NDLI: Flagellar Motility Is a Key Determinant of the Magnitude of the Inflammasome Response to Pseudomonas aeruginosa

Content Provider	PubMed Central
Author	Patankar, Yash R. Lovewell, Rustin R. Poynter, Matthew E. Jeevan, Jyot Kazmierczak, Barbara I. Brent, Berwin
Editor	Camilli, A.
Copyright Year	2013
Abstract	We previously demonstrated that bacterial flagellar motility is a fundamental mechanism by which host phagocytes bind and ingest bacteria. Correspondingly, loss of bacterial motility, consistently observed in clinical isolates from chronic Pseudomonas aeruginosa infections, enables bacteria to evade association and ingestion of P. aeruginosa by phagocytes both in vitro and in vivo. Since bacterial interactions with the phagocyte cell surface are required for type three secretion system-dependent NLRC4 inflammasome activation by P. aeruginosa, we hypothesized that reduced bacterial association with phagocytes due to loss of bacterial motility, independent of flagellar expression, will lead to reduced inflammasome activation. Here we report that inflammasome activation is reduced in response to nonmotile P. aeruginosa. Nonmotile P. aeruginosa elicits reduced IL-1β production as well as caspase-1 activation by peritoneal macrophages and bone marrow-derived dendritic cells in vitro. Importantly, nonmotile P. aeruginosa also elicits reduced IL-1β levels in vivo in comparison to those elicited by wild-type P. aeruginosa. This is the first demonstration that loss of bacterial motility results in reduced inflammasome activation and antibacterial IL-1β host response. These results provide a critical insight into how the innate immune system responds to bacterial motility and, correspondingly, how pathogens have evolved mechanisms to evade the innate immune system.
Related Links	http://dx.doi.org/10.1128/iai.00054-13
Ending Page	2052
Page Count	10
Starting Page	2043
File Format	PDF
ISSN	00199567
e-ISSN	10985522
Journal	Infection and Immunity
Issue Number	6
Volume Number	81
Language	English
Publisher	American Society for Microbiology
Publisher Date	2013-06-01
Access Restriction	Open
Rights Holder	American Society for Microbiology
Subject Keyword	Immunology Microbiology Parasitology Infectious Diseases Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Infectious Diseases Parasitology Immunology Microbiology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

The Pseudomonas aeruginosa Flagellar Cap Protein, FliD, Is Responsible for Mucin Adhesion

Pseudomonas aeruginosa Triggers Macrophage Autophagy To Escape Intracellular Killing by Activation of the NLRP3 Inflammasome

Pseudomonas aeruginosa Evasion of Phagocytosis Is Mediated by Loss of Swimming Motility and Is Independent of Flagellum Expression▿ †

Twitching Motility Contributes to the Role of Pili in Corneal Infection Caused by Pseudomonas aeruginosa

Recognition of Lewis x Derivatives Present on Mucins by Flagellar Components of Pseudomonas aeruginosa

Interleukin-18 Impairs the Pulmonary Host Response to Pseudomonas aeruginosa

Flagellar preparations from Pseudomonas aeruginosa: animal protection studies.

Flagellar preparations from Pseudomonas aeruginosa: isolation and characterization.

Alveolar Response to Pseudomonas aeruginosa: Role of the Type III Secretion System

Flagellar Motility Is a Key Determinant of the Magnitude of the Inflammasome Response to Pseudomonas aeruginosa

Similar Documents

The Pseudomonas aeruginosa Flagellar Cap Protein, FliD, Is Responsible for Mucin Adhesion

Pseudomonas aeruginosa Triggers Macrophage Autophagy To Escape Intracellular Killing by Activation of the NLRP3 Inflammasome

Pseudomonas aeruginosa Evasion of Phagocytosis Is Mediated by Loss of Swimming Motility and Is Independent of Flagellum Expression▿ †

Twitching Motility Contributes to the Role of Pili in Corneal Infection Caused by Pseudomonas aeruginosa

Recognition of Lewis x Derivatives Present on Mucins by Flagellar Components of Pseudomonas aeruginosa

Interleukin-18 Impairs the Pulmonary Host Response to Pseudomonas aeruginosa

Flagellar preparations from Pseudomonas aeruginosa: animal protection studies.

Flagellar preparations from Pseudomonas aeruginosa: isolation and characterization.

Alveolar Response to Pseudomonas aeruginosa: Role of the Type III Secretion System

Flagellar Motility Is a Key Determinant of the Magnitude of the Inflammasome Response to Pseudomonas aeruginosa