymbiont provocateur' and merits further evaluation in mouse models of human disease.
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male syrian hamsters experimentally infected with Helicobacter spp of the h Bilis cluster develop malt associated gastrointestinal lymphomas
PMC, 2016Co-Authors: Stephanie E Woods, Zeli Shen, Mark T Whary, Yan Feng, Sureshkumar Muthupalani, James G FoxAbstract:BACKGROUND Aged hamsters naturally infected with novel Helicobacter spp. classified in the H. Bilis cluster develop hepatobiliary lesions and typhlocolitis. METHODS To determine whether enterohepatic H. spp. contribute to disease, Helicobacter-free hamsters were experimentally infected with H. spp. after suppression of intestinal bacteria by tetracycline treatment of dams and pups. After antibiotic withdrawal, weanlings were gavaged with four H. Bilis-like Helicobacter spp. isolated from hamsters or H. Bilis ATCC 43879 isolated from human feces and compared to controls (n = 7 per group). RESULTS Helicobacter Bilis 43879-dosed hamsters were necropsied at 33 weeks postinfection (WPI) due to the lack of detectable infection by fecal PCR; at necropsy, 5 of 7 were weakly PCR positive but lacked intestinal lesions. The remaining hamsters were maintained for ~95 WPI; chronic H. spp. infection in hamsters (6/7) was confirmed by PCR, bacterial culture, fluorescent in situ hybridization, and ELISA. Hamsters had mild-to-moderate typhlitis, and three of the male H. spp.-infected hamsters developed small intestinal lymphoma, in contrast to one control. Of the three lymphomas in H. spp.-infected hamsters, one was a focal ileal mucosa-associated lymphoid tissue (MALT) B-cell lymphoma, while the other two were multicentric small intestinal large B-cell lymphomas involving both the MALT and extra-MALT mucosal sites with lymphoepithelial lesions. The lymphoma in the control hamster was a diffuse small intestinal lymphoma with a mixed population of T and B cells. CONCLUSIONS Results suggest persistent H. spp. infection may augment risk for gastrointestinal MALT origin lymphomas. This model is consistent with H. pylori/heilmannii-associated MALT lymphoma in humans and could be further utilized to investigate the mechanisms of intestinal lymphoma development.
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infection with Helicobacter Bilis but not Helicobacter hepaticus was associated with extrahepatic cholangiocarcinoma
Helicobacter, 2015Co-Authors: Fany Karina Seguralopez, James G Fox, Francisco Avilesjimenez, Alfredo Guitroncantu, Hilda A Valdezsalazar, Samuel Leoncarballo, Leoncio Guerreroperez, Javier TorresAbstract:Background and Aims: The biliary tract cancer or cholangiocarcinoma (CCA) represents the sixth leading cause of gastrointestinal tumors in the Western world, and mortality varies across the world, with regions such as Chile, Thailand, Japan, and northeastern India presenting the highest rates. CCA may develop in the bile duct, gallbladder, or ampulla of Vater; and risk factors include obesity, parity, genetic background, geographical and environmental factors. Inflammation induced by bacterial infections might play a role in the pathogenesis of CCA. In this work, we investigated whether there is an association between extrahepatic cholangiocarcinoma (ECCA) and infection with S. typhi, H. hepaticus, or H. Bilis in a Mexican population. Methods: A total of 194 patients were included and divided into 91 patients with benign biliary pathology (controls) and 103 with ECCA (cases). Tumor samples were taken during endoscopic retrograde cholangiopancreatography by biliary brushing, followed by DNA extraction and PCR testing for infections. Results: We found that 44/103 cases were positive for H. Bilis, compared with 19/91 controls (p = 0.002; OR 2.83, 95% CI 1.49–5.32), and when analyzed by sub-site, H. Bilis infection was significantly more associated with cancer in the common bile duct (p = 0.0005; OR 3.56, 95% CI 1.77–7.17). In contrast, H. hepaticus infection was not different between cases (17/103) and controls (13/91) (p = 0.82; OR 1.19, 95% CI 0.54–2.60). None of the samples were positive for S. typhi infection. Conclusion: In conclusion, infection with H. Bilis but neither H. Hepaticus nor S. typhi was significantly associated with ECCA, particularly with tumors located in the common bile duct.
