Secretor Status and Human Leucocyte Antigens in Coeliac Disease

Heneghan, Michael A.; Kearns, M.; Goulding, Joseph; Egan, E. L.; Stevens, Fiona; McCarthy, C. F.

doi:10.3109/00365529609003116

“…The prevalence of Le expression among patients with or without H. pylori infection was not signi¢cantly di¡erent from the prevalence of Le antigen expression (27%), as reported previously in a group of controls originating in the region from which our patient sample was drawn [17]. In our current sample of dyspeptic patients, non-secretors exhibited a combination of endoscopically visible antral gastritis, duodenitis, gastric ulcer or duodenal ulcer no more frequently than secretors.…”

Section: Discussionsupporting

confidence: 75%

Effect of host Lewis and ABO blood group antigen expression on Helicobacter pylori colonisation density and the consequent inflammatory response

Heneghan¹

1998

FEMS Immunology and Medical Microbiology

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The Lewis(b) blood group antigen has been implicated as a putative receptor for Helicobacter pylori in the gastric mucosa. Furthermore, an increased prevalence of duodenal ulcer was found in non-secretors and it has been suggested that secretor status may influence bacterial colonisation density. Other investigators have hypothesised that severity of antral gastritis may be related to colonisation density of the bacterium alone, and that a critical bacterial load is necessary for the development of duodenal ulcer. Our objectives were to investigate whether a relationship existed between host Lewis and ABO blood group phenotype and prevalence of H. pylori infection. In addition we investigated whether bacterial colonisation density and the ensuing inflammatory response was influenced by secretor status and ABO blood group phenotype. The Lewis and ABO blood group phenotype of 207 patients undergoing upper endoscopy was determined. Of these, 136 were secretors and 62 were nonsecretors. Forty-five percent of patients were infected with H. pylori. No significant association was found between H. pylori infection and expression of Lewis(a) or Lewis(b) blood group antigen. The mean histological density of H. pylori was 1.8 +/- 0.2 among non-secretors and 1.51 +/- 0.13 among secretors (P = 0.209), with a mean grade of lymphocytic infiltration significantly greater in H. pylori-infected non-secretors (2.23 +/- 0.123 vs 1.8 +/- 0.074; P = 0.003). In addition, blood group O non-secretors had a significantly higher grade of lymphocyte infiltration of their gastric mucosa compared to non-O non-secretors (2.53 +/- 0.133 vs 1.93 +/- 0.181, P = 0.027). These results suggest that although no in vivo relationship exists between H. pylori and preferential adhesion to the putative Lewis(b) receptor, bacterial colonisation and the ensuing inflammatory response may be influenced at least in part by host expression of ABO and Lewisa blood group antigens.

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“…The prevalence of Le a expression among patients with or without H. pylori infection was not significantly different from the prevalence of Le a antigen expression (27%), as reported previously in a group of controls originating in the region from which our patient sample was drawn [17]. In our current sample of dyspeptic patients, non‐secretors exhibited a combination of endoscopically visible antral gastritis, duodenitis, gastric ulcer or duodenal ulcer no more frequently than secretors.…”

Section: Discussionsupporting

confidence: 76%

Effect of host Lewis and ABO blood group antigen expression onHelicobacter pyloricolonisation density and the consequent inflammatory response

