A non-secretor is a person who does not release their ABO blood group antigens into their body fluids and mucosal secretions, such as saliva, tears, and mucus. This characteristic is a common genetic trait, inherited from one’s parents, and about one-fifth of the global population shares this status. The presence or absence of these antigens subtly influences various biological processes, particularly those involving interactions with the environment and the body’s internal systems. This difference affects everything from the types of bacteria that colonize the gut to the susceptibility to certain infectious diseases.
The Genetics Behind Secretor Status
The ability to secrete ABO antigens is governed by a single instruction set within the human genome, found in the FUT2 gene. This gene provides the blueprint for an enzyme called Fucosyltransferase 2. This enzyme is responsible for adding a specific sugar molecule, fucose, to the precursor molecules of the ABO antigens on the surface of cells lining the gastrointestinal tract and other mucosal surfaces.
An individual becomes a non-secretor by inheriting two copies of a non-functional FUT2 gene, which is a recessive trait. If a person inherits even one functional copy, they will produce the active enzyme and become a secretor. The non-functional gene results in a lack of the Fucosyltransferase 2 enzyme, meaning the ABO antigens are not properly constructed on the mucosal surfaces, although they are still expressed on the red blood cells.
The consequence is that a non-secretor’s mucosal surfaces, which line the respiratory, digestive, and genitourinary tracts, lack the H antigen structure, which is the precursor for A and B antigens. This structural difference in the protective mucus layer directly alters how the body interacts with both its resident microbes and external pathogens.
Impact on the Gut Microbiome
The difference in mucosal structure profoundly affects the ecosystem within the digestive tract, known as the gut microbiome. In secretors, the secreted ABO antigens are complex sugar molecules released into the gut mucus. These molecules, which include specific human milk oligosaccharides like 2′-fucosyllactose (2’FL), serve as a primary food source for certain beneficial bacteria.
Non-secretors lack the enzyme to produce these fucosylated sugar structures, thus not providing this food source for these microbes. This absence leads to a measurable difference in the composition of the gut flora compared to secretors. Specifically, non-secretors often exhibit a significantly lower abundance and reduced diversity of bacteria, most notably those belonging to the genus Bifidobacterium.
Bifidobacterium are recognized for their beneficial role in gut health, including producing short-chain fatty acids that support the intestinal lining. The altered environment in non-secretors influences the overall balance of the microbial community. Consequently, the unique intestinal environment may be linked to varying metabolic and immune responses.
Susceptibility to Specific Infections
The molecular difference in mucosal surfaces creates a trade-off, conferring both protection against some diseases and increased vulnerability to others. A primary example is the resistance non-secretors exhibit to the most common strains of Norovirus, often referred to as the “stomach flu.” Noroviruses cause acute gastroenteritis, but they require specific histo-blood group antigens (HBGAs) to bind to the intestinal cells and initiate infection.
Since non-secretors do not express these antigens on their gut lining, the virus cannot effectively attach and infect the host cells. This makes them naturally resistant to infection by major strains like the GII.4 variants. However, some newer or less common Norovirus strains utilize different binding mechanisms, meaning non-secretors are not immune to all forms of the virus.
Conversely, non-secretor status increases susceptibility to certain bacterial infections. The bacterium Helicobacter pylori, strongly associated with stomach ulcers, more easily colonizes the gastric lining of non-secretors. In this instance, the secreted antigens in secretors act as a decoy, binding to the bacteria in the mucus layer and preventing them from adhering to the host cells.
The lack of this decoy mechanism in non-secretors allows H. pylori to attach directly to the mucosal surface and cause persistent inflammation. This status has also been associated with an increased risk for infections in other areas, such as recurrent urinary tract infections and certain respiratory illnesses.
Testing and Prevalence
Determining an individual’s secretor status can be achieved through two primary methods. Historically, a simple saliva test based on the principle of hemagglutination inhibition was used. This test checks whether the ABO antigens are present in the saliva by seeing if the saliva can neutralize specific antibodies.
Today, secretor status is often determined more precisely through genetic testing, which analyzes the FUT2 gene for the presence of the non-functional variant. Since the status is determined by genetics, the result remains consistent throughout a person’s life. Globally, the non-secretor trait is found in approximately 20% of the population.
Prevalence varies significantly across different ethnic and geographical groups. For example, the frequency of non-secretors is relatively high in European populations. Conversely, in some indigenous groups, such as certain Native American and Aboriginal Australian populations, the non-secretor trait is extremely rare or non-existent.