Salmonella Typhimurium and inflammation: a pathogen-centric affair

Microbial infections are controlled by host inflammatory responses that are initiated by innate immune receptors after recognition of conserved microbial products. As inflammation can also lead to disease, tissues that are exposed to microbial products such as the intestinal epithelium are subject t...

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Published inNature reviews. Microbiology Vol. 19; no. 11; pp. 716 - 725
Main Author Galán, Jorge E.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.11.2021
Nature Publishing Group
Subjects
631/250/254
631/326/421
631/326/88
Animals
Biomedical and Life Sciences
Coevolution
Development and progression
Epithelium
Homeostasis
Host-bacteria relationships
Host-Pathogen Interactions
Humans
Infectious Diseases
Inflammation
Inflammation - microbiology
Inflammation - pathology
Inflammatory response
Intestine
Life Sciences
Medical Microbiology
Microbiology
Microorganisms
Parasitology
Pathogens
Physiological aspects
Proteins
Receptors
Regulatory mechanisms (biology)
Review Article
Salmonella
Salmonella enterica
Salmonella Infections - microbiology
Salmonella Infections - pathology
Salmonella typhimurium
Salmonella typhimurium - metabolism
Salmonellosis
Virology
United States
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Abstract Microbial infections are controlled by host inflammatory responses that are initiated by innate immune receptors after recognition of conserved microbial products. As inflammation can also lead to disease, tissues that are exposed to microbial products such as the intestinal epithelium are subject to stringent regulatory mechanisms to prevent indiscriminate signalling through innate immune receptors. The enteric pathogen Salmonella enterica subsp. enterica serovar Typhimurium, which requires intestinal inflammation to sustain its replication in the intestinal tract, uses effector proteins of its type III secretion systems to trigger an inflammatory response without the engagement of innate immune receptors. Furthermore, S . Typhimurium uses a different set of effectors to restrict the inflammatory response to preserve host homeostasis. The S . Typhimurium–host interface is a remarkable example of the unique balance that emerges from the co-evolution of a pathogen and its host. In this Review, Galán discusses the mechanisms by which Salmonella enterica subsp. enterica serovar Typhimurium triggers inflammation in the intestinal tract through the activities of effector proteins as well as the mechanisms that are aimed at recovering host homeostasis after the inflammatory response.
AbstractList Microbial infections are controlled by host inflammatory responses that are initiated by innate immune receptors after recognition of conserved microbial products. As inflammation can also lead to disease, tissues that are exposed to microbial products such as the intestinal epithelium are subject to stringent regulatory mechanisms to prevent indiscriminate signalling through innate immune receptors. The enteric pathogen Salmonella enterica subsp. enterica serovar Typhimurium, which requires intestinal inflammation to sustain its replication in the intestinal tract, uses effector proteins of its type III secretion systems to trigger an inflammatory response without the engagement of innate immune receptors. Furthermore, S. Typhimurium uses a different set of effectors to restrict the inflammatory response to preserve host homeostasis. The S. Typhimurium-host interface is a remarkable example of the unique balance that emerges from the co-evolution of a pathogen and its host.Microbial infections are controlled by host inflammatory responses that are initiated by innate immune receptors after recognition of conserved microbial products. As inflammation can also lead to disease, tissues that are exposed to microbial products such as the intestinal epithelium are subject to stringent regulatory mechanisms to prevent indiscriminate signalling through innate immune receptors. The enteric pathogen Salmonella enterica subsp. enterica serovar Typhimurium, which requires intestinal inflammation to sustain its replication in the intestinal tract, uses effector proteins of its type III secretion systems to trigger an inflammatory response without the engagement of innate immune receptors. Furthermore, S. Typhimurium uses a different set of effectors to restrict the inflammatory response to preserve host homeostasis. The S. Typhimurium-host interface is a remarkable example of the unique balance that emerges from the co-evolution of a pathogen and its host.
Microbial infections are most often controlled by host inflammatory responses that are initiated by innate immune receptors after recognition of conserved microbial products. As inflammation can also lead to pathology, tissues that are exposed to microbial products such as the intestinal epithelium, are subject to stringent regulatory mechanisms to prevent indiscriminate signaling through innate immune receptors. The enteric pathogen Salmonella Typhimurium, which requires intestinal inflammation to sustain its replication in the intestinal tract, uses effector proteins of its type III secretion systems to trigger an inflammatory response without the engagement of innate immune receptors. Furthermore, Salmonella Typhimurium utilizes a different set of effectors to restrict the inflammatory response in order to preserve the host’s homeostasis. The Salmonella -host interface is a remarkable example of the unique balance that emerges from the co-evolution of a pathogen and its host.
