Innate immune encounters of the (Type) 4th kind: Brucella

Maarten F. de Jong, Hortensia G. Rolán, Renee M Tsolis

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Summary: In humans, pathogenic Brucella species cause a febrile illness known as brucellosis. A key pathogenic trait of this group of organisms is their ability to survive in immune cells and persist in tissues of the reticuloendothelial system, a process that requires the function of a Type IV secretion system. In contrast to other well-studied Gram-negative bacteria, Brucella spp. do not cause inflammation at the site of invasion, but have a latency period of 2-4 weeks before the onset of symptoms. This review discusses several mechanisms that allow Brucella spp. both to evade detection by pattern recognition receptors of the innate immune system and suppress their signalling. In contrast to these stealth features, the VirB Type IV secretion system, which mediates survival within phagocytic cells, stimulates innate immune responses in vivo. The responses stimulated by this virulence factor are sufficient to check bacterial growth, but not to elicit sterilizing immunity. The result is a stand-off between host and pathogen that results in persistent infection.

Original languageEnglish (US)
Pages (from-to)1195-1202
Number of pages8
JournalCellular Microbiology
Volume12
Issue number9
DOIs
StatePublished - Sep 2010

Fingerprint

Brucella
Pattern Recognition Receptors
Mononuclear Phagocyte System
Brucellosis
Virulence Factors
Phagocytes
Gram-Negative Bacteria
Innate Immunity
Immune System
Immunity
Fever
Inflammation
Survival
Growth
Infection
Type IV Secretion Systems

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Virology

Cite this

Innate immune encounters of the (Type) 4th kind : Brucella. / de Jong, Maarten F.; Rolán, Hortensia G.; Tsolis, Renee M.

In: Cellular Microbiology, Vol. 12, No. 9, 09.2010, p. 1195-1202.

Research output: Contribution to journalArticle

de Jong, Maarten F. ; Rolán, Hortensia G. ; Tsolis, Renee M. / Innate immune encounters of the (Type) 4th kind : Brucella. In: Cellular Microbiology. 2010 ; Vol. 12, No. 9. pp. 1195-1202.
@article{e529e70a6fec4ce79e8103c9151b1143,
title = "Innate immune encounters of the (Type) 4th kind: Brucella",
abstract = "Summary: In humans, pathogenic Brucella species cause a febrile illness known as brucellosis. A key pathogenic trait of this group of organisms is their ability to survive in immune cells and persist in tissues of the reticuloendothelial system, a process that requires the function of a Type IV secretion system. In contrast to other well-studied Gram-negative bacteria, Brucella spp. do not cause inflammation at the site of invasion, but have a latency period of 2-4 weeks before the onset of symptoms. This review discusses several mechanisms that allow Brucella spp. both to evade detection by pattern recognition receptors of the innate immune system and suppress their signalling. In contrast to these stealth features, the VirB Type IV secretion system, which mediates survival within phagocytic cells, stimulates innate immune responses in vivo. The responses stimulated by this virulence factor are sufficient to check bacterial growth, but not to elicit sterilizing immunity. The result is a stand-off between host and pathogen that results in persistent infection.",
author = "{de Jong}, {Maarten F.} and Rol{\'a}n, {Hortensia G.} and Tsolis, {Renee M}",
year = "2010",
month = "9",
doi = "10.1111/j.1462-5822.2010.01498.x",
language = "English (US)",
volume = "12",
pages = "1195--1202",
journal = "Cellular Microbiology",
issn = "1462-5814",
publisher = "Wiley-Blackwell",
number = "9",

}

TY - JOUR

T1 - Innate immune encounters of the (Type) 4th kind

T2 - Brucella

AU - de Jong, Maarten F.

AU - Rolán, Hortensia G.

AU - Tsolis, Renee M

PY - 2010/9

Y1 - 2010/9

N2 - Summary: In humans, pathogenic Brucella species cause a febrile illness known as brucellosis. A key pathogenic trait of this group of organisms is their ability to survive in immune cells and persist in tissues of the reticuloendothelial system, a process that requires the function of a Type IV secretion system. In contrast to other well-studied Gram-negative bacteria, Brucella spp. do not cause inflammation at the site of invasion, but have a latency period of 2-4 weeks before the onset of symptoms. This review discusses several mechanisms that allow Brucella spp. both to evade detection by pattern recognition receptors of the innate immune system and suppress their signalling. In contrast to these stealth features, the VirB Type IV secretion system, which mediates survival within phagocytic cells, stimulates innate immune responses in vivo. The responses stimulated by this virulence factor are sufficient to check bacterial growth, but not to elicit sterilizing immunity. The result is a stand-off between host and pathogen that results in persistent infection.

AB - Summary: In humans, pathogenic Brucella species cause a febrile illness known as brucellosis. A key pathogenic trait of this group of organisms is their ability to survive in immune cells and persist in tissues of the reticuloendothelial system, a process that requires the function of a Type IV secretion system. In contrast to other well-studied Gram-negative bacteria, Brucella spp. do not cause inflammation at the site of invasion, but have a latency period of 2-4 weeks before the onset of symptoms. This review discusses several mechanisms that allow Brucella spp. both to evade detection by pattern recognition receptors of the innate immune system and suppress their signalling. In contrast to these stealth features, the VirB Type IV secretion system, which mediates survival within phagocytic cells, stimulates innate immune responses in vivo. The responses stimulated by this virulence factor are sufficient to check bacterial growth, but not to elicit sterilizing immunity. The result is a stand-off between host and pathogen that results in persistent infection.

UR - http://www.scopus.com/inward/record.url?scp=77957121832&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77957121832&partnerID=8YFLogxK

U2 - 10.1111/j.1462-5822.2010.01498.x

DO - 10.1111/j.1462-5822.2010.01498.x

M3 - Article

C2 - 20670294

AN - SCOPUS:77957121832

VL - 12

SP - 1195

EP - 1202

JO - Cellular Microbiology

JF - Cellular Microbiology

SN - 1462-5814

IS - 9

ER -