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S1696 TL1A Expression Is Induced During Dendritic Cell Differentiation
S1696
the prevalence of ASCA and anti-I2 were similar in CD patients (30%, 38% respectively), only anti-I2 positive CD patients had high frequency of IgG antibodies to food antigens. CD patients with anal fistulas, extraintestinal manifestations, high serum CRP levels, high platelet or white blood cell numbers in blood had significantly higher frequency of IgG antibodies to food antigens. Gender, location or behavior of CD lesion, history of medical and surgical treatment was not related to the frequency of IgG antibodies against food. DISCUSSION: CD patients have high immunoreactivity to many kinds of food antigens, especially in patients with severe clinical features (anal fistulas, extraintestinal manifestations or high serum CRP levels). Combined with our recent results using murine IL-10 KO colitis model, in which elimination of food antigens from standard diet exhibited marked suppression of colitis (Mori et al., DDW abstract, 2009), food antigens could play an aggravating role in the inflammatory response in CD patients and the control of food intake might regulate disease activity.
AGA Abstracts
TL1A Expression Is Induced During Dendritic Cell Differentiation Rivkah Gonsky, Richard L. Deem, Stephan R. Targan IFN-γ plays an important role in the generation and perpetuation of mucosal inflammation in IBD. TL1A, a TNF superfamily member, synergizes with IL-12 and IL-18 to augment IFN-γ production in human T cells. Enhanced TL1A expression is detected in IBD with a strong TL1A SNP association reported in Crohn's disease. We have previously shown TL1A expression is induced in peripheral monocytes and in-vitro derived dendritic cells (DC). The molecular mechanisms regulating TL1A expression during DC differentiation however, remain poorly defined. The human monocytic cell line, KG-1, provides a valuable model for dendritic cell differentiation. The round non-adherent KG1 cells develop a DC-like phenotype following activation by PMA/ionomycin. These cells become loosely adherent with long cytoplasmic projections. A concomitant induction of membrane TL1A and mRNA is observed with mRNA expression being detectable within 2 hours and peaking at 8 hours following stimulation. A strikingly similar kinetics of TL1A expression was likewise noted following PMA/ionomycin stimulation of peripheral monocytes. Further DC maturation of KG-1 cells following treatment with LPS results in additional enhancement of TL1A expression. Transient transfection of KG-1 with TL1A promoter-constructs up to 1.5 kb in length reveals up to 90-fold enhanced expression compared to cells transfected with the promoterless vector. EMSA analysis demonstrates PMA/ionomycin mediated upregulation of nucleo-protein binding to a putative TL1A NFκB binding site. Binding is competed by excess unlabeled wt TL1A NFκB, but not mutant oligonucleotide and is likewise attenuated following proteasomal inhibition by MG132. Our data suggests in the human monocytic KG-1 cell line, differentiation of immature cells towards a mature DC phenotype is associated with functional upregulation of surface TL1A expression and binding of NFκB to the TL1A promoter. These studies provide a molecular basis for future studies which may help elucidate the mechanism modulating TL1A expression during DC maturation.
S1699 Genetic and Experimental Murine Models of Inflammatory Bowel Disease Are Characterized By Novel Distinct Immune Profiles Philip Alex, Thuan Nguyen, Maxim Suhodrev-Saksonov, Igor Dozmorov, Fong-Fong Chu, Michael Centola, Xuhang Li Early effective treatment of IBD requires sensitive diagnostic tools and accurate means to evaluate disease activity. We performed comprehensive cytokine profiling in experimental and genetic models of murine IBD and have identified distinct patterns that can distinguish UC-like from CD-like colitis, indeterminate from IBD-like colitis, and severe from selflimited disease. Six models were established: [i,ii] acute and chronic DSS-induced, [iii,iv] acute and chronic TNBS-induced, [v] IL-10 knockout (KO), and [vi] mice with the combined disruption of Gpx1 and Gpx2 genes (Gpx DKO). Serum, intestinal tissues and mucosal scrapings were obtained from a total of 201 mice (12-17 mice/group; 6-9 wks). Disease activity index (DAI), MPO, and histological activity index (HAI) were obtained. A novel