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Advances in ETEC Virulence, New Adjuvants, and Vaccine Development

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 4440

Special Issue Editors


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Guest Editor
College of Veterinary Medicine, Yangzhou University, Yangzhou, China
Interests: ETEC; STEC; flagellin; enterotoxin; new adjuvant; vaccines; host-pathogen interaction

E-Mail Website
Co-Guest Editor
College of Veterinary Medicine, Yangzhou University, Yangzhou, China
Interests: ETEC; Salmonella; vaccines; innate immunity; adjuvant

Special Issue Information

Dear Colleagues,

Enterotoxigenic Escherichia coli (ETEC) strains remain a leading cause of diarrhea in young children and livestock. Adhesins and enterotoxins are known to be required for ETEC infection; however, how these interactions between virulence factors and hosts occur, and the mechanisms of host immune systems are poorly understood. In addition, the heterogeneity of ETEC bacterial virulence factors is a major challenge for the development of a broadly protective vaccine. The aim of this Special Issue is to present the recent advances in this field and cover all topics concerning the molecular pathogenesis, virulence determinants, and control strategies of pathogenic E. coli, addressing topics that include but are not limited to: the molecular mechanism of virulence factors, newfound virulence factors contributing to ETEC infection, the mechanisms of invading the host immune system, host-pathogen interactions, new broadly protective vaccines, and new adjuvants applied in ETEC vaccines.

Prof. Dr. Qiangde Duan
Prof. Dr. Guoqiang Zhu
Guest Editors

Manuscript Submission Information

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Keywords

  • ETEC
  • virulence factors
  • adhesins
  • enterotoxins
  • innate immune
  • host-pathogen interaction
  • vaccines
  • adjuvant

Published Papers (2 papers)

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Research

17 pages, 2653 KiB  
Article
Both LTA and LTB Subunits Are Equally Important to Heat-Labile Enterotoxin (LT)-Enhanced Bacterial Adherence
by Qiangde Duan, Shengmei Pang, Lili Feng, Baoliang Li, Linfen Lv, Yuxuan Liang and Guoqiang Zhu
Int. J. Mol. Sci. 2023, 24(2), 1245; https://doi.org/10.3390/ijms24021245 - 8 Jan 2023
Cited by 1 | Viewed by 1698
Abstract
There is increasing evidence indicating that the production of heat-labile enterotoxin (LT) enhances bacterial adherence within in vitro and in vivo models. However, which subunit plays the main role, and the precise regulatory mechanisms remain unclear. To further elucidate the contribution of the [...] Read more.
There is increasing evidence indicating that the production of heat-labile enterotoxin (LT) enhances bacterial adherence within in vitro and in vivo models. However, which subunit plays the main role, and the precise regulatory mechanisms remain unclear. To further elucidate the contribution of the A subunit of LT (LTA) and the B subunit of LT (LTB) in LT-enhanced bacterial adherence, we generated several LT mutants where their ADP-ribosylation activity or GM1 binding ability was impaired and evaluated their abilities to enhance the two LT-deficient E. coli strains (1836-2 and EcNc) adherence. Our results showed that the two LT-deficient strains, expressing either the native LT or LT derivatives, had a significantly greater number of adhesions to host cells than the parent strains. The adherence abilities of strains expressing the LT mutants were significantly reduced compared with the strains expressing the native LT. Moreover, E. coli 1836-2 and EcNc strains when exogenously supplied with cyclic AMP (cAMP) highly up-regulated the adhesion molecules expression and improved their adherence abilities. Ganglioside GM1, the receptor for LTB subunit, is enriched in lipid rafts. The results showed that deletion of cholesterol from cells also significantly decreased the ability of LT to enhance bacterial adherence. Overall, our data indicated that both subunits are equally responsible for LT-enhanced bacterial adherence, the LTA subunit contributes to this process mainly by increasing bacterial adhesion molecules expression, while LTB subunit mainly by mediating the initial interaction with the GM1 receptors of host cells. Full article
(This article belongs to the Special Issue Advances in ETEC Virulence, New Adjuvants, and Vaccine Development)
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19 pages, 4187 KiB  
Article
Whole Genome Sequencing and CRISPR/Cas9 Gene Editing of Enterotoxigenic Escherichia coli BE311 for Fluorescence Labeling and Enterotoxin Analyses
by Shuang Lu, Ting Tao, Yating Su, Jia Hu, Li Zhang, Guoliang Wang, Xiangyu Li and Xiaohua Guo
Int. J. Mol. Sci. 2022, 23(14), 7502; https://doi.org/10.3390/ijms23147502 - 6 Jul 2022
Cited by 6 | Viewed by 2284
Abstract
Some prevention strategies, including vaccines and antibiotic alternatives, have been developed to reduce enterotoxigenic Escherichia coli proliferation in animal production. In this study, a wild-type strain of BE311 with a virulent heat-stable enterotoxin gene identical to E. coli K99 was isolated for its [...] Read more.
Some prevention strategies, including vaccines and antibiotic alternatives, have been developed to reduce enterotoxigenic Escherichia coli proliferation in animal production. In this study, a wild-type strain of BE311 with a virulent heat-stable enterotoxin gene identical to E. coli K99 was isolated for its high potential for gene expression ability. The whole genome of E. coli BE311 was sequenced for gene analyses and editing. Subsequently, the fluorescent gene mCherry was successfully knocked into the genome of E. coli BE311 by CRISPR/Cas9. The E. coli BE311–mCherry strain was precisely quantified through the fluorescence intensity and red colony counting. The inflammatory factors in different intestinal tissues all increased significantly after an E. coli BE311–mCherry challenge in Sprague–Dawley rats (p < 0.05). The heat-stable enterotoxin gene of E. coli BE311 was knocked out, and an attenuated vaccine host E. coli BE311-STKO was constructed. Flow cytometry showed apoptotic cell numbers were lower following a challenge of IPEC-J2 cells with E. coli BE311-STKO than with E. coli BE311. Therefore, the E. coli BE311–mCherry and E. coli BE311-STKO strains that were successfully constructed based on the gene knock-in and knock-out technology could be used as ideal candidates in ETEC challenge models and for the development of attenuated vaccines. Full article
(This article belongs to the Special Issue Advances in ETEC Virulence, New Adjuvants, and Vaccine Development)
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