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systemic macrophage depletion inhibits Helicobacter Bilis induced proinflammatory cytokine mediated typhlocolitis and impairs bacterial colonization dynamics in a balb c rag2 mouse model of inflammatory bowel disease
Infection and Immunity, 2012Co-Authors: Sureshkumar Muthupalani, Yan Feng, Barry H Rickman, Melissa W Mobley, Amanda Mccabe, Nico Van Rooijen, James G FoxAbstract:Helicobacter Bilis, an enterohepatic Helicobacter, is associated with chronic hepatitis in aged immunocompetent inbred mice and inflammatory bowel disease (IBD) in immunodeficient mice. To evaluate the role of macrophages in H. Bilis-induced IBD, Rag2−/− BALB/c or wild-type (WT) BALB/c mice were either sham dosed or infected with H. Bilis Missouri strain under specific-pathogen-free conditions, followed by an intravenous injection of a 0.2-ml suspension of liposomes coated with either phosphate-buffered saline (control) or clodronate (a macrophage depleting drug) at 15 weeks postinfection (wpi). At 16 wpi, the ceca of H. Bilis-infected Rag2−/− mice treated with control liposomes had significantly higher histopathological lesional scores (for cumulative typhlitis index, inflammation, edema, epithelial defects, and hyperplasia) and higher counts of F4/80+ macrophages and MPO+ neutrophils compared to H. Bilis-infected Rag2−/− mice treated with clodronate liposomes. In addition, cecal quantitative PCR analyses revealed a significant suppression in the expression of macrophage-related cytokine genes, namely, Tnfa, Il-1β, Il-10, Cxcl1, and iNos, in the clodronate-treated H. Bilis-infected Rag2−/− mice compared to the H. Bilis-infected Rag2−/− control mice. Finally, cecal quantitative PCR analyses also revealed a significant reduction in bacterial colonization in the clodronate-treated Rag2−/− mice. Taken together, our results suggest that macrophages are critical inflammatory cellular mediators for promoting H. Bilis-induced typhlocolitis in mice.
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cross reactivity between immune responses to Helicobacter Bilis and Helicobacter pylori in a population in thailand at high risk of developing cholangiocarcinoma
Clinical and Vaccine Immunology, 2008Co-Authors: Paola Pisani, Mark T Whary, Åsa Ljungh, James G Fox, Torkel Wadström, Ingrid Nilsson, Supannee Sriamporn, David FormanAbstract:Helicobacter Bilis DNA has been detected in human tissue and is a candidate for etiologic investigations on the causes of hepatic and biliary tract diseases, but reliable serologic tests need to be developed in order to pursue such investigations. The scope of this study was to assess the specificity of two assays for H. Bilis immune response allowing for H. pylori, and their cross-reactivity in a population in Thailand at high risk for cholangiocarcinoma. Plasma samples from 92 Thai volunteers were independently tested in two laboratories (Massachusetts Institute of Technology [MIT] and Lund). MIT performed three analyses of H. pylori and H. Bilis based either on (i) outer membrane protein (OMP) with no preabsorption or on antigens derived from whole-cell sonicate before (ii) or after (iii) preabsorption with H. pylori sonicate protein. Lund used cell surface proteins from H. pylori and H. Bilis as antigens. Testing for H. Bilis was preabsorbed with a whole-cell lysate of H. pylori. More than 80% of the samples were positive for H. pylori in both laboratories. As tested by MIT, 58.7% (95% confidence interval, 47.9 to 68.9%) were positive for H. Bilis by OMP and 44.5% (34.1 to 55.3%) were positive for H. Bilis sonicate protein, but only 15.2% (8.6 to 24.2%) remained positive after preabsorption with H. pylori sonicate protein. Lund found 34.5% of the samples positive for H. Bilis (22.0 to 41.0%), which was statistically compatible with all three MIT results. Serologic responses to OMPs of the two bacteria coincided in 66 and 45% of the samples in the MIT and Lund assays, respectively. We found high cross-reactivity between the immune responses to H. pylori and H. Bilis antigens. More-specific H. Bilis antigens need to be isolated to develop serologic tests suitable for epidemiological studies.
