It was known early in the century that ABO blood group substances occur in human tissues and secretions in two forms, water-soluble and alcohol-soluble, and that persons with these substances in saliva (secretors) have more water-soluble substances in their tissues than those lacking the substance in their saliva (non-secretors). One of the primary differences in physiology between secretors and non-secretors has to do with qualitative and quantitative differences in blood type antigen components of their saliva, mucus, and other body secretions. Two alleles, Se, and se control ABH secretion. Se is dominant and se is recessive (or amorphic). Approximately 80% of people are secretors (SeSe or Sese).

The term ABH secretor, as used in blood banking, refers to secretion of ABO blood group antigens in fluids such as saliva, sweat, tears, semen, and serum. If people are ABH secretors, they will secrete antigens according to their blood groups. For example, group O people will secrete H antigen, group A people will secrete A and H antigens, etc. Soluble (secreted) antigens are called substances. To test for secretor status, an inhibition or neutralization test is done using saliva. The principle of the test is that if ABH antigens are present in a soluble form in a fluid (e.g., saliva) they will neutralize their corresponding antibodies and the antibodies will no longer be able to agglutinate red cells possessing the same antigens.

It's often not what you are eating, but what is eating you.

In the most rudimentary sense, the secretor gene (FUT2 at 19q13.3) codes for the activity of the glycosyltransferases needed to assemble aspects of both the ABO and Lewis blood groups. This it does in concert with the gene for group O, or H (FUT1). These enzymes are then active in places like goblet and mucous gland cells, resulting in the presence of the corresponding antigens in body fluids. (1)

Secretor status and Candida albicans

ABH non-secretors are much more likely to be carriers of Candida species and to have problems with persistent Candida infections. Blood group O non-secretors are the most affected of the non-secretor blood types. One of the innate defenses against superficial infections by Candida species appears to be the ability of an individual to secrete the water-soluble form of his ABO blood group antigens into body fluids. The protective effect afforded by the secretor gene might be due to the ability of glycocompounds in the body fluids of secretors to inhibit adhesins (attachment lectins) on the surface of the yeast. In attachment studies, preincubation of certain bacterial spores with boiled secretor saliva significantly reduced their ability to bind to epithelial cells. ABH non-secretor saliva did not reduce the binding and often enhanced the numbers of attached yeasts. (2,3) In one study, among individuals with Type II diabetes, 44% of ABH non-secretors were oral carriers of this yeast. (4)

Although non-secretors make up only about 26% of the population, they are significantly over represented among individuals with either oral or vaginal Candida infections, making up almost 50% of affected individuals. (5) The inability to secrete blood group antigens in saliva also appears to be a risk factor in the development or persistence of chronic hyperplastic candidosis. In one study, the proportion of non-secretors of blood group antigens among patients with chronic hyperplastic candidosis was 68%. (6)

Women with recurrent idiopathic vulvovaginal candidosis are much more likely to be ABH non-secretors. Combining both ABH non-secretor phenotype and absence of the Lewis gene, Lewis (a- b-), the relative risk of chronic recurring vulvovaginal candidosis is between 2.41-4.39, depending on the analysis technique and control group. (7)

Oral carriage of Candida is also significantly associated with blood group O (p < 0.001) and independently, with non-secretion of blood group antigens (p < 0.001), with the trend towards carriage being greatest in group O non-secretors. (8)

Blood Groups and Microbiome

This is especially interesting in light of the fact that many of the fucosyltransferase enzymes convey blood group and/or secretor status. (9) Human feces contain enzymes produced by enteric bacteria that degrade the A, B, and H blood group antigens of gut mucin glycoproteins. The autosomal dominant ABH secretor gene together with the ABO blood group gene controls the presence and specificity of A, B, and H blood group antigens in human gut mucin glycoproteins. There is evidence that the host’s ABO blood group and secretor status affects the specificity of blood group-degrading enzymes produced by his fecal bacteria in vitro. (10) Comparatively small populations of fecal bacteria produce blood group-degrading enzymes but their presence is highly correlated with the ABO /secretor phenotype of the host: Fecal populations of B-degrading bacteria were stable over time, and their population density averaged 50,000-fold greater in blood group B secretors than in other subjects. In fact, the large populations of fecal anaerobes may be an additional source of blood group antigen substrate for blood group antigen degrading bacteria: antigens cross-reacting with blood group antigens were detected on cell walls of anaerobic bacteria from three of 10 cultures inoculated. (11)

1. Henderson J, Seagroatt V, Goldacre M. Ovarian cancer and ABO blood groups. J Epidemiol Community Health. 1993 Aug; 47(4):287-9.
2. Toft AD, Blackwell CC, Saadi AT, et al. Secretor status and infection in patients with Graves” disease. Autoimmunity 1990; 7(4):279-89.
3. Blackwell CC, Aly FZ, James VS, et al. Blood group, secretor status and oral carriage of yeasts among patients with diabetes mellitus. Diabetes Res 1989 Nov; 12(3):101-4.
4. Thom SM, Blackwell CC, MacCallum CJ, et al. Non-secretion of blood group antigens and susceptibility to infection by Candida species. FEMS Microbiol Immunol 1989 Jun; 1(6-7):401-5.
5. Thom SM, Blackwell CC, MacCallum CJ, et al. Non-secretion of blood group antigens and susceptibility to infection by Candida species. FEMS Microbiol Immunol 1989 Jun; 1(6-7):401-5.
6. Lamey PJ, Darwazeh AM, Muirhead J, et al. Chronic hyperplastic candidosis and secretor status. J Oral Pathol Med 1991 Feb; 20(2):64-7.
7. Chaim W, Foxman B, Sobel JD. Association of recurrent vaginal candidiasis and secretory ABO and Lewis phenotype. J Infect Dis 1997 Sep; 176(3):828-30.
8. Burford-Mason AP, Weber JC, Willoughby JM. Oral carriage of Candida albicans, ABO blood group and secretor status in healthy subjects. J Med Vet Mycol 1988 Feb; 26(1):49-56.
9. D’Adamo PJ, Kelly GS. Metabolic and immunologic consequences of ABH secretor and Lewis subtype status. Altern Med Rev. Aug;6(4):390-405; 2001
10. Hoskins LC, Boulding ET. Degradation of blood group antigens in human colon ecosystems. I. In vitro production of ABH blood group-degrading enzymes by enteric bacteria. J Clin Invest Jan;57(1):63-73;1976
11. Hoskins LC, Boulding ET. Degradation of blood group antigens in human colon ecosystems. II. A gene interaction in man that affects the fecal population density of certain enteric bacteria. J Clin Invest Jan;57(1):74-82; 1976

Tags: abo blood group | candida | secretor status