Host restriction of Salmonella enterica serotype typhi is not caused by functional alteration of SipA, SopB, or SopB

Manuela Raffatellu, Yao Hui Sun, R. Paul Wilson, Quynh T. Tran, Daniela Chessa, Helene L. Andrews-Polymenis, Sara D. Lawhon, Josely F. Figueiredo, Renee M Tsolis, L. Garry Adams, Andreas J Baumler

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Salmonella enterica serotype Typhi is a strictly human adapted pathogen that does not cause disease in nonprimate vertebrate hosts, while Salmonella enterica serotype Typhimurium is a broad-host-range pathogen. Serotype Typhi lacks some of the proteins (effectors) exported by the invasion-associated type III secretion system that are required by serotype Typhimurium for eliciting fluid secretion and inflammation in bovine ligated ileal loops. We investigated whether the remaining serotype Typhi effectors implicated in enteropathogenicity (SipA, SopB, and SopD) are functionally exchangeable with their serotype Typhimurium homologues. Serotype Typhi elicited fluid accumulation in bovine ligated ileal loops at levels similar to those elicited by a noninvasive serotype Typhimurium strain (the sipA sopABDE2 mutant) or by sterile culture medium. However, introduction of the cloned serotype Typhi sipA, sopB, and sopD genes complemented the ability of a serotype Typhimurium sipA sopABDE2 mutant to elicit fluid secretion in bovine ligated ileal loops. Introduction of the cloned serotype Typhi sipA, sopB, and sopD genes increased the invasiveness of a serotype Typhimurium sipA sopABDE2 mutant for human colon carcinoma epithelial (HT-29 and T84) cells and bovine kidney (MDBK) cells. Translational fusions between the mature TEM-1 β-lactamase reporter and SipA or SopD demonstrated that serotype Typhi translocates these effectors into host cells. We conclude that the inability of serotype Typhi to cause fluid accumulation in bovine ligated ileal loops is not caused by a functional alteration of its SipA, SopB, and SopD effector proteins with respect to their serotype Typhimurium homologues.

Original languageEnglish (US)
Pages (from-to)7817-7826
Number of pages10
JournalInfection and Immunity
Volume73
Issue number12
DOIs
StatePublished - Dec 2005

Fingerprint

Salmonella enterica
Fluids and Secretions
Serogroup
HT29 Cells
Host Specificity
Genes

ASJC Scopus subject areas

  • Immunology

Cite this

Host restriction of Salmonella enterica serotype typhi is not caused by functional alteration of SipA, SopB, or SopB. / Raffatellu, Manuela; Sun, Yao Hui; Wilson, R. Paul; Tran, Quynh T.; Chessa, Daniela; Andrews-Polymenis, Helene L.; Lawhon, Sara D.; Figueiredo, Josely F.; Tsolis, Renee M; Adams, L. Garry; Baumler, Andreas J.

In: Infection and Immunity, Vol. 73, No. 12, 12.2005, p. 7817-7826.

Research output: Contribution to journalArticle

Raffatellu, M, Sun, YH, Wilson, RP, Tran, QT, Chessa, D, Andrews-Polymenis, HL, Lawhon, SD, Figueiredo, JF, Tsolis, RM, Adams, LG & Baumler, AJ 2005, 'Host restriction of Salmonella enterica serotype typhi is not caused by functional alteration of SipA, SopB, or SopB', Infection and Immunity, vol. 73, no. 12, pp. 7817-7826. https://doi.org/10.1128/IAI.73.12.7817-7826.2005
Raffatellu, Manuela ; Sun, Yao Hui ; Wilson, R. Paul ; Tran, Quynh T. ; Chessa, Daniela ; Andrews-Polymenis, Helene L. ; Lawhon, Sara D. ; Figueiredo, Josely F. ; Tsolis, Renee M ; Adams, L. Garry ; Baumler, Andreas J. / Host restriction of Salmonella enterica serotype typhi is not caused by functional alteration of SipA, SopB, or SopB. In: Infection and Immunity. 2005 ; Vol. 73, No. 12. pp. 7817-7826.
@article{7edc913f3ad84856a16bab0137b85b93,
title = "Host restriction of Salmonella enterica serotype typhi is not caused by functional alteration of SipA, SopB, or SopB",
abstract = "Salmonella enterica serotype Typhi is a strictly human adapted pathogen that does not cause disease in nonprimate vertebrate hosts, while Salmonella enterica serotype Typhimurium is a broad-host-range pathogen. Serotype Typhi lacks some of the proteins (effectors) exported by the invasion-associated type III secretion system that are required by serotype Typhimurium for eliciting fluid secretion and inflammation in bovine ligated ileal loops. We investigated whether the remaining serotype Typhi effectors implicated in enteropathogenicity (SipA, SopB, and SopD) are functionally exchangeable with their serotype Typhimurium homologues. Serotype Typhi elicited fluid accumulation in bovine ligated ileal loops at levels similar to those elicited by a noninvasive serotype Typhimurium strain (the sipA sopABDE2 mutant) or by sterile culture medium. However, introduction of the cloned serotype Typhi sipA, sopB, and sopD genes complemented the ability of a serotype Typhimurium sipA sopABDE2 mutant to elicit fluid secretion in bovine ligated ileal loops. Introduction of the cloned serotype Typhi sipA, sopB, and sopD genes increased the invasiveness of a serotype Typhimurium sipA sopABDE2 mutant for human colon carcinoma epithelial (HT-29 and T84) cells and bovine kidney (MDBK) cells. Translational fusions between the mature TEM-1 β-lactamase reporter and SipA or SopD demonstrated that serotype Typhi translocates these effectors into host cells. We conclude that the inability of serotype Typhi to cause fluid accumulation in bovine ligated ileal loops is not caused by a functional alteration of its SipA, SopB, and SopD effector proteins with respect to their serotype Typhimurium homologues.",
author = "Manuela Raffatellu and Sun, {Yao Hui} and Wilson, {R. Paul} and Tran, {Quynh T.} and Daniela Chessa and Andrews-Polymenis, {Helene L.} and Lawhon, {Sara D.} and Figueiredo, {Josely F.} and Tsolis, {Renee M} and Adams, {L. Garry} and Baumler, {Andreas J}",
year = "2005",
month = "12",
doi = "10.1128/IAI.73.12.7817-7826.2005",
language = "English (US)",
volume = "73",
pages = "7817--7826",
journal = "Infection and Immunity",
issn = "0019-9567",
publisher = "American Society for Microbiology",
number = "12",

