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A murine model of pediatric inflammatory bowel disease causes
microbiota-gut-brain axis deficits in adulthood.
Salvo E, Stokes P, Keogh CE, Brust-Mascher I, Hennessey C, Knotts TA, Sladek JA,
Rude KM, Swedek M, Rabasa G, Gareau MG
Submitted Externally on 9/28/2020
American journal of physiology. Gastrointestinal and liver physiology
Volume : Pages
319 : G361 - G374
Inflammatory bowel diseases (IBDs) are chronic intestinal diseases, frequently
associated with comorbid psychological and cognitive deficits. These
neuropsychiatric effects include anxiety, depression, and memory impairments
that can be seen both during active disease and following remission and are more
frequently seen in pediatric patients. The mechanism(s) through which these
extraintestinal deficits develop remain unknown, and the study of these
phenomenon is hampered by a lack of murine pediatric IBD models. Herein we
describe microbiota-gut-brain (MGB) axis deficits following induction of colitis
in a pediatric setting. Acute colitis was induced by administration of 2%
dextran sodium sulfate (DSS) for 5 days starting at weaning [postnatal day
(P)21] causing reduced weight gain, colonic shortening, and colonic inflammation
by 8 days post-DSS (P29), which were mostly resolved in adult (P56) mice.
Despite resolution of acute disease, cognitive deficits (novel object
recognition task) and anxiety-like behavior (light/dark box) were identified in
the absence of changes in exploratory behavior (open field test) in P56 mice
previously treated with DSS at weaning. Behavioral deficits were found in
conjunction with neuroinflammation, decreased neurogenesis, and altered
expression of pattern recognition receptor genes in the hippocampus.
Additionally, persistent alterations in the gut microbiota composition were
observed at P56, including reduced butyrate-producing species. Taken together,
these results describe for the first time the presence of MGB axis deficits
following induction of colitis at weaning, which persist in adulthood.NEW &
NOTEWORTHY Here we describe long-lasting impacts on the microbiota-gut-brain
(MGB) axis following administration of low-dose dextran sodium sulfate (DSS) to
weaning mice (P21), including gut dysbiosis, colonic inflammation, and
brain/behavioral deficits in adulthood (P56). Early-life DSS leads to acute
colonic inflammation, similar to adult mice; however, it results in long-lasting
deficits in the MGB axis in adulthood (P56), in contrast to the transient
deficits seen in adult DSS. This model highlights the unique features of
pediatric inflammatory bowel disease.
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Financial support for this work was provided by the NIDDK Mouse Metabolic Phenotyping Centers (National MMPC, RRID:SCR_008997,
) under the MICROMouse Program, grants DK076169.
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