Michael J Wannemuehler - One of the best experts on this subject based on the ideXlab platform.
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Helicobacter Bilis Infection Alters Mucosal Bacteria and Modulates Colitis Development in Defined Microbiota Mice
Inflammatory Bowel Diseases, 2016Co-Authors: Todd Atherly, Meghan Wymore Brand, Alexandra Proctor, Curtis Mosher, Jesse M Hostetter, Michael J Wannemuehler, Gregory J Phillips, Chong Wang, Albert E JergensAbstract:Background:Helicobacter Bilis infection of C3H/HeN mice harboring the altered Schaedler flora (ASF) triggers progressive immune responsiveness and the development of colitis. We sought to investigate temporal alterations in community structure of a defined (ASF-colonized) microbiota in normal and in
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Helicobacter Bilis colonization enhances susceptibility to typhlocolitis following an inflammatory trigger
Digestive Diseases and Sciences, 2011Co-Authors: Zhiping Liu, Abigail Henderson, Jesse M Hostetter, Albert E Jergens, Chong Wang, Amanda E Ramertait, Cumhur Yusuf Demirkale, Dan Nettleton, Michael J WannemuehlerAbstract:Aberrant mucosal immune responses to antigens of the resident microbiota are a significant cause of inflammatory bowel diseases (IBD), as are genetic and environmental factors. Previous work from our laboratory demonstrated that Helicobacter Bilis colonization of immunocompetent, defined microbiota mice induced antigen-specific immune responses to the resident microbiota, yet these mice failed to develop colitis, suggesting that the immunological provocation induced by H. Bilis alone was insufficient to induce disease. The purpose of this study was to test the hypothesis that the introduction of a bacterial provocateur such as H. Bilis enhances the host’s susceptibility to IBD following an inflammatory event. Defined microbiota (DM) mice colonized with H. Bilis were administered low dose (1.5%) dextran sodium sulfate (DSS) in drinking water for 5 days followed by a 4-day restitution period. Severity of lesions was assessed grossly and microscopically. Differential expression of select mucosal genes and histopathologic lesions was characterized. Helicobacter Bilis colonization increased the severity of intestinal inflammation induced by an inflammatory trigger in the form of low-dose DSS. An analysis of the molecular and cellular mechanisms associated with H. Bilis colonization revealed significant increases in expression of mucosal genes associated with lymphocyte activation and inflammatory cell chemotaxis as well as increased infiltration of mucosal macrophages and T cells in mice colonized with H. Bilis prior to DSS treatment versus DSS treatment alone. These results indicate that prior colonization with H. Bilis heightens the host’s sensitivity to enteric inflammation by altering mucosal homeostasis and initiating immune cell activation and migration.
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mucosal gene expression profiles following the colonization of immunocompetent defined flora c3h mice with Helicobacter Bilis a prelude to typhlocolitis
Microbes and Infection, 2009Co-Authors: Zhiping Liu, Abigail Henderson, Jesse M Hostetter, Albert E Jergens, Amanda E Ramertait, Dan Nettleton, Jennifer H Wilsonwelder, Michael J WannemuehlerAbstract:An aberrant immune response to the commensal microbiota is widely hypothesized to contribute to the development of inflammatory bowel disease. Helicobacter Bilis colonization of defined-flora mice has been shown to trigger host immune responses to the commensal flora. However, the magnitude of the effects on mucosal homeostasis following colonization with H. Bilis has not been determined. Using microarray analysis, differential gene expression within the cecal mucosa was assessed at 15, 30, or 45 days following H. Bilis colonization using Affymetrix Genechips. H. Bilis colonization induced marked upregulation of genes associated with protein metabolism, immune responses, and downregulation of genes associated with fatty acid metabolism and detoxification which peaked at 15 days postinfection. A set of genes associated with glycoprotein synthesis and detoxification including Fut2, B3galt5, Ceacam12, Cyp4b1, and Ugt8a were uniquely identified and found to be similarly expressed following the induction of typhlocolitis by dextran sodium sulfate or Brachyspira hyodysenteriae. This study provides preliminary evidence as to the types of factors or changes in the intestinal mucosa that potentially predispose the host to the development of typhlocolitis.