approach of serum multiplex cytokine profiling utilizing robotic ultra-sensitive, highlyreproducible biometric immunosandwich ELISA's was used to assess the modulation of 16 cytotoxic and humoral cytokines and chemokines. SDS-PAGE, Western blots, and immunofluorescent studies were performed on colonic tissue and mucosa. Novel distinctive systemic cytokine patterns were readily identified with significant correlations to disease activity and duration of disease (p<0.01). As the disease becomes chronic, TNBS colitis exhibited heightened Th1-Th17 response (IL-12 and IL-17), and DSS colitis switched from Th1-Th17 (TNF-a, IL-6, IL-17, and KC) to a predominant Th2 profile (IL-4 and IL-10). IL-10 KO mice had a distinct Th1-chemotactic profile (IL-2, TNF-a, IL-12 and MIP), while the Gpx DKO model had a Th2-Th17 profile (IL-17, IL-5, and IL-10). When DAI, HAI and MPO were compared to cytokine profiles, partial correlational analysis identified distinct UC-like & CD-like subsets with significant correlations (r > 0.8) to disease severity. These data also showed that the GPX DKO model was a potential reproducible model of indeterminate colitis (comparable to patients). Multivariate analyses identified 8 significant variables (Wilk's λ: 0.031-0.149), which on a 3D plot mapped groups into distinct positions that were able to discriminate UC-like (DSS) from CD-like colitis (TNBS, IL-10 KO), and indeterminate (GPX DKO) from IBD-like colitis (DSS, TNBS, and IL-10 KO). Intestinal immunoblot and immunofluorescence studies validated and provided further insight into these distinct cytokine patterns. Our studies have identified (i) novel distinct systemic cytokine profiles as a means to effectively differentiate and subclassify IBD-like colitis, (ii) as practical indicators to monitor disease severity, and (iii) has given us important insight into the immunopathogenesis of IBD.
S1697 Human Neutrophil Peptide-1 Has Cytotoxic Effects On Colon Cancer Cells and Aggravates Dextran Sulfate Sodium-Induced Colitis Shinichi Hashimoto, Hirofumi Uto, Shuji Kanmura, Yuko Nakamura, Manei Oku, Shirou Tanoue, Yuichiro Nasu, Fumisato Sasaki, Akihiro Moriuchi, Hiroshi Fujita, Takafumi Yamamoto, Makoto Oketani, Akio Ido, Hirohito Tsubouchi Background & Aims: We previously used a proteomic approach to show that peaks of human neutrophil peptide-1, -2, and -3 (HNP-1-3) were increased in the serum of ulcerative colitis (UC) patients compared to healthy controls and that plasma HNP-1-3 were useful biomarkers to diagnose and predict treatment outcomes in UC patients. However, the relationship between HNP-1-3 and the intestinal mucosa during UC has not been investigated. The aim of this study was to determine whether HNP-1 affects colon epithelial cell proliferation and exacerbates disease activity in mice with experimental colitis. Methods: The colon cancer cell line HT-29 was cultured in serum free medium for 24 hours, and then treated with 0, 5, 10, 100 or 200 μg/ml HNP-1 for 24 hours. The proliferation of HT-29 cells was assessed by the Tetracolor One assay and BrdU ELISA. In addition, experimental colitis was induced in BALB/c mice by administering dextran sulfate sodium (DSS, 1.5%, w/v) in the drinking water for seven days. Mice were treated intraperitoneally with HNP-1 (30 μg/body/ day; HNP-1 group, n=6) or phosphate buffered saline (control group, n=6) from day 0 to day 6. Mice were sacrificed and the severity of colitis was evaluated based on the disease activity index (DAI) and histological score. Results: HNP-1 at concentrations above 100 μg/ ml significantly inhibited HT-29 cell proliferation. The proliferation of HT-29 cells treated with 100 μg/ml HNP-1 was inhibited by 46% compared to untreated cells as evaluated by the Tetracolor One assay, and the BrdU uptake rate was inhibited by 33%. Although the body weight of the control mice was unchanged (26.8 g →26.8 g), the body weight of HNP-1-treated mice decreased from 26.8 g to 25.4 g. In addition, the histological score was significantly higher in the HNP-1 group than in the control group (2.91 vs. 2.09, P=0.026), and the DAI score tended to be higher in the HNP-1 group. Conclusions: HNP-1 inhibited the proliferation of a colon cancer cell line and aggravated DSS-induced colitis. These results indicate that high concentrations of HNP-1-3 in UC patients may prevent tissue repair in the colon by inhibiting colon epithelial cell proliferation and exacerbate colitis activity.
