Abstract
Escherichia coli (E. coli) infection is very common among
young growing animals, and zinc supplementation is often
used to alleviate inflammation induced by this disease. Therefore,
the objective of this study was to evaluate whether chitosan-
chelated zinc (CS-Zn) supplementation could attenuate
gut injury induced by E. coli challenge and to explore how CSZn
modulates cecal microbiota and alleviates intestinal inflammation
in weaned rats challenged with E. coli. 36 weaned
rats (55.65 ± 2.18 g of BW, n = 12) were divided into three
treatment groups consisting of unchallenged rats fed a basal
diet (Control) and two groups of rats challenged with E. coli
and fed a basal diet or a diet containing 640 mg/kg CS-Zn
(E. coli + CS-Zn, containing 50 mg/kg Zn) for a 14-day experiment.
On days 10 to 12, each rat was given 4 ml of E. coli
solution with a total bacteria count of 1010 CFU by oral gavage
daily or normal saline of equal dosage. CS-Zn supplementation
mitigated intestinal morphology impairment (e.g.
higher crypt depth and lower macroscopic damage index)
induced by E. coli challenge (P < 0.05), and alleviated the increase
of Myeloperoxidase (MPO) activity after E. coli challenge
(P < 0.05). 16S rRNA sequencing analyses revealed that
E. coli challenge significantly increased the abundance of Verrucomicrobia
and E. coli (P < 0.05). However, CS-Zn supplementation
increased the abundance of Lactobacillus and decreased
the relative abundance of Proteobacteria, Desulfovibrio
and E. coli (P < 0.05). The concentrations of butyrate in
the cecal digesta, which decreased due to the challenge, were
higher in the E. coli + CS-Zn group (P < 0.05). In addition,
CS-Zn supplementation significantly prevented the elevation
of pro-inflammatory cytokines IL-6 concentration and upregulated
the level of anti-inflammatory cytokines IL-10 in
cecal mucosa induced by E. coli infection (P < 0.05). In conclusion,
these results indicate that CS-Zn produces beneficial
effects in alleviating gut mucosal injury of E. coli challenged
rats by enhancing the intestinal morphology and modulating
cecal bacterial composition, as well as attenuating inflammatory
response.
Citations
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