Author:
Abdelgawad Ahmed,Nicola Teodora,Martin Isaac,Halloran Brian A.,Tanaka Kosuke,Adegboye Comfort Y.,Jain Pankaj,Ren Changchun,Lal Charitharth V.,Ambalavanan Namasivayam,O’Connell Amy E.,Jilling Tamás,Willis Kent A.
Abstract
Abstract
Background
Mammalian mucosal barriers secrete antimicrobial peptides (AMPs) as critical, host-derived regulators of the microbiota. However, mechanisms that support microbiota homeostasis in response to inflammatory stimuli, such as supraphysiologic oxygen, remain unclear.
Results
We show that supraphysiologic oxygen exposure to neonatal mice, or direct exposure of intestinal organoids to supraphysiologic oxygen, suppresses the intestinal expression of AMPs and alters intestinal microbiota composition. Oral supplementation of the prototypical AMP lysozyme to hyperoxia-exposed neonatal mice reduced hyperoxia-induced alterations in their microbiota and was associated with decreased lung injury.
Conclusions
Our results identify a gut-lung axis driven by intestinal AMP expression and mediated by the intestinal microbiota that is linked to lung injury in newborns. Together, these data support that intestinal AMPs modulate lung injury and repair.
Funder
National Heart, Lung, and Blood Institute
National Institute of Diabetes and Digestive and Kidney Diseases
Publisher
Springer Science and Business Media LLC
Subject
Microbiology (medical),Microbiology
Cited by
1 articles.
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