S1700 The Role of Human γδ T-Cells in Inflammatory Bowel Disease Elizabeth R. Mann, Neil E. McCarthy, Andrew N. Milestone, Stella A. Cochrane, Andrew J. Stagg, Ailsa Hart, Stella C. Knight INTRODUCTION: γδ T-cells are innate lymphocytes, which play a pivotal role in modification of inflammatory responses. Some mouse models of inflammatory bowel disease (IBD) suggest that γδ T-cells are immuno-protective in gut mucosa, while others indicate a role in exacerbation of disease. The role of γδ T-cells in gut immunity and IBD is far from clear. METHODS: Human peripheral blood was obtained from patients (n=12) with Crohn's disease or ulcerative colitis on minimal treatment (5-aminosalicylic acid or azathioprine) or healthy volunteers (n=11). Mononuclear cells were isolated on Ficoll gradients. Rectal biopsies were obtained from patients with active Crohn's disease (n=2) or healthy volunteers (n=2). Blood mononuclear cells and mucosal “walkout” cells were labelled with monoclonal antibodies for analysis by flow cytometry. γδ T-cells were analysed for expression of tissue-homing molecules such as β7 integrin, a molecule associated with leukocyte homing to the gut. RESULTS: In healthy control subjects, blood and rectal γδ T-cells were CD3hi and the majority expressed β7 and memory cell marker, CD45RO. The co-stimulatory receptor CD28 was expressed on 2030% of γδ T-cells. Expression of skin homing markers was absent. There was a significant decrease in both number and proportion of γδ T-cells in blood of IBD patients compared with healthy controls. Early indications also suggest a loss from non-inflamed rectum in IBD. The proportion of blood γδ T-cells exhibiting memory cell phenotype was also significantly reduced in IBD, and preliminary data indicate alterations in expression of CD28. One patient with skin manifestations of (inactive) IBD (erythema nodosum) exhibited a separate, unique population of β7- blood γδ T-cells expressing skin homing molecule cutaneous lymphocyte antigen (CLA). CONCLUSION: Taken with reports that γδ T-cells are increased in the gut of IBD patients, it seems likely that reduced numbers of γδ T-cells in the circulation and non-inflamed rectum is a result of γδ T-cell migration to inflamed areas of the gut. Epidermal γδ T-cells in mice limit tissue damage associated with αβ T-cell mediated inflammation in contact hypersensitivity. Taken with the unique population of skin homing γδ Tcells in the blood of an erythema nodosum patient, it seems likely that γδ T-cells in humans play an immuno-protective role at epidermal and mucosal sites. The reduced proportion of blood γδ T-cells expressing CD45RO in IBD, and possible alterations in CD28 expression suggest differences in activation status of γδ T-cells in IBD. Further work will determine the role and possible therapeutic potential of γδ T-cells in inflammatory disease.
S1698 High Sero-Reactivity to Food Antigens Correlates with Disease Severity in Crohn's Disease, But Not in Ulcerative Colitis Patients Takaaki Kawaguchi, Keiko Saito, Yasuyo Suga, Masaki Hashimoto, Akira Mitsui, Mayuki Nakajima, Minako Sako, Naoki Yoshimura, Manabu Suzuki, Masakazu Takazoe BACKGROUND: Although the etiology of inflammatory bowel disease (IBD) is not clear, complex food proteins and enteric flora may act as antigenic stimuli in IBD, especially in Crohn's disease (CD). Only a few studies that assess clinical relevance of immune reaction against food antigens in IBD patients are reported. AIMS & METHODS: The aim of the study was 1) to investigate the prevalence of IgG antibodies against specific food antigens in patients with CD compared to ulcerative colitis (UC) patients and healthy controls (HC), 2) to compare the frequency of the development of IgG antibodies against foods with microbial antigens (Anti-Saccharomyces cerevisiae antibodies (ASCA) and antibodies to I2 from Pseudomonas fluorescens (anti-I2)) in CD patients, and 3) to investigate the correlation of numbers of IgG positive food items and clinical features in CD patients. Patients with CD or UC were sequentially enrolled from Social Insurance Central General Hospital. Serum IgG of 88 food antigens were examined by the IgG Food Antibody Assessment (Genova Diagnostics, USA). Statistical analysis was performed using SAS system. RESULTS: Between September 2007 and October 2008, 80 CD patients, 44 UC patients and 52 HC were enrolled. CD patients had significantly higher IgG antibody prevalence against food compared to both UC and HC (number of antibody-positive food items; CD; 10.6 (95% CI 8.1-13.1), UC; 1.8 (CI 0.5-3.1), HC; 0.9 (CI 0.5-1.3), p<0.001; CD vs. UC and/or HC). CD patients but not UC and HC, had high immune response to vegetables, nuts and grains. Although
AGA Abstracts
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the prevalence of ASCA and anti-I2 were similar in CD patients (30%, 38% respectively), only anti-I2 positive CD patients had high frequency of IgG antibodies to food antigens. CD patients with anal fistulas, extraintestinal manifestations, high serum CRP levels, high platelet or white blood cell numbers in blood had significantly higher frequency of IgG antibodies to food antigens. Gender, location or behavior of CD lesion, history of medical and surgical treatment was not related to the frequency of IgG antibodies against food. DISCUSSION: CD patients have high immunoreactivity to many kinds of food antigens, especially in patients with severe clinical features (anal fistulas, extraintestinal manifestations or high serum CRP levels). Combined with our recent results using murine IL-10 KO colitis model, in which elimination of food antigens from standard diet exhibited marked suppression of colitis (Mori et al., DDW abstract, 2009), food antigens could play an aggravating role in the inflammatory response in CD patients and the control of food intake might regulate disease activity.
AGA Abstracts
TL1A Expression Is Induced During Dendritic Cell Differentiation Rivkah Gonsky, Richard L. Deem, Stephan R. Targan IFN-γ plays an important role in the generation and perpetuation of mucosal inflammation in IBD. TL1A, a TNF superfamily member, synergizes with IL-12 and IL-18 to augment IFN-γ production in human T cells. Enhanced TL1A expression is detected in IBD with a strong TL1A SNP association reported in Crohn's disease. We have previously shown TL1A expression is induced in peripheral monocytes and in-vitro derived dendritic cells (DC). The molecular mechanisms regulating TL1A expression during DC differentiation however, remain poorly defined. The human monocytic cell line, KG-1, provides a valuable model for dendritic cell differentiation. The round non-adherent KG1 cells develop a DC-like phenotype following activation by PMA/ionomycin. These cells become loosely adherent with long cytoplasmic projections. A concomitant induction of membrane TL1A and mRNA is observed with mRNA expression being detectable within 2 hours and peaking at 8 hours following stimulation. A strikingly similar kinetics of TL1A expression was likewise noted following PMA/ionomycin stimulation of peripheral monocytes. Further DC maturation of KG-1 cells following treatment with LPS results in additional enhancement of TL1A expression. Transient transfection of KG-1 with TL1A promoter-constructs up to 1.5 kb in length reveals up to 90-fold enhanced expression compared to cells transfected with the promoterless vector. EMSA analysis demonstrates PMA/ionomycin mediated upregulation of nucleo-protein binding to a putative TL1A NFκB binding site. Binding is competed by excess unlabeled wt TL1A NFκB, but not mutant oligonucleotide and is likewise attenuated following proteasomal inhibition by MG132. Our data suggests in the human monocytic KG-1 cell line, differentiation of immature cells towards a mature DC phenotype is associated with functional upregulation of surface TL1A expression and binding of NFκB to the TL1A promoter. These studies provide a molecular basis for future studies which may help elucidate the mechanism modulating TL1A expression during DC maturation.
S1699 Genetic and Experimental Murine Models of Inflammatory Bowel Disease Are Characterized By Novel Distinct Immune Profiles Philip Alex, Thuan Nguyen, Maxim Suhodrev-Saksonov, Igor Dozmorov, Fong-Fong Chu, Michael Centola, Xuhang Li Early effective treatment of IBD requires sensitive diagnostic tools and accurate means to evaluate disease activity. We performed comprehensive cytokine profiling in experimental and genetic models of murine IBD and have identified distinct patterns that can distinguish UC-like from CD-like colitis, indeterminate from IBD-like colitis, and severe from selflimited disease. Six models were established: [i,ii] acute and chronic DSS-induced, [iii,iv] acute and chronic TNBS-induced, [v] IL-10 knockout (KO), and [vi] mice with the combined disruption of Gpx1 and Gpx2 genes (Gpx DKO). Serum, intestinal tissues and mucosal scrapings were obtained from a total of 201 mice (12-17 mice/group; 6-9 wks). Disease activity index (DAI), MPO, and histological activity index (HAI) were obtained. A novel approach of serum multiplex cytokine profiling utilizing robotic ultra-sensitive, highlyreproducible biometric immunosandwich ELISA's was used to assess the modulation of 16 cytotoxic and humoral cytokines and chemokines. SDS-PAGE, Western blots, and immunofluorescent studies were performed on colonic tissue and mucosa. Novel distinctive systemic cytokine patterns were readily identified with significant correlations to disease activity and duration of disease (p<0.01). As the disease becomes chronic, TNBS colitis exhibited heightened Th1-Th17 response (IL-12 and IL-17), and DSS colitis switched from Th1-Th17 (TNF-a, IL-6, IL-17, and KC) to a predominant Th2 profile (IL-4 and IL-10). IL-10 KO mice had a distinct Th1-chemotactic profile (IL-2, TNF-a, IL-12 and MIP), while the Gpx DKO model had a Th2-Th17 profile (IL-17, IL-5, and IL-10). When DAI, HAI and MPO were compared to cytokine profiles, partial correlational analysis identified distinct UC-like & CD-like subsets with significant correlations (r > 0.8) to disease severity. These data also showed that the GPX DKO model was a potential reproducible model of indeterminate colitis (comparable to patients). Multivariate analyses identified 8 significant variables (Wilk's λ: 0.031-0.149), which on a 3D plot mapped groups into distinct positions that were able to discriminate UC-like (DSS) from CD-like colitis (TNBS, IL-10 KO), and indeterminate (GPX DKO) from IBD-like colitis (DSS, TNBS, and IL-10 KO). Intestinal immunoblot and immunofluorescence studies validated and provided further insight into these distinct cytokine patterns. Our studies have identified (i) novel distinct systemic cytokine profiles as a means to effectively differentiate and subclassify IBD-like colitis, (ii) as practical indicators to monitor disease severity, and (iii) has given us important insight into the immunopathogenesis of IBD.
S1697 Human Neutrophil Peptide-1 Has Cytotoxic Effects On Colon Cancer Cells and Aggravates Dextran Sulfate Sodium-Induced Colitis Shinichi Hashimoto, Hirofumi Uto, Shuji Kanmura, Yuko Nakamura, Manei Oku, Shirou Tanoue, Yuichiro Nasu, Fumisato Sasaki, Akihiro Moriuchi, Hiroshi Fujita, Takafumi Yamamoto, Makoto Oketani, Akio Ido, Hirohito Tsubouchi Background & Aims: We previously used a proteomic approach to show that peaks of human neutrophil peptide-1, -2, and -3 (HNP-1-3) were increased in the serum of ulcerative colitis (UC) patients compared to healthy controls and that plasma HNP-1-3 were useful biomarkers to diagnose and predict treatment outcomes in UC patients. However, the relationship between HNP-1-3 and the intestinal mucosa during UC has not been investigated. The aim of this study was to determine whether HNP-1 affects colon epithelial cell proliferation and exacerbates disease activity in mice with experimental colitis. Methods: The colon cancer cell line HT-29 was cultured in serum free medium for 24 hours, and then treated with 0, 5, 10, 100 or 200 μg/ml HNP-1 for 24 hours. The proliferation of HT-29 cells was assessed by the Tetracolor One assay and BrdU ELISA. In addition, experimental colitis was induced in BALB/c mice by administering dextran sulfate sodium (DSS, 1.5%, w/v) in the drinking water for seven days. Mice were treated intraperitoneally with HNP-1 (30 μg/body/ day; HNP-1 group, n=6) or phosphate buffered saline (control group, n=6) from day 0 to day 6. Mice were sacrificed and the severity of colitis was evaluated based on the disease activity index (DAI) and histological score. Results: HNP-1 at concentrations above 100 μg/ ml significantly inhibited HT-29 cell proliferation. The proliferation of HT-29 cells treated with 100 μg/ml HNP-1 was inhibited by 46% compared to untreated cells as evaluated by the Tetracolor One assay, and the BrdU uptake rate was inhibited by 33%. Although the body weight of the control mice was unchanged (26.8 g →26.8 g), the body weight of HNP-1-treated mice decreased from 26.8 g to 25.4 g. In addition, the histological score was significantly higher in the HNP-1 group than in the control group (2.91 vs. 2.09, P=0.026), and the DAI score tended to be higher in the HNP-1 group. Conclusions: HNP-1 inhibited the proliferation of a colon cancer cell line and aggravated DSS-induced colitis. These results indicate that high concentrations of HNP-1-3 in UC patients may prevent tissue repair in the colon by inhibiting colon epithelial cell proliferation and exacerbate colitis activity.
S1700 The Role of Human γδ T-Cells in Inflammatory Bowel Disease Elizabeth R. Mann, Neil E. McCarthy, Andrew N. Milestone, Stella A. Cochrane, Andrew J. Stagg, Ailsa Hart, Stella C. Knight INTRODUCTION: γδ T-cells are innate lymphocytes, which play a pivotal role in modification of inflammatory responses. Some mouse models of inflammatory bowel disease (IBD) suggest that γδ T-cells are immuno-protective in gut mucosa, while others indicate a role in exacerbation of disease. The role of γδ T-cells in gut immunity and IBD is far from clear. METHODS: Human peripheral blood was obtained from patients (n=12) with Crohn's disease or ulcerative colitis on minimal treatment (5-aminosalicylic acid or azathioprine) or healthy volunteers (n=11). Mononuclear cells were isolated on Ficoll gradients. Rectal biopsies were obtained from patients with active Crohn's disease (n=2) or healthy volunteers (n=2). Blood mononuclear cells and mucosal “walkout” cells were labelled with monoclonal antibodies for analysis by flow cytometry. γδ T-cells were analysed for expression of tissue-homing molecules such as β7 integrin, a molecule associated with leukocyte homing to the gut. RESULTS: In healthy control subjects, blood and rectal γδ T-cells were CD3hi and the majority expressed β7 and memory cell marker, CD45RO. The co-stimulatory receptor CD28 was expressed on 2030% of γδ T-cells. Expression of skin homing markers was absent. There was a significant decrease in both number and proportion of γδ T-cells in blood of IBD patients compared with healthy controls. Early indications also suggest a loss from non-inflamed rectum in IBD. The proportion of blood γδ T-cells exhibiting memory cell phenotype was also significantly reduced in IBD, and preliminary data indicate alterations in expression of CD28. One patient with skin manifestations of (inactive) IBD (erythema nodosum) exhibited a separate, unique population of β7- blood γδ T-cells expressing skin homing molecule cutaneous lymphocyte antigen (CLA). CONCLUSION: Taken with reports that γδ T-cells are increased in the gut of IBD patients, it seems likely that reduced numbers of γδ T-cells in the circulation and non-inflamed rectum is a result of γδ T-cell migration to inflamed areas of the gut. Epidermal γδ T-cells in mice limit tissue damage associated with αβ T-cell mediated inflammation in contact hypersensitivity. Taken with the unique population of skin homing γδ Tcells in the blood of an erythema nodosum patient, it seems likely that γδ T-cells in humans play an immuno-protective role at epidermal and mucosal sites. The reduced proportion of blood γδ T-cells expressing CD45RO in IBD, and possible alterations in CD28 expression suggest differences in activation status of γδ T-cells in IBD. Further work will determine the role and possible therapeutic potential of γδ T-cells in inflammatory disease.
S1698 High Sero-Reactivity to Food Antigens Correlates with Disease Severity in Crohn's Disease, But Not in Ulcerative Colitis Patients Takaaki Kawaguchi, Keiko Saito, Yasuyo Suga, Masaki Hashimoto, Akira Mitsui, Mayuki Nakajima, Minako Sako, Naoki Yoshimura, Manabu Suzuki, Masakazu Takazoe BACKGROUND: Although the etiology of inflammatory bowel disease (IBD) is not clear, complex food proteins and enteric flora may act as antigenic stimuli in IBD, especially in Crohn's disease (CD). Only a few studies that assess clinical relevance of immune reaction against food antigens in IBD patients are reported. AIMS & METHODS: The aim of the study was 1) to investigate the prevalence of IgG antibodies against specific food antigens in patients with CD compared to ulcerative colitis (UC) patients and healthy controls (HC), 2) to compare the frequency of the development of IgG antibodies against foods with microbial antigens (Anti-Saccharomyces cerevisiae antibodies (ASCA) and antibodies to I2 from Pseudomonas fluorescens (anti-I2)) in CD patients, and 3) to investigate the correlation of numbers of IgG positive food items and clinical features in CD patients. Patients with CD or UC were sequentially enrolled from Social Insurance Central General Hospital. Serum IgG of 88 food antigens were examined by the IgG Food Antibody Assessment (Genova Diagnostics, USA). Statistical analysis was performed using SAS system. RESULTS: Between September 2007 and October 2008, 80 CD patients, 44 UC patients and 52 HC were enrolled. CD patients had significantly higher IgG antibody prevalence against food compared to both UC and HC (number of antibody-positive food items; CD; 10.6 (95% CI 8.1-13.1), UC; 1.8 (CI 0.5-3.1), HC; 0.9 (CI 0.5-1.3), p<0.001; CD vs. UC and/or HC). CD patients but not UC and HC, had high immune response to vegetables, nuts and grains. Although
AGA Abstracts
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