The manifestations of the immune response in the course of food allergy are highly variable between individuals, so much so that some individuals, while producing specific IgE in some hapten protein, show no symptoms after taking the food incriminated, although the increased intake is related to an increased risk.
The biochemical characteristics of a food alone can not explain its allergenicity. In fact the natural consequence of exposure to new foods is the development of a physiological immune tolerance . The oral immune tolerance depends on a barrier intact and immunologically active the entire gastrointestinal tract. This barrier includes the epithelial cells joined by tight junctions and a thick layer of mucus , as well as the ' brush border , also enzymes, bile salts , and peak pH degrading them to help make it less immunogenic protein antigens.
Among the factors responsible for the triggering of an event-related allergic guests there is the activity of PAF acetilidrolasi , enzyme that degrades PAF , and this causes an increase in the severity of anaphylactoid reactions.
Among the factors to be considered the stability of food proteins to digestion and fragmentation of chemical / enzymatic intestinal absorption of certain seeds ( groundnuts , cumin , cashews ). These proteins, in fact, remain intact and can more easily trigger allergic reactions, food also very severe.
Assumptions acid hyposecretion
So closely related to the previous assumptions, the growing incidence of eosinophilic esophagitis, a form of food allergy, which has increased in recent years must seem attributable to the use of PPIs (proton pump inhibitors), and this decreased because the resulting chloride use of these drugs makes it more difficult digestion of proteins by the body resulting in increased permeability of the same proteins in the intestinal mucosa. The hypothesis although not yet confirmed by human studies, it is very plausible and interesting.
The scientific literature to support this effect is relatively large and recent: and correlates well with the hypothesis of the resistance protein.
A recent study relates the quantity of production of IL-9 with intestinal permeability to proteins and the subsequent exasperated response of mast cells. The IL-9, in fact, stimulates the release of histamine by mast cells and proteases and promotes the expression of FcεRI α. TNF also plays a role in the genesis of enteropathy of food allergies.
Assumptions Leaky gut
A large recent literature and lays the foundation for understanding the molecular causes of sensitization by food protein antigens in susceptible individuals. One of the predisposing factors, long hypothesized to gastrointestinal diseases is impaired barrier function, referred to as leaky gut.
The first-degree relatives of patients with inflammatory bowel disease (IBD) have an increased intestinal permeability in the absence of clinical symptoms.
Patients with food allergies who also have increased intestinal permeability, have increased the severity of their clinical symptoms. Although constitutive abnormalities in intestinal permeability were not always observed in patients with food allergy, it is assumed that environmental events, including infection and stress, can alter intestinal permeability and promote food antigen sensitization by.
Another issue recently highlighted correlates with food allergies, intestinal microbial balance dell'ecositema and host defense mechanisms. According to Japanese authors, in fact, to avoid excessive inflammatory reactions in the intestine play a role in the microbial components directly regulate the functions of mast cells through Toll-like receptors . This may explain the reason by which allergic reactions are a function of a non-symbiotic intestinal flora proper maintenance.
Recent research links the viral infection Reoviridae to cause immunological changes such as to trigger the pathological response of food allergies.
The protective role of probiotics in health human extends to a range of disease manifestations and among these there are the allergic reactions.
Probably all the assumptions described above contribute to varying degrees in etiopagenesi food allergies, and all offer important keys to understanding and research for understanding and finding solutions to this widespread disease of the well-being.