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Protection from environmental enteric dysfunction and growth improvement in malnourished newborns by amplification of secretory IgA

ABSTRACT: Protection from environmental enteric dysfunction and growth improvement in malnourished newborns by amplification of secretory IgA

PROVIDER: PRJEB68326 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR12259302_1.fastq.gz	Fastqsanger.gz
	ERR12259302_2.fastq.gz	Fastqsanger.gz
	ERR12259303_1.fastq.gz	Fastqsanger.gz
	ERR12259303_2.fastq.gz	Fastqsanger.gz
	ERR12259304_1.fastq.gz	Fastqsanger.gz

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Apyrase-mediated amplification of secretory IgA promotes intestinal homeostasis

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Protection from environmental enteric dysfunction and growth improvement in malnourished newborns by amplification of secretory IgA.

Project description: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. Extracellular ATP (eATP) released by microbiota limits T follicular helper (Tfh) cell activity and SIgA generation in Peyer's patches (PPs). 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.

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Apyrase-mediated amplification of secretory IgA promotes intestinal homeostasis

Project description:Morphogenesis of epithelial tissues relies on the precise developmental control of cell polarity and architecture. In the early Drosophila embryo, the primarSecretory IgA (SIgA) interaction with commensal bacteria regulates the composition and function of the microbiota, contributing to gut ecosystem homeostasis. However, mechanisms regulating the reciprocal control of microbiota and SIgA are not defined. Bacteria-derived ATP limits T follicular helper (Tfh) cells activity in the Peyer’s patches (Pps) of the small intestine via the P2X7 receptor and thereby SIgA generation. Here we show that inhibition of bacteria derived ATP signaling by delivery of the ATP-degrading enzyme apyrase to the intestine results in the amplification of the SIgA repertoire. The enhanced breadth of SIgA in mice colonized with apyrase-releasing E. Coli conditioned topographical distribution of bacteria and expression of genes involved in metabolic versus immune functions in the intestinal epithelium. SIgA mediated conditioning of bacteria and enterocyte function was also reflected by selective differences in nutrients absorption in mice colonized with apyrase expressing bacteria. Hydrolysis of bacteria derived ATP was particularly helpful in restoring intestinal homeostasis via SIgA in antibiotics induced dysbiosis. Administration of apyrase expressing bacteria attenuated intestinal barrier impairment, glucose metabolism perturbation and susceptibility to infection by enteric pathogens induced by antibiotic treatments. Therefore, microbiota derived ATP regulates SIgA, and amplification of SIgA response by apyrase can be leveraged to restore intestinal fitness in dysbiotic conditions.y epithelium forms during cellularisation, following a tightly controlled genetic programme where specific sets of genes are up-regulated. Some of them, for instance, control membrane invagination between the nuclei anchored at the apical surface of the syncytium.

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