Cephalosporins-induced intestinal dysbiosis exacerbated pulmonary endothelial barrier disruption in streptococcus pneumoniae-infected mice
Antibiotic abuse is growing more severe in clinic, and even short-term antibiotic treatment can cause long-term gut dysbiosis, which may promote the development and aggravation of diseases. Cephalosporins as the broad-spectrum antibiotics are widely used for prevention and treatment of community-acq...
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Published in | Frontiers in cellular and infection microbiology Vol. 12; p. 997368 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Frontiers Media S.A
24.08.2022
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Subjects | |
Online Access | Get full text |
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Summary: | Antibiotic abuse is growing more severe in clinic, and even short-term antibiotic treatment can cause long-term gut dysbiosis, which may promote the development and aggravation of diseases. Cephalosporins as the broad-spectrum antibiotics are widely used for prevention and treatment of community-acquired respiratory tract infection in children. However, their potential consequences in health and disease have not been fully elaborated. In this study, the effects of cefaclor, cefdinir and cefixime on intestinal microbiota and lung injury were investigated in
Streptococcus pneumoniae
(Spn)-infected mice. The results showed that the proportion of coccus and bacillus in intestinal microbiota were changed after oral administration with cefaclor, cefdinir and cefixime twice for 10 days, respectively. Compared with the Spn-infected group, the proportion of
Bifidobacterium
and
Lactobacillus
in intestine were significantly reduced, while
Enterococcus
and
Candida
was increased after cephalosporin treatment. Furthermore, 3 cephalosporins could obviously increase the number of total cells, neutrophils and lymphocytes in BALF as well as the serum levels of endotoxin, IL-2, IL-1β, IL-6 and TNF-α. Mechanically, cephalosporins accelerated Spn-induced pulmonary barrier dysfunction
via
mediating the mRNA expressions of endothelial barrier-related proteins (Claudin 5, Occludin, and ZO-1) and inflammation-related proteins (TLR4, p38 and NF-κB). However, all of those consequences could be partly reversed by
Bifidobacterium bifidum
treatment, which was closely related to the elevated acetate production, indicating the protective effects of probiotic against antibiotic-induced intestinal dysbiosis. Therefore, the present study demonstrated that oral administration with cephalosporins not only disrupted intestinal microecological homeostasis, but also increased the risk of Spn infection, resulting in severer respiratory inflammation and higher bacterial loads in mice. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Reviewed by: Dan-Li Xie, Wenzhou Medical University, China; Longhuan Ma, University of Florida, United States; Kai Wang, Chinese Academy of Agricultural Sciences (CAAS), China Edited by: Ping Li, Zhejiang Gongshang University, China These authors have contributed equally to this work This article was submitted to Intestinal Microbiome, a section of the journal Frontiers in Cellular and Infection Microbiology |
ISSN: | 2235-2988 2235-2988 |
DOI: | 10.3389/fcimb.2022.997368 |