Sep 29 2010
new study on the role of mucosal immunity and host genetics in defining intestinal commensal bacteria indicates that basic elements of gut immunity, such as antibody class known as secretory IgA (sIgA) exert profound effects on the composition of the bacterial flora that inhabit the gut. This reinforces the prior observations about the influence of ABO and secretor genetics on the microbiome. It has been known since the 1950’s that ABH secretor status correlates with sIgA levels (non-secretors having lower levels), while some strains of enteric bacteria are up to 50,000 time more likely to be found in on ABO blood group versus another.
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 control 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. ( Free Text) 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 3 of 10 cultures inoculated. (Free Text)
Although it is well recognized that blood group antigens can serve as points of attachment for microbial adhesins, perhaps less appreciated (at least with regard to the ABO group) is the sheer destructive potential of the opposing blood group antibodies (isohemagglutinins.)
When an isohemagglutinin antibody encounters a foreign antigen, a reaction called agglutination occurs. This means that the antibody attaches to the antigen and makes it very sticky. When cells, viruses, parasites and bacteria are agglutinated, they stick together and “clump up,” which makes the job of their disposal much easier. As microbes must rely on their slippery powers of evasion, this is a very powerful defense mechanism. It is rather like handcuffing criminals together; they become far less dangerous than when allowed to move around freely.
Unlike IgG class antibodies, which require the assistance of the immune system to do their business, these isohemagglutinins kill things all by themselves, which is why getting the wrong blood group in a transfusion is so dangerous.
It is an interesting dichotomy that polymorphisms such as the blood groups that are capable of producing such a toxic reaction to the presence of an opposing blood group antigen but are themselves really just non-lethal mutations. Nobody dies just because they are one blood group or another, although there are many physiologic distinctions and consequences.
It is difficult to understand how agglutinins are produced in individuals who do not have the respective antigenic substances in their red blood cells. However, group A and B antigens are believed to enter the body in the food, in bacteria, or by other means, and these substances presumably initiate the development of anti-A or anti-B agglutinins.
—Arthur Guyton, Textbook of Medical Physiology
Although most scientists are aware of the relationship between the blood group antigens and antibodies that are the determining factor behind the classic transfusion relationships discovered by Landsteiner in 1900. However not very well known is the fact that foods and bacteria that possess many of these same opposing ABO blood group antigens are the source of induction for these IgM class antibodies.