Microbial infections are controlled by host inflammatory responses that are initiated by innate immune receptors after recognition of conserved microbial products. As inflammation can also lead to disease, tissues that are exposed to microbial products such as the intestinal epithelium are subject to stringent regulatory mechanisms to prevent indiscriminate signalling through innate immune receptors. The enteric pathogen Salmonella enterica subsp. enterica serovar Typhimurium, which requires intestinal inflammation to sustain its replication in the intestinal tract, uses effector proteins of its type III secretion systems to trigger an inflammatory response without the engagement of innate immune receptors. Furthermore, S. Typhimurium uses a different set of effectors to restrict the inflammatory response to preserve host homeostasis. The S. Typhimurium-host interface is a remarkable example of the unique balance that emerges from the co-evolution of a pathogen and its host.
Microbial infections are controlled by host inflammatory responses that are initiated by innate immune receptors after recognition of conserved microbial products. As inflammation can also lead to disease, tissues that are exposed to microbial products such as the intestinal epithelium are subject to stringent regulatory mechanisms to prevent indiscriminate signalling through innate immune receptors. The enteric pathogen Salmonella enterica subsp. enterica serovar Typhimurium, which requires intestinal inflammation to sustain its replication in the intestinal tract, uses effector proteins of its type III secretion systems to trigger an inflammatory response without the engagement of innate immune receptors. Furthermore, S. Typhimurium uses a different set of effectors to restrict the inflammatory response to preserve host homeostasis. The S. Typhimurium-host interface is a remarkable example of the unique balance that emerges from the co-evolution of a pathogen and its host. In this Review, Galán discusses the mechanisms by which Salmonella enterica subsp. enterica serovar Typhimurium triggers inflammation in the intestinal tract through the activities of effector proteins as well as the mechanisms that are aimed at recovering host homeostasis after the inflammatory response.
Microbial infections are controlled by host inflammatory responses that are initiated by innate immune receptors after recognition of conserved microbial products. As inflammation can also lead to disease, tissues that are exposed to microbial products such as the intestinal epithelium are subject to stringent regulatory mechanisms to prevent indiscriminate signalling through innate immune receptors. The enteric pathogen Salmonella enterica subsp. enterica serovar Typhimurium, which requires intestinal inflammation to sustain its replication in the intestinal tract, uses effector proteins of its type III secretion systems to trigger an inflammatory response without the engagement of innate immune receptors. Furthermore, S . Typhimurium uses a different set of effectors to restrict the inflammatory response to preserve host homeostasis. The S . Typhimurium–host interface is a remarkable example of the unique balance that emerges from the co-evolution of a pathogen and its host. In this Review, Galán discusses the mechanisms by which Salmonella enterica subsp. enterica serovar Typhimurium triggers inflammation in the intestinal tract through the activities of effector proteins as well as the mechanisms that are aimed at recovering host homeostasis after the inflammatory response.
Audience Academic
Author Galán, Jorge E.
Author_xml – sequence: 1
  givenname: Jorge E.
  orcidid: 0000-0002-6531-0355
  surname: Galán
  fullname: Galán, Jorge E.
  email: jorge.galan@yale.edu
  organization: Department of Microbial Pathogenesis, Yale University School of Medicine
BackLink https://www.ncbi.nlm.nih.gov/pubmed/34012042$$D View this record in MEDLINE/PubMed
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Snippet Microbial infections are controlled by host inflammatory responses that are initiated by innate immune receptors after recognition of conserved microbial...
Microbial infections are most often controlled by host inflammatory responses that are initiated by innate immune receptors after recognition of conserved...
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Enrichment Source
Publisher
StartPage 716
SubjectTerms 631/250/254
631/326/421
631/326/88
Animals
Biomedical and Life Sciences
Coevolution
Development and progression
Epithelium
Homeostasis
Host-bacteria relationships
Host-Pathogen Interactions
Humans
Infectious Diseases
Inflammation
Inflammation - microbiology
Inflammation - pathology
Inflammatory response
Intestine
Life Sciences
Medical Microbiology
Microbiology
Microorganisms
Parasitology
Pathogens
Physiological aspects
Proteins
Receptors
Regulatory mechanisms (biology)
Review Article
Salmonella
Salmonella enterica
Salmonella Infections - microbiology
Salmonella Infections - pathology
Salmonella typhimurium
Salmonella typhimurium - metabolism
Salmonellosis
Virology
Title Salmonella Typhimurium and inflammation: a pathogen-centric affair
URI https://link.springer.com/article/10.1038/s41579-021-00561-4
https://www.ncbi.nlm.nih.gov/pubmed/34012042
https://www.proquest.com/docview/2580826890
https://www.proquest.com/docview/2529932490
https://pubmed.ncbi.nlm.nih.gov/PMC9350856
Volume 19
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