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Helicobacter Bilis triggers persistent immune reactivity to antigens derived from the commensal bacteria in gnotobiotic c3h hen mice
Gut, 2007Co-Authors: Albert E Jergens, Andrea Dorn, Abigail Henderson, Jesse M Hostetter, Richard B Evans, Zhiping Liu, Jennifer H Wilsonwelder, Michael J WannemuehlerAbstract:Background: Infection with Helicobacter species has been associated with the development of mucosal inflammation and inflammatory bowel disease (IBD) in several mouse models. However, consensus regarding the role of Helicobacter as a model organism to study microbial-induced IBD is confounded by the presence of a complex colonic microbiota. Aim: To investigate the kinetics and inflammatory effects of immune system activation to commensal bacteria following H Bilis colonisation in gnotobiotic mice. Methods: C3H/HeN mice harbouring an altered Schaedler flora (ASF) were selectively colonised with H Bilis and host responses were investigated over a 10-week period. Control mice were colonised only with the defined flora (DF). Tissues were analysed for gross/histopathological lesions, and bacterial antigen-specific antibody and T-cell responses. Results: Gnotobiotic mice colonised with H Bilis developed mild macroscopic and microscopic lesions of typhlocolitis beginning 3 weeks postinfection. ASF-specific IgG responses were demonstrable within 3 weeks, persisted throughout the 10-week study, and presented as a mixed IgG1:IgG2a profile. Lymphocytes recovered from the mesenteric lymph node of H Bilis -colonised mice produced increased levels of interferon γ, tumour necrosis factor α (TNFα), interleukin 6 (IL6) and IL12 in response to stimulation with commensal- or H Bilis -specific bacterial lysates. In contrast, DF mice not colonised with H Bilis did not develop immune responses to their resident flora and remained disease free. Conclusions: Colonisation of gnotobiotic C3H/HeN mice with H Bilis perturbs the host’s response to its resident flora and induces progressive immune reactivity to commensal bacteria that contributes to the development of immune-mediated intestinal inflammation.
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Induction of differential immune reactivity to members of the flora of gnotobiotic mice following colonization with Helicobacter Bilis or Brachyspira hyodysenteriae
Microbes and Infection, 2006Co-Authors: Albert E Jergens, Andrea Dorn, Krystal Dingbaum, Abigail Henderson, Jesse M Hostetter, Richard B Evans, Jenny Wilson, Michael J WannemuehlerAbstract:Abstract Aberrant host immune responses to bacterial components of the resident microflora may initiate and perpetuate gastrointestinal inflammation. To investigate how microbial perturbation promotes host immunological responsiveness to commensal bacteria and contributes to the development of typhlocolitis, we selectively colonized defined (altered Schaedler) flora C3H mice with either Helicobacter Bilis or Brachyspira hyodysenteriae. Following selective colonization, tissues were analyzed for gross/histopathologic lesions and bacterial antigen-specific B- and T-cell responses. Gnotobiotic mice colonized with H. Bilis or B. hyodysenteriae developed typhlocolitis of varying severity, with the most severe gross and histopathogical lesions observed in B. hyodysenteriae-colonized mice. Antigen-specific IgG1 and IgG2a responses to the resident microflora were increased in both H. Bilis-and B. hyodysenteriae-colonized mice. The greater antibody responses were associated with less severe cecal inflammation in H. Bilis-colonized mice. Altered Schaedler flora (ASF)-stimulated mesenteric lymphocytes from B. hyodysenteriae-colonized mice produced higher levels of interferon-γ and interleukin (IL)-4 than did lymphocytes from H. Bilis-colonized mice. However, ASF-stimulated mesenteric and splenic lymphocytes from both H. Bilis and B. hyodysenteriae-colonized mice secreted higher amounts of IL-10 compared to similarly stimulated lymphocytes recovered from control mice. These results indicate that microbial perturbation may induce differential immune responses to nonpathogenic resident bacteria that can lead to intestinal inflammation.