Heneghan

¹

,

Moran

²

,

Feeley

³

et al. 1998

FEMS Immunology &Amp; Medical Microbiology

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The Lewis(b) blood group antigen has been implicated as a putative receptor for Helicobacter pylori in the gastric mucosa. Furthermore, an increased prevalence of duodenal ulcer was found in non-secretors and it has been suggested that secretor status may influence bacterial colonisation density. Other investigators have hypothesised that severity of antral gastritis may be related to colonisation density of the bacterium alone, and that a critical bacterial load is necessary for the development of duodenal ulcer. Our objectives were to investigate whether a relationship existed between host Lewis and ABO blood group phenotype and prevalence of H. pylori infection. In addition we investigated whether bacterial colonisation density and the ensuing inflammatory response was influenced by secretor status and ABO blood group phenotype. The Lewis and ABO blood group phenotype of 207 patients undergoing upper endoscopy was determined. Of these, 136 were secretors and 62 were nonsecretors. Forty-five percent of patients were infected with H. pylori. No significant association was found between H. pylori infection and expression of Lewis(a) or Lewis(b) blood group antigen. The mean histological density of H. pylori was 1.8 +/- 0.2 among non-secretors and 1.51 +/- 0.13 among secretors (P = 0.209), with a mean grade of lymphocytic infiltration significantly greater in H. pylori-infected non-secretors (2.23 +/- 0.123 vs 1.8 +/- 0.074; P = 0.003). In addition, blood group O non-secretors had a significantly higher grade of lymphocyte infiltration of their gastric mucosa compared to non-O non-secretors (2.53 +/- 0.133 vs 1.93 +/- 0.181, P = 0.027). These results suggest that although no in vivo relationship exists between H. pylori and preferential adhesion to the putative Lewis(b) receptor, bacterial colonisation and the ensuing inflammatory response may be influenced at least in part by host expression of ABO and Lewisa blood group antigens.

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“…The association of non-secretor status with CelD was first suggested by Dickey et al (31). In a follow-up study by Heneghan et al (32), the non-secretor status did not associate significantly with CelD and the authors concluded that the 'secretor gene' was unlikely to be a CelD susceptibility gene.…”

Section: Discussionmentioning

confidence: 93%

“…The association of non‐secretor status with CelD was first suggested by Dickey et al . In a follow‐up study by Heneghan et al , the non‐secretor status did not associate significantly with CelD and the authors concluded that the ‘secretor gene’ was unlikely to be a CelD susceptibility gene. Recent studies have however shown that there is a relationship between the composition of gut microbiota and protection from or susceptibility to certain infections .…”

Section: Discussionmentioning

confidence: 94%

Association study of FUT2 (rs601338) with celiac disease and inflammatory bowel disease in the Finnish population

Parmar

¹

,

Alakulppi

²

,

Paavola–Sakki

³

et al. 2012

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Homozygosity for a nonsense mutation in the fucosyltransferase 2 (FUT2) gene (rs601338G>A) leads to the absence of ABH blood groups (FUT2 non-secretor status) in body fluids. As the secretor status has been shown to be a major determinant for the gut microbial spectrum, assumed to be important in the gut immune homeostasis, we studied the association of rs601338-FUT2 with celiac disease (CelD) and inflammatory bowel disease (IBD) in the Finnish population. Rs601338 was genotyped in CelD (n = 909), dermatitis herpetiformis (DH) (n = 116), ulcerative colitis (UC) (n = 496) and Crohn's disease (CD) (n = 280) patients and healthy controls (n = 2738). CelD showed significant genotypic [P = 0.0074, odds ratio (OR): 1.28] and recessive (P = 0.015, OR: 1.28) association with the rs601338-AA genotype. This was also found in the combined CelD+DH dataset (genotype association: P = 0.0060, OR: 1.28; recessive association: P < 0.011, OR: 1.28). The A allele of rs601338 showed nominal association with dominant protection from UC (P = 0.044, OR: 0.82) and UC+CD (P = 0.035, OR: 0.84). The frequency of non-secretors (rs601338-GG) in controls, CelD, DH, UC and CD datasets was 14.7%, 18%, 18.1%, 14.3% and 16.1%, respectively. No association was evident in the DH or CD datasets alone. In conclusion, FUT2 non-secretor status is associated with CelD susceptibility and FUT2 secretor status may also play a role in IBD in the Finnish population.

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Secretor Status and Human Leucocyte Antigens in Coeliac Disease

Abstract: This study shows no firm relationship between the non-secretor state and coeliac disease, nor any difference in the distribution of HLA markers among secretor and non-secretor coeliacs. It is unlikely, therefore, that the secretor gene is the much sought-after second coeliac gene.

Cited by 6 publications

References 27 publications

Effect of host Lewis and ABO blood group antigen expression on Helicobacter pylori colonisation density and the consequent inflammatory response

Effect of host Lewis and ABO blood group antigen expression on Helicobacter pylori colonisation density and the consequent inflammatory response

Effect of host Lewis and ABO blood group antigen expression onHelicobacter pyloricolonisation density and the consequent inflammatory response

Association study of FUT2 (rs601338) with celiac disease and inflammatory bowel disease in the Finnish population

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