}

TY - JOUR

T1 - Host restriction of Salmonella enterica serotype typhi is not caused by functional alteration of SipA, SopB, or SopB

AU - Raffatellu, Manuela

AU - Sun, Yao Hui

AU - Wilson, R. Paul

AU - Tran, Quynh T.

AU - Chessa, Daniela

AU - Andrews-Polymenis, Helene L.

AU - Lawhon, Sara D.

AU - Figueiredo, Josely F.

AU - Tsolis, Renee M

AU - Adams, L. Garry

AU - Baumler, Andreas J

PY - 2005/12

Y1 - 2005/12

N2 - Salmonella enterica serotype Typhi is a strictly human adapted pathogen that does not cause disease in nonprimate vertebrate hosts, while Salmonella enterica serotype Typhimurium is a broad-host-range pathogen. Serotype Typhi lacks some of the proteins (effectors) exported by the invasion-associated type III secretion system that are required by serotype Typhimurium for eliciting fluid secretion and inflammation in bovine ligated ileal loops. We investigated whether the remaining serotype Typhi effectors implicated in enteropathogenicity (SipA, SopB, and SopD) are functionally exchangeable with their serotype Typhimurium homologues. Serotype Typhi elicited fluid accumulation in bovine ligated ileal loops at levels similar to those elicited by a noninvasive serotype Typhimurium strain (the sipA sopABDE2 mutant) or by sterile culture medium. However, introduction of the cloned serotype Typhi sipA, sopB, and sopD genes complemented the ability of a serotype Typhimurium sipA sopABDE2 mutant to elicit fluid secretion in bovine ligated ileal loops. Introduction of the cloned serotype Typhi sipA, sopB, and sopD genes increased the invasiveness of a serotype Typhimurium sipA sopABDE2 mutant for human colon carcinoma epithelial (HT-29 and T84) cells and bovine kidney (MDBK) cells. Translational fusions between the mature TEM-1 β-lactamase reporter and SipA or SopD demonstrated that serotype Typhi translocates these effectors into host cells. We conclude that the inability of serotype Typhi to cause fluid accumulation in bovine ligated ileal loops is not caused by a functional alteration of its SipA, SopB, and SopD effector proteins with respect to their serotype Typhimurium homologues.

AB - Salmonella enterica serotype Typhi is a strictly human adapted pathogen that does not cause disease in nonprimate vertebrate hosts, while Salmonella enterica serotype Typhimurium is a broad-host-range pathogen. Serotype Typhi lacks some of the proteins (effectors) exported by the invasion-associated type III secretion system that are required by serotype Typhimurium for eliciting fluid secretion and inflammation in bovine ligated ileal loops. We investigated whether the remaining serotype Typhi effectors implicated in enteropathogenicity (SipA, SopB, and SopD) are functionally exchangeable with their serotype Typhimurium homologues. Serotype Typhi elicited fluid accumulation in bovine ligated ileal loops at levels similar to those elicited by a noninvasive serotype Typhimurium strain (the sipA sopABDE2 mutant) or by sterile culture medium. However, introduction of the cloned serotype Typhi sipA, sopB, and sopD genes complemented the ability of a serotype Typhimurium sipA sopABDE2 mutant to elicit fluid secretion in bovine ligated ileal loops. Introduction of the cloned serotype Typhi sipA, sopB, and sopD genes increased the invasiveness of a serotype Typhimurium sipA sopABDE2 mutant for human colon carcinoma epithelial (HT-29 and T84) cells and bovine kidney (MDBK) cells. Translational fusions between the mature TEM-1 β-lactamase reporter and SipA or SopD demonstrated that serotype Typhi translocates these effectors into host cells. We conclude that the inability of serotype Typhi to cause fluid accumulation in bovine ligated ileal loops is not caused by a functional alteration of its SipA, SopB, and SopD effector proteins with respect to their serotype Typhimurium homologues.

UR - http://www.scopus.com/inward/record.url?scp=28444443764&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=28444443764&partnerID=8YFLogxK

U2 - 10.1128/IAI.73.12.7817-7826.2005

DO - 10.1128/IAI.73.12.7817-7826.2005

M3 - Article

C2 - 16299271

AN - SCOPUS:28444443764

VL - 73

SP - 7817

EP - 7826

JO - Infection and Immunity

JF - Infection and Immunity

SN - 0019-9567

IS - 12

ER -