Antigen absorption by the jejunal epithelium of children with cow's milk allergy
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Infants with cow's milk allergy (CMA) show increased intestinal permeability to horseradish peroxidase (HRP), indicating a role for gut barrier function in CMA. This permeability returns to normal after a milk-free diet.
Area of Science:
- Gastroenterology
- Immunology
- Pediatrics
Background:
- Cow's milk allergy (CMA) is a common condition in infants.
- The role of intestinal permeability in CMA pathogenesis is not fully understood.
Purpose of the Study:
- To investigate intestinal permeability to exogenous antigens in infants with CMA.
- To assess the impact of a milk-free diet and milk challenge on gut barrier function.
Main Methods:
- Assessed intestinal permeability using horseradish peroxidase (HRP) transport across jejunal biopsies in infants with CMA and controls.
- Utilized Ussing chamber technique to measure HRP fluxes and electrical parameters.
- Performed biopsies during diagnosis, 1 year later, and before/after milk challenge.
Main Results:
- Infants with CMA exhibited significantly higher transepithelial HRP fluxes (8-fold increase) compared to controls.
- Increased short-circuit current was observed in CMA infants, while conductance remained unchanged.
- HRP flux and short-circuit current normalized after a milk-free diet, and a milk challenge caused a non-significant rise in HRP permeability.
Conclusions:
- Increased intestinal permeability to intact HRP is a feature of active cow's milk allergy in infants.
- Gut barrier function improves with a milk-free diet, suggesting reversibility.
- Intestinal permeability may play a significant role in the development and persistence of CMA.
Abstract:
To establish if intestinal permeability to exogenous antigens is involved in cow's milk allergy (CMA) in infants, 33 children 1 to 24 months old (18 controls and 15 with CMA) were tested for intestinal permeability to the protein marker horseradish peroxidase (HRP). Jejunal biopsies were performed either during the initial period of diagnosis, at the mean (and SE) age of 3 +/- 1 months, and/or 1 yr later, at the age of 13 +/- 2 months, just before and after a milk challenge. A small fragment of the biopsy was studied for histology and the remainder was mounted in an Ussing chamber for simultaneous measurement of mucosal to serosal transport of HRP in its intact and degraded forms and electrical parameters including short-circuit current and conductance. No modification in HRP absorption was noted in control children aged from 2 months to 11 yr, indicating that gut closure probably occurred earlier in life. During the initial period of CMA, transepithelial HRP fluxes were significantly higher, about 8-fold, in children with CMA (intact HRP flux = 48.5 +/- 15.2, 95% confidence interval, 11.2 to 85.7 versus 5.9 +/- 1.2, 95% confidence interval 2.9 to 8.3, in control children). In addition, short-circuit current was increased but conductance was unchanged. After several months on a milk-free diet, HRP flux and short-circuit current returned to control values. Just after the milk challenge and independently of the clinical issue, a slight rise in HRP permeability was observed but it was not significant and remained within control values.(ABSTRACT TRUNCATED AT 250 WORDS)