The p47 GTPases Iigp2 and Irgb10 regulate innate immunity and inflammation to murine Chlamydia psittaci infection.

The p47 GTPases Iigp2 and Irgb10 regulate innate immunity and inflammation to murine Chlamydia psittaci infection. Research Abstract Details 

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The p47 GTPases Iigp2 and Irgb10 regulate innate immunity and inflammation to murine Chlamydia psittaci infection. Abstract Text:

Isao Miyairi,Venkat R R Arva Tatireddigari,Olaimatu S Mahdi,Lorne A Rose,Robert J Belland,Lu Lu,Robert W Williams,Gerