Anti-Saccharomyces Cerevisiae Antibodies (ASCA), Phenotypes of IBD, and Intestinal Permeability: A Study in IBD Families

Vermeire, Séverine; Peeters, Marc; Vlietinck, Robert; Joossens, Sofie; Hond, Elly Den; Bulteel, Veerle; Bossuyt, Xavier; Geypens, Benny; Rutgeerts, Paul

doi:10.1097/00054725-200102000-00002

Cited by 158 publications

(113 citation statements)

References 37 publications

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“…20 This group, however, only included patients on medical therapy and did not observe patients post-operatively. Interestingly, Vermeire et al could not associate ASCA serum levels with the degree of intestinal permeability in patients with CD as measured by 51Cr-EDTA intestinal permeation, 21 which supports the hypothesis that loss of tolerance towards Saccharomyces cerevisiae in CD is independent of a breach of intestinal integrity. Concordantly, in our cohort there was neither a difference in ASCA seropositivity nor ASCA serum levels in patients experiencing mild vs. severe post-operative endoscopic recurrence.…”

Section: Discussionmentioning

confidence: 84%

The impact of intestinal resection on serum levels of anti‐Saccharomyces cerevisiae antibodies (ASCA) in patients with Crohn’s disease

Eser

Papay

Primas

et al. 2011

Aliment Pharmacol Ther

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Section: Discussionmentioning

confidence: 84%

The impact of intestinal resection on serum levels of anti‐Saccharomyces cerevisiae antibodies (ASCA) in patients with Crohn’s disease

Eser

Papay

Primas

et al. 2011

Aliment Pharmacol Ther

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“…The markers studied most are intestinal permeability, and a number of anti-microbial antibodies: anti-Saccharomyces cerevisiae antibodies (ASCA) and atypical pANCA (perinuclear antineutrophil cytoplasmic antibodies). [11][12][13][14][15] Other microbial antibodies found in IBD patients as antiOmpC (directed against the outermembrane porin C of Escherichia coli), I2 (antibodies directed against Pseudomonas fluorescens) and Cbir 1 (anti-flagellin antibodies) have not been studied in asymptomatic family members. [16][17][18] However, the presence of these subclinical markers has no clinical implications yet and longitudinal studies are needed first to evaluate their exact meaning.…”

Section: Genetic Epidemiologymentioning

confidence: 99%

Current status of genetics research in inflammatory bowel disease

Vermeire¹,

Rutgeerts²

2005

Genes Immun

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The research on genetic susceptibility of inflammatory bowel diseases (IBD) has been tremendous and over 10 chromosomal regions have been identified by genome-wide scanning. Further fine mapping as well as candidate gene studies have already led to the identification of a number of susceptibility genes including CARD15, DLG5, OCTN1 and 2, NOD1, HLA, and TLR4. The CARD15 gene is undoubtedly replicated most widely and most understood at present. CARD15 is involved in the recognition of bacterial peptidoglycan-derived muramyl dipeptide (MDP) and will stimulate secretion of antimicrobial peptides including alpha-defensins (also called cryptdins) to protect the host from invasion. Genetic research in IBD has advanced our understanding of the clinical heterogeneity of the disease and has started to tackle the complex interactions between genetic risk factors and environmental risk factors in IBD. Genes also interfere with the metabolization of drugs and may influence the clinical response and the drug-related toxicity. Interesting pharmacogenetic data with respect to steroids, azathioprine, and infliximab have been generated in IBD. Overall, it is anticipated that genetic markers in the future will be implemented in an integrated molecular diagnostic and prognostic approach of our patients. Genes and Immunity (2005) 6, 637-645.

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“…It was, thus, concluded that ASCA may result from a mucosal permeability defect. However, Vermeire et al [20] were not able to show a correlation between ASCA and intestinal permeability.…”

Section: Introductionmentioning

confidence: 89%

Anti-Saccharomyces cerevisiaeantibody titers are stable over time in Crohn’s patients and are not inducible in murine models of colitis

Müller

Styner

Seibold-Schmid

et al. 2005

WJG

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AIM: To investigate ASCA production over time in CD and murine colitis in order to further our understanding of their etiology. MATERIALS AND METHODS:Sixty-six CD patients were compared to ulcerative colitis (UC) and irritable b o w e l s y n d r o m e p a t i e n t s w i t h r e s p e c t t o A S C A production as measured by ELISA. ASCA IgG or IgA positivity as well as change in titers over a period of up to 3 years (∆IgG/A) was correlated with clinical parameters such as CD activity index (CDAI) and C-reactive protein levels (CRP). Moreover, two murine models of colitis (DSS and IL-10 knock out) were compared to control animals with respect to ASCA titers after oral yeast exposure. RESULTS:ASCA IgG and IgA titers are stable over time in CD and non-CD patients. Fistular disease was associated with a higher rate of ASCA IgA positivity (P = 0.014). Ileal disease was found to have a significant influence on the ∆IgG of ASCA (P = 0.032). There was no correlation found between ASCA positivity or ∆IgG/A and clinical parameters of CD: CDAI and CRP. In mice, neither healthy animals nor animals with DSS-induced or spontaneous colitis exhibited a marked increase in ASCA titers after high-dose yeast exposure. On the other hand, mice immunized intraperitoneally with mannan plus adjuvant showed a marked and significant increase in ASCA titers compared to adjuvant-only immunized controls (P = 0.014). CONCLUSION:The propensity to produce ASCA in a subgroup of CD patients is largely genetically predetermined as evidenced by their stability and lack of correlation with clinical disease activity parameters. Furthermore, in animal models of colitis, mere oral exposure of mice to yeast does not lead to the induction of marked ASCA titers irrespective of concomitant colonic inflammation. Hence, environment may play only a minor role in inducing ASCA.

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Anti-Saccharomyces Cerevisiae Antibodies (ASCA), Phenotypes of IBD, and Intestinal Permeability: A Study in IBD Families

Abstract: ASCA is strongly associated with familial CD in Belgium, and 21% of healthy family members also display the marker. The association is much weaker in patients belonging to mixed families. ASCA is a stable marker and is not a secondary phenomenon due to increased intestinal permeability.

Cited by 158 publications

References 37 publications

The impact of intestinal resection on serum levels of anti‐Saccharomyces cerevisiae antibodies (ASCA) in patients with Crohn’s disease

The impact of intestinal resection on serum levels of anti‐Saccharomyces cerevisiae antibodies (ASCA) in patients with Crohn’s disease

Current status of genetics research in inflammatory bowel disease

Anti-Saccharomyces cerevisiaeantibody titers are stable over time in Crohn’s patients and are not inducible in murine models of colitis

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