Albert E Jergens - One of the best experts on this subject based on the ideXlab platform.
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Helicobacter Bilis Infection Alters Mucosal Bacteria and Modulates Colitis Development in Defined Microbiota Mice
Inflammatory Bowel Diseases, 2016Co-Authors: Todd Atherly, Meghan Wymore Brand, Alexandra Proctor, Curtis Mosher, Jesse M Hostetter, Michael J Wannemuehler, Gregory J Phillips, Chong Wang, Albert E JergensAbstract:Background:Helicobacter Bilis infection of C3H/HeN mice harboring the altered Schaedler flora (ASF) triggers progressive immune responsiveness and the development of colitis. We sought to investigate temporal alterations in community structure of a defined (ASF-colonized) microbiota in normal and in
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Helicobacter Bilis colonization enhances susceptibility to typhlocolitis following an inflammatory trigger
Digestive Diseases and Sciences, 2011Co-Authors: Zhiping Liu, Abigail Henderson, Jesse M Hostetter, Albert E Jergens, Chong Wang, Amanda E Ramertait, Cumhur Yusuf Demirkale, Dan Nettleton, Michael J WannemuehlerAbstract:Aberrant mucosal immune responses to antigens of the resident microbiota are a significant cause of inflammatory bowel diseases (IBD), as are genetic and environmental factors. Previous work from our laboratory demonstrated that Helicobacter Bilis colonization of immunocompetent, defined microbiota mice induced antigen-specific immune responses to the resident microbiota, yet these mice failed to develop colitis, suggesting that the immunological provocation induced by H. Bilis alone was insufficient to induce disease. The purpose of this study was to test the hypothesis that the introduction of a bacterial provocateur such as H. Bilis enhances the host’s susceptibility to IBD following an inflammatory event. Defined microbiota (DM) mice colonized with H. Bilis were administered low dose (1.5%) dextran sodium sulfate (DSS) in drinking water for 5 days followed by a 4-day restitution period. Severity of lesions was assessed grossly and microscopically. Differential expression of select mucosal genes and histopathologic lesions was characterized. Helicobacter Bilis colonization increased the severity of intestinal inflammation induced by an inflammatory trigger in the form of low-dose DSS. An analysis of the molecular and cellular mechanisms associated with H. Bilis colonization revealed significant increases in expression of mucosal genes associated with lymphocyte activation and inflammatory cell chemotaxis as well as increased infiltration of mucosal macrophages and T cells in mice colonized with H. Bilis prior to DSS treatment versus DSS treatment alone. These results indicate that prior colonization with H. Bilis heightens the host’s sensitivity to enteric inflammation by altering mucosal homeostasis and initiating immune cell activation and migration.
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mucosal gene expression profiles following the colonization of immunocompetent defined flora c3h mice with Helicobacter Bilis a prelude to typhlocolitis
Microbes and Infection, 2009Co-Authors: Zhiping Liu, Abigail Henderson, Jesse M Hostetter, Albert E Jergens, Amanda E Ramertait, Dan Nettleton, Jennifer H Wilsonwelder, Michael J WannemuehlerAbstract:An aberrant immune response to the commensal microbiota is widely hypothesized to contribute to the development of inflammatory bowel disease. Helicobacter Bilis colonization of defined-flora mice has been shown to trigger host immune responses to the commensal flora. However, the magnitude of the effects on mucosal homeostasis following colonization with H. Bilis has not been determined. Using microarray analysis, differential gene expression within the cecal mucosa was assessed at 15, 30, or 45 days following H. Bilis colonization using Affymetrix Genechips. H. Bilis colonization induced marked upregulation of genes associated with protein metabolism, immune responses, and downregulation of genes associated with fatty acid metabolism and detoxification which peaked at 15 days postinfection. A set of genes associated with glycoprotein synthesis and detoxification including Fut2, B3galt5, Ceacam12, Cyp4b1, and Ugt8a were uniquely identified and found to be similarly expressed following the induction of typhlocolitis by dextran sodium sulfate or Brachyspira hyodysenteriae. This study provides preliminary evidence as to the types of factors or changes in the intestinal mucosa that potentially predispose the host to the development of typhlocolitis.
