Official websites use. Share sensitive information only on official, secure websites. Environmental enteric dysfunction EED is a condition associated with malnutrition that can progress to malabsorption and villous atrophy. Severe EED results in linear growth stunting, slowed neurocognitive development, and unresponsiveness to oral vaccines. Prenatal exposure to malnutrition and breast feeding by malnourished mothers replicates EED.
Pups are characterized by deprivation of secretory IgA SIgA and altered development of the gut immune system and microbiota. Administration of a live biotherapeutic releasing the ATP-degrading enzyme apyrase to malnourished pups restores SIgA levels and ameliorates stunted growth. SIgA is instrumental in improving the growth and intestinal immune competence of mice while they are continuously fed a malnourished diet.
The analysis of microbiota composition suggests that amplification of endogenous SIgA may exert a dominant function in correcting malnourishment dysbiosis and its consequences on host organisms, irrespective of the actual microbial ecology. Keywords: malnutrition, environmental enteric dysfunction, microbiota, breast milk, secretory immunoglobulin, live biotherapeutic, purinergic signaling, mucosal immunity, T follicular helper cell.
Malnourished mothers and offspring are characterized by SIgA impoverishment. An apyrase-releasing live biotherapeutic induces SIgA amplification in pups. Environmental enteric dysfunction EED is a causal factor of stunting and neurocognitive defects in malnourished infants.
Perruzza et al. In , almost million children under 5 years of age were affected by stunting due to living in impoverished environments, Sub-Saharan Africa and Southern Asia comprising more than two-third of affected children.
