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Non-pathogenic Escherichia coli Enhance Stx2a Production of E. coli O157:H7 Through Both bamA-Dependent and Independent Mechanisms.
Front Microbiol. 2018; 9:1325.FM

Abstract

Intestinal colonization by the foodborne pathogen Escherichia coli O157:H7 leads to serious disease symptoms, including hemolytic uremic syndrome (HUS) and hemorrhagic colitis (HC). Synthesis of one or more Shiga toxins (Stx) is essential for HUS and HC development. The genes encoding Stx, including Stx2a, are found within a lambdoid prophage integrated in the E. coli O157:H7 chromosome. Enhanced Stx2a expression was reported when specific non-pathogenic E. coli strains were co-cultured with E. coli O157:H7, and it was hypothesized that this phenotype required the non-pathogenic E. coli to be sensitive to stx-converting phage infection. We tested this hypothesis by generating phage resistant non-pathogenic E. coli strains where bamA (an essential gene and Stx phage receptor) was replaced with an ortholog from other species. Such heterologous gene replacement abolished the ability of the laboratory strain E. coli C600 to enhance toxin production when co-cultured with E. coli O157:H7 strain PA2, which belongs to the hypervirulent clade 8. The extracellular loops of BamA (loop 4, 6, 7) were further shown to be important for infection by stx2a-converting phages. However, similar gene replacement in another commensal E. coli, designated 1.1954, revealed a bamA-independent mechanism for toxin amplification. Toxin enhancement by 1.1954 was not the result of phage infection through an alternative receptor (LamB or FadL), lysogen formation by stx2a-converting phages, or the production of a secreted molecule. Collectively, these data suggest that non-pathogenic E. coli can enhance toxin production through at least two mechanisms.

Authors+Show Affiliations

Department of Food Science, The Pennsylvania State University, University Park, PA, United States.Huck Institutes of Life Sciences, The Pennsylvania State University, University Park, PA, United States.Department of Food Science, The Pennsylvania State University, University Park, PA, United States.Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, Santa Barbara, CA, United States.Department of Food Science, The Pennsylvania State University, University Park, PA, United States. Center for Immunology and Infectious Disease, The Pennsylvania State University, University Park, PA, United States.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29973923

Citation

Xiaoli, Lingzi, et al. "Non-pathogenic Escherichia Coli Enhance Stx2a Production of E. Coli O157:H7 Through Both bamA-Dependent and Independent Mechanisms." Frontiers in Microbiology, vol. 9, 2018, p. 1325.
Xiaoli L, Figler HM, Goswami Banerjee K, et al. Non-pathogenic Escherichia coli Enhance Stx2a Production of E. coli O157:H7 Through Both bamA-Dependent and Independent Mechanisms. Front Microbiol. 2018;9:1325.
Xiaoli, L., Figler, H. M., Goswami Banerjee, K., Hayes, C. S., & Dudley, E. G. (2018). Non-pathogenic Escherichia coli Enhance Stx2a Production of E. coli O157:H7 Through Both bamA-Dependent and Independent Mechanisms. Frontiers in Microbiology, 9, 1325. https://doi.org/10.3389/fmicb.2018.01325
Xiaoli L, et al. Non-pathogenic Escherichia Coli Enhance Stx2a Production of E. Coli O157:H7 Through Both bamA-Dependent and Independent Mechanisms. Front Microbiol. 2018;9:1325. PubMed PMID: 29973923.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Non-pathogenic Escherichia coli Enhance Stx2a Production of E. coli O157:H7 Through Both bamA-Dependent and Independent Mechanisms. AU - Xiaoli,Lingzi, AU - Figler,Hillary M, AU - Goswami Banerjee,Kakolie, AU - Hayes,Christopher S, AU - Dudley,Edward G, Y1 - 2018/06/15/ PY - 2018/03/20/received PY - 2018/05/30/accepted PY - 2018/7/6/entrez PY - 2018/7/6/pubmed PY - 2018/7/6/medline KW - BamA KW - E. coli O157:H7 KW - Shiga toxin KW - Stx2a KW - commensal E. coli SP - 1325 EP - 1325 JF - Frontiers in microbiology JO - Front Microbiol VL - 9 N2 - Intestinal colonization by the foodborne pathogen Escherichia coli O157:H7 leads to serious disease symptoms, including hemolytic uremic syndrome (HUS) and hemorrhagic colitis (HC). Synthesis of one or more Shiga toxins (Stx) is essential for HUS and HC development. The genes encoding Stx, including Stx2a, are found within a lambdoid prophage integrated in the E. coli O157:H7 chromosome. Enhanced Stx2a expression was reported when specific non-pathogenic E. coli strains were co-cultured with E. coli O157:H7, and it was hypothesized that this phenotype required the non-pathogenic E. coli to be sensitive to stx-converting phage infection. We tested this hypothesis by generating phage resistant non-pathogenic E. coli strains where bamA (an essential gene and Stx phage receptor) was replaced with an ortholog from other species. Such heterologous gene replacement abolished the ability of the laboratory strain E. coli C600 to enhance toxin production when co-cultured with E. coli O157:H7 strain PA2, which belongs to the hypervirulent clade 8. The extracellular loops of BamA (loop 4, 6, 7) were further shown to be important for infection by stx2a-converting phages. However, similar gene replacement in another commensal E. coli, designated 1.1954, revealed a bamA-independent mechanism for toxin amplification. Toxin enhancement by 1.1954 was not the result of phage infection through an alternative receptor (LamB or FadL), lysogen formation by stx2a-converting phages, or the production of a secreted molecule. Collectively, these data suggest that non-pathogenic E. coli can enhance toxin production through at least two mechanisms. SN - 1664-302X UR - https://www.unboundmedicine.com/medline/citation/29973923/Non_pathogenic_Escherichia_coli_Enhance_Stx2a_Production_of_E__coli_O157:H7_Through_Both_bamA_Dependent_and_Independent_Mechanisms_ L2 - https://doi.org/10.3389/fmicb.2018.01325 DB - PRIME DP - Unbound Medicine ER -
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