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Helicobacter Bilis triggers persistent immune reactivity to antigens derived from the commensal bacteria in gnotobiotic c3h hen mice
Gut, 2007Co-Authors: Albert E Jergens, Andrea Dorn, Abigail Henderson, Jesse M Hostetter, Richard B Evans, Zhiping Liu, Jennifer H Wilsonwelder, Michael J WannemuehlerAbstract:Background: Infection with Helicobacter species has been associated with the development of mucosal inflammation and inflammatory bowel disease (IBD) in several mouse models. However, consensus regarding the role of Helicobacter as a model organism to study microbial-induced IBD is confounded by the presence of a complex colonic microbiota. Aim: To investigate the kinetics and inflammatory effects of immune system activation to commensal bacteria following H Bilis colonisation in gnotobiotic mice. Methods: C3H/HeN mice harbouring an altered Schaedler flora (ASF) were selectively colonised with H Bilis and host responses were investigated over a 10-week period. Control mice were colonised only with the defined flora (DF). Tissues were analysed for gross/histopathological lesions, and bacterial antigen-specific antibody and T-cell responses. Results: Gnotobiotic mice colonised with H Bilis developed mild macroscopic and microscopic lesions of typhlocolitis beginning 3 weeks postinfection. ASF-specific IgG responses were demonstrable within 3 weeks, persisted throughout the 10-week study, and presented as a mixed IgG1:IgG2a profile. Lymphocytes recovered from the mesenteric lymph node of H Bilis -colonised mice produced increased levels of interferon γ, tumour necrosis factor α (TNFα), interleukin 6 (IL6) and IL12 in response to stimulation with commensal- or H Bilis -specific bacterial lysates. In contrast, DF mice not colonised with H Bilis did not develop immune responses to their resident flora and remained disease free. Conclusions: Colonisation of gnotobiotic C3H/HeN mice with H Bilis perturbs the host’s response to its resident flora and induces progressive immune reactivity to commensal bacteria that contributes to the development of immune-mediated intestinal inflammation.
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Induction of differential immune reactivity to members of the flora of gnotobiotic mice following colonization with Helicobacter Bilis or Brachyspira hyodysenteriae
Microbes and Infection, 2006Co-Authors: Albert E Jergens, Andrea Dorn, Krystal Dingbaum, Abigail Henderson, Jesse M Hostetter, Richard B Evans, Jenny Wilson, Michael J WannemuehlerAbstract:Abstract Aberrant host immune responses to bacterial components of the resident microflora may initiate and perpetuate gastrointestinal inflammation. To investigate how microbial perturbation promotes host immunological responsiveness to commensal bacteria and contributes to the development of typhlocolitis, we selectively colonized defined (altered Schaedler) flora C3H mice with either Helicobacter Bilis or Brachyspira hyodysenteriae. Following selective colonization, tissues were analyzed for gross/histopathologic lesions and bacterial antigen-specific B- and T-cell responses. Gnotobiotic mice colonized with H. Bilis or B. hyodysenteriae developed typhlocolitis of varying severity, with the most severe gross and histopathogical lesions observed in B. hyodysenteriae-colonized mice. Antigen-specific IgG1 and IgG2a responses to the resident microflora were increased in both H. Bilis-and B. hyodysenteriae-colonized mice. The greater antibody responses were associated with less severe cecal inflammation in H. Bilis-colonized mice. Altered Schaedler flora (ASF)-stimulated mesenteric lymphocytes from B. hyodysenteriae-colonized mice produced higher levels of interferon-γ and interleukin (IL)-4 than did lymphocytes from H. Bilis-colonized mice. However, ASF-stimulated mesenteric and splenic lymphocytes from both H. Bilis and B. hyodysenteriae-colonized mice secreted higher amounts of IL-10 compared to similarly stimulated lymphocytes recovered from control mice. These results indicate that microbial perturbation may induce differential immune responses to nonpathogenic resident bacteria that can lead to intestinal inflammation.
