Antibiotic-Induced Gut Microbiota Dysbiosis Damages the Intestinal Barrier, Increasing Food Allergy in Adult Mice

Abstract

(1) Background: The use of antibiotics affects the composition of gut microbiota. Studies have suggested that the colonization of gut microbiota in early life is related to later food allergies. Still, the relationship between altered intestinal microbiota in adulthood and food allergies is unclear. (2) Methods: We established three mouse models to analyze gut microbiota dysbiosis’ impact on the intestinal barrier and determine whether this effect can increase the susceptibility to and severity of food allergy in later life. (3) Results: The antibiotic-induced gut microbiota dysbiosis significantly reduced Lachnospiraceae, Muribaculaceae, and Ruminococcaceae, and increased Enterococcaceae and Clostridiales. At the same time, the metabolic abundance was changed, including decreased short-chain fatty acids and tryptophan, as well as enhanced purine. This change is related to food allergies. After gut microbiota dysbiosis, we sensitized the mice. The content of specific IgE and IgG1 in mice serum was significantly increased, and the inflammatory response was enhanced. The dysbiosis of gut microbiota caused the sensitized mice to have more severe allergic symptoms, ruptured intestinal villi, and a decrease in tight junction proteins (TJs) when re-exposed to the allergen. (4) Conclusions: Antibiotic-induced gut microbiota dysbiosis increases the susceptibility and severity of food allergies. This event may be due to the increased intestinal permeability caused by decreased intestinal tight junction proteins and the increased inflammatory response.

Fucoxanthin Prevents the Ovalbumin-Induced Food Allergic Response by Enhancing the Intestinal Epithelial Barrier and Regulating the Intestinal Flora

“…20 Antibiotic intake by adult mice increases FA susceptibility and severity due to higher intestinal permeability and dysbiosis of the gut microbiota. 4 Another study has shown that feces from healthy infants transplanted into germ-free mice can prevent cow milk allergy. 21 Therefore, it is reasonable to hypothesize that fucoxanthin may prevent FA by enhancing the intestinal epithelial barrier and microbial regulation pathways.…”

“…Food allergy (FA) is an adverse immune reaction that occurs when people are exposed to certain foods and can be divided into IgE-mediated or non-IgE-mediated reactions. , It is widely accepted that the FA is associated with immunological abnormalities, inflammatory mediator expansion, increased intestinal permeability, and gut microbiota dysbiosis. − However, current immunotherapy treatment (oral immunotherapy, sublingual immunotherapy, and epicutaneous immunotherapy) and medication remain limited and can produce various adverse effects. , Therefore, natural anti-FA substances have attracted significant attention due to their milder effect, fewer side effects, and safety. , …”

ProbResist: a database for drug-resistant probiotic bacteria

“…Indeed, it was shown in mice that antibiotic-associated reduction in intestinal microbiota and metabolic abundance such as short-chain fatty acids and tryptophan resulted in an increase in inflammatory response as evidenced by elevated immunoglobulins IgE and IgG1 after sensitization. Upon re-exposure to the allergens, the mice showed evidence for damaged intestinal barrier such as ruptured intestinal villi and a decrease in tight junction proteins ( 66 ). Thus, excessive or irresponsible use of probiotics, many of which are phenotypically resistant to clinically important antibiotics and harbor resistance genes on mobile genetic elements, could further exacerbate the current public health crisis especially in the clinical settings where those with underlying health conditions are most vulnerable.…”

Claudin-1 Mediated Tight Junction Dysfunction as a Contributor to Atopic March

“…A food allergen challenge induced a rapid degradation of intestinal intercellular junction proteins, including claudin-1, in a mouse model of food allergy ( 126 ). Downregulation of CLDN1 expression level in the GI tract was also associated with an increased serum IgE level ( 127 ).…”