Serum Antibodies Reactive with &lt;i&gt;Saccharomyces cerevisiae&lt;/i&gt; in Inflammatory Bowel Disease: Is IgA Antibody a Marker for Crohn’s Disease?

Barnes, R. M. R.; Allan, Susan; Taylor-Robinson, C.H.; Finn, Ronald D.; Johnson, Patricia R.

doi:10.1159/000235217

Cited by 76 publications

(40 citation statements)

References 4 publications

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“…In a second publication, the same group confirmed their initial data and showed that the antibody response was specific for baker's yeast and did not include Candida albicans [8], By excluding yeast from the diet, these authors were also able to significantly reduce the Crohn's disease activity index in their patients [16]. Subsequently, the existence of ele vated antibody titers against baker's yeast in Crohn's dis ease has been supported by several publications from oth 41 er groups [9][10][11]. Lindberg et al [10] investigated 26 monozygotic twin pairs with inflammatory bowel disease and 52 healthy controls.…”

Section: Discussionmentioning

confidence: 71%

“…An elevated titer to a dietary compo nent like baker's yeast might have been considered an unspecific immune response that is unrelated to the pri mary mechanisms underlying Crohn's disease. Patients with Crohn's disease are known to have a leaky epithe lium which may lead to increased exposure of their immune system to foreign antigens [17], Serum anti bodies to cow's milk proteins have been claimed to be higher in Crohn's disease patients than controls [18,19], Lymphocyte proliferation may represent a more specific cellular immune response than elevated antibody titers, although the evidence accumulated by other groups sug gests that the elevated titers, particularly of IgA, represent a primary phenomenon rather than an epiphenomenon resulting from an impaired mucosal barrier [7][8][9][10][11], The results described in the present paper corroborate these previous findings. The similar baseline proliferation rate and the similar response to PHA among patients and con trols speak against a generally altered reactivity of lym phocytes in patients with Crohn's disease.…”

Section: Discussionmentioning

confidence: 99%

“…There is strong epidemiologic evidence to suggest that the occur ence of Crohn's disease is influenced by exogenous risk factors [1][2][3]. Nutritional surveys and studies testing the stepwise exclusion of dietary components have suggested that a dietary factor associated with wheat might be linked to the occurrence of Crohn's disease [4][5][6], Several groups have found increased IgG and IgA antibodies to baker's yeast in patients with Crohn's disease, but not healthy controls or patients with ulcerative colitis [7][8][9][10][11], The occupational distribution of Crohn's disease in En gland and Germany is characterized by a strikingly high azine (D ipcntum ') for maintenance treatment. None were treated with active corticosteroid medication for at least I month prior to study.…”

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confidence: 99%

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Lymphocyte Proliferation Response to Baker’s Yeast in Crohn’s Disease

1994

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The etiology of Crohn’s disease is still unknown. The present study served to test the hypothesis that baker’s yeast (Saccharomyces cerevisiae) plays a role in Crohn’s disease. Blood samples were obtained from 12 patients and 15 healthy controls. Peripheral blood leukocytes were isolated and incubated alone or with different concentrations of baker’s yeast. After 3 days, the cultures were pulsed with tritiated thymidine. None of the lymphocyte cultures from healthy controls, including 3 bakers, proliferated in response to yeast. In striking contrast, all 9 patients with Crohn’s disease in remission, on no medication, showed a threefold increase in their lymphocyte proliferation rate. Lymphocytes from 3 patients on 1.5 g of olsalazine maintenance therapy failed to respond. These results are consistent with previous findings that showed increased titers of IgG and IgA antibodies to baker’s yeast in patients with Crohn’s disease as compared to healthy controls. They confirm the suspicion that baker’s yeast itself or a related antigen play a role in Crohn’s disease and suggest that anti-inflammatory agents may act, in part, by inhibiting lymphocyte proliferation.

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Lymphocyte Proliferation Response to Baker’s Yeast in Crohn’s Disease

1994

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“…ASCA (IgA and IgG) are detected through their reactivity with sequences of mannose residues expressed in the cell wall mannan of Saccharomyces cerevisiae [21,25,26]. Saccharomyces cerevisiae is a "ubiquitous" yeast and occurs in diverse places naturally, on plants and in the ground.…”

Section: Discussionmentioning

confidence: 99%

Anti-Saccharomyces cerevisiae Antibody Does Not Differentiate Between Crohn's Disease and Intestinal Tuberculosis

et al. 2006

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The clinical, morphological, and histological features of intestinal tuberculosis (IT) and Crohn's disease (CD) mimic so much, that it becomes difficult to differentiate between them. The sensitivity of anti-Saccharomyces cerevisiae antibody (ASCA) IgG and ASCA IgA in CD is 60%-80%, whereas the specificity is almost 90%. There are no reports of study of ASCA in patients with IT, nor has it ever been used to differentiate CD from IT. Patients with ulcerative colitis (UC; n=25), CD (n=59), and IT (n=30) and 21 healthy controls were included in this study. The location and behavior of CD were classified according to the Modified Montreal classification. Five milliliters of blood was taken from them and serum was stored at -70 degrees C. ASCA antibodies (both IgG and IgA) were estimated using commercially available ELISA kits (AESKU Diagnostics, Germany). Anti-neutrophilic cytoplasmic antibody was measured by indirect immunofluorescence test. ASCA IgA was positive in 4.7%, 28%, 33.9%, and 43.3% and ASCA IgG was positive in 4.7%, 24%, 50.8%, and 46.6% of healthy controls and patients with UC, CD, and IT, respectively. Either ASCA IgG or ASCA IgA was positive in 9.5%, 40%, 61% and 66.6% of healthy controls, UC, CD, and IT, respectively. ANCA was positive in 0%, 32%, 10.1%, and 6.6% of healthy controls, UC, CD, and IT, respectively. ASCA IgG was positive in a significantly higher number of patients with CD (P<0.0001) and IT (P<0.0001) in comparison to healthy controls. ASCA IgA was positive in a significantly higher number of patients with UC (P<0.04), CD (P<0.013), and IT (P<0.006) in comparison to healthy controls. In comparisons between diseases, ASCA IgG was positive in significantly more patients with CD (P<0.001) and IT (P<0.001) in comparison to UC. There was no significant difference in ASCA IgA (33.9% vs. 43.3%), ASCA IgG (50.86% vs. 46.6%), or ANCA (10.7%, 7.4%) in patients with CD and IT, respectively. There was no correlation between ASCA and duration, location and behavior of CD, and IT. We conclude that ASCA IgG and ASCA IgA do not help to differentiate between IT and CD.

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“…Nevertheless, some of the familial studies have yielded conflicting data. For example, one group showed increased ASCA production in familial vs sporadic CD [7] , but others have shown equal or increased ASCA prevalence for sporadic CD [9,[16][17][18] . Thus, the case for an environmental etiology for ASCA has been articulated as well.…”

Section: Introductionmentioning

confidence: 99%

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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Serum Antibodies Reactive with <i>Saccharomyces cerevisiae</i> in Inflammatory Bowel Disease: Is IgA Antibody a Marker for Crohn’s Disease?

Cited by 76 publications

References 4 publications

Lymphocyte Proliferation Response to Baker’s Yeast in Crohn’s Disease

Lymphocyte Proliferation Response to Baker’s Yeast in Crohn’s Disease

Anti-Saccharomyces cerevisiae Antibody Does Not Differentiate Between Crohn's Disease and Intestinal Tuberculosis

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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