Carlo La Vecchia - One of the best experts on this subject based on the ideXlab platform.
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gallbladder cancer worldwide geographical distribution and risk factors
International Journal of Cancer, 2006Co-Authors: Giorgia Randi, Silvia Franceschi, Carlo La VecchiaAbstract:Gallbladder cancer is a relatively rare neoplasm that shows, however, high incidence rates in certain world populations. The interplay of genetic susceptibility, lifestyle factors and infections in gallbladder carcinogenesis is still poorly understood. Age-adjusted rates were calculated by cancer registry-based data. Epidemiological studies on gallbladder cancer were selected through searches of literature, and relative risks were abstracted for major risk factors. The highest gallbladder cancer incidence rates worldwide were reported for women in Delhi, India (21.5/100,000), South Karachi, Pakistan (13.8/100,000) and Quito, Ecuador (12.9/100,000). High incidence was found in Korea and Japan and some central and eastern European countries. Female-to-male incidence ratios were generally around 3, but ranged from 1 in Far East Asia to over 5 in Spain and Colombia. History of gallstones was the strongest risk factor for gallbladder cancer, with a pooled relative risk (RR) of 4.9 [95% confidence interval (CI): 3.3-7.4]. Consistent associations were also present with obesity, multiparity and chronic infections like Salmonella typhi and S. paratyphi [pooled RR 4.8 (95% CI: 1.4-17.3)] and Helicobacter Bilis and H. pylori [pooled RR 4.3 (95% CI: 2.1-8.8)]. Differences in incidence ratios point to variations in gallbladder cancer aetiology in different populations. Diagnosis of gallstones and removal of gallbladder currently represent the keystone to gallbladder cancer prevention, but interventions able to prevent obesity, cholecystitis and gallstone formation should be assessed.
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Gallbladder cancer worldwide : Geographical distribution and risk factors
'Wiley', 2006Co-Authors: Giorgia Randi, Silvia Franceschi, Carlo La VecchiaAbstract:Gallbladder cancer is a relatively rare neoplasm that shows, however, high incidence rates in certain world populations. The interplay of genetic susceptibility, lifestyle factors and infections in gallbladder carcinogenesis is still poorly understood. Age-adjusted rates were calculated by cancer registry-based data. Epidemiological studies on gallbladder cancer were selected through searches of literature, and relative risks were abstracted for major risk factors. The highest gallbladder. cancer incidence rates worldwide were reported for women in Delhi, India (21.5/100,000), South Karachi, Pakistan (13.8/100,000) and Quito, Ecuador (12.9/100,000). High incidence was found in Korea and Japan and some central and eastern European countries. Female-to-male incidence ratios were generally around 3, but ranged from I in Far East Asia to over 5 in Spain and Colombia. History of gallstones was the strongest risk factor for gallbladder cancer, with a pooled relative risk (RR) of 4.9 [95% confidence interval (Cl): 3.3-7.4]. Consistent associations were also present with obesity, multiparity and chronic infections like Salmonella typhi and S. paratyphi [pooled RR 4.8 (95% CI: 1.4-17.3)] and Helicobacter Bilis and H. pylori [pooled RR 4.3 (95% CI: 2.1-8.8)]. Differences in incidence ratios point to variations in gallbladder cancer aetiology in different populations. Diagnosis of gallstones and removal of gallbladder currently represent the keystone to gallbladder cancer prevention, but interventions able to prevent obesity, cholecystitis and gallstone formation should be assessed. (c) 2005 Wiley-Liss, Inc
Joanne L Viney - One of the best experts on this subject based on the ideXlab platform.
