Avian intestinal ultrastructure changes provide insight into the pathogenesis of enteric diseases and probiotic mode of action

Epithelial damage and loss of barrier integrity occur following intestinal infections in humans and animals. Gut health was evaluated by electron microscopy in an avian model that exposed birds to subclinical necrotic enteritis (NE) and fed them a diet supplemented with the probiotic Bacillus amylol...

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Veröffentlicht in:Scientific reports 2021-01, Vol.11 (1), p.167-167, Article 167
Hauptverfasser: Shini, Shaniko, Aland, R. Claire, Bryden, Wayne L.
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Sprache:eng
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Zusammenfassung:Epithelial damage and loss of barrier integrity occur following intestinal infections in humans and animals. Gut health was evaluated by electron microscopy in an avian model that exposed birds to subclinical necrotic enteritis (NE) and fed them a diet supplemented with the probiotic Bacillus amyloliquefaciens strain H57 (H57). Scanning electron microscopy of ileal mucosa revealed significant villus damage, including focal erosions of epithelial cells and villous atrophy, while transmission electron microscopy demonstrated severe enterocyte damage and loss of cellular integrity in NE-exposed birds. In particular, mitochondria were morphologically altered, appearing irregular in shape or swollen, and containing electron-lucent regions of matrix and damaged cristae. Apical junctional complexes between adjacent enterocytes were significantly shorter, and the adherens junction was saccular, suggesting loss of epithelial integrity in NE birds. Segmented filamentous bacteria attached to villi, which play an important role in intestinal immunity, were more numerous in birds exposed to NE. The results suggest that mitochondrial damage may be an important initiator of NE pathogenesis, while H57 maintains epithelium and improves the integrity of intestinal mucosa. Potential actions of H57 are discussed that further define the mechanisms responsible for probiotic bacteria’s role in maintaining gut health.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-020-80714-2