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dual infection with Helicobacter Bilis and Helicobacter hepaticus in p glycoprotein deficient mdr1a mice results in colitis that progresses to dysplasia
American Journal of Pathology, 2005Co-Authors: Lillian Maggioprice, Piper M Treuting, Donna Shows, Weiping Zeng, Phil Morrissey, Helle Bielefeldtohmann, Brian M Iritani, Andrea Nicks, Mark Tsang, Joanne L VineyAbstract:Patients with inflammatory bowel disease (IBD) are at increased risk for developing high-grade dysplasia and colorectal cancer. Animal IBD models that develop dysplasia and neoplasia may help elucidate the link between inflammation and colorectal cancer. Mdr1a−/− mice lack the membrane efflux pump p-glycoprotein and spontaneously develop IBD that can be modulated by infection with Helicobacter sp: H. Bilis accelerates development of colitis while H. hepaticus delays disease. In this study, we determined if H. hepaticus infection could prevent H. Bilis-induced colitis. Unexpectedly, a proportion of dual-infected mdr1a−/− mice showed IBD with foci of low- to high-grade dysplasia. A group of dual-infected mdr1a−/− animals were maintained long term (39 weeks) by intermittent feeding of medicated wafers to model chronic and relapsing disease. These mice showed a higher frequency of high-grade crypt dysplasia, including invasive adenocarcinoma, possibly because H. hepaticus, in delaying the development of colitis, allows time for transformation of epithelial cells. Colonic epithelial preparations from co-infected mice showed increased expression of c-myc (5- to 12-fold) and interleukin-1α/β (600-fold) by real-time polymerase chain reaction relative to uninfected wild-type and mdr1a−/− animals. This animal model may have particular relevance to human IBD and colorectal cancer because certain human MDR1 polymorphisms have been linked to ulcerative colitis and increasedrisk for colorectal cancer.
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Helicobacter Bilis infection accelerates and h hepaticus infection delays the development of colitis in multiple drug resistance deficient mdr1a mice
American Journal of Pathology, 2002Co-Authors: Lillian Maggioprice, Donna Shows, Kim Waggie, Andrew Burich, Weiping Zeng, Sabine S Escobar, Phil Morrissey, Joanne L VineyAbstract:mdr1a-deficient mice lack P-glycoprotein and spontaneously develop colitis with age. Helicobacter spp. are gram-negative organisms that have been associated with colitis in certain mouse strains, but Helicobacter spp. have been excluded as contributing to the spontaneous colitis that develops in mdr1a−/− mice. We wished to determine whether infection with either H. Bilis or H. hepaticus would accelerate the development of inflammatory bowel disease (IBD) in mdr1a−/− mice. We found that H. Bilis infection induced diarrhea, weight loss, and IBD in mdr1a−/− mice within 6 to 17 weeks post-inoculation and before the expected onset of spontaneous IBD. Histopathology of H. Bilis-induced IBD included crypt hyperplasia, inflammatory cell infiltrates, crypt abscesses, and obliteration of normal gut architecture. Reverse transcription-polymerase chain reaction and Taqman analysis from colonic tissue showed increased transcripts for interferon-γ and interleukin-10 from H. Bilis-infected colitic mdr1a−/− mice. Additionally, mesenteric lymph nodes had increased cellularity with expansion of CD4+ and CD8+ T cells and B cells and increased proliferation to soluble H. Bilis antigens with elaboration of interferon-γ, tumor necrosis factor-α and interleukin-10. In contrast, H. hepaticus infection of mdr1a−/− mice did not accelerate disease but rather delayed the onset of spontaneous colitis which was milder in severity. mdr1a−/− mice infected with Helicobacter spp. may provide a useful tool to explore the pathogenesis of microbial-induced IBD in a model with a presumed epithelial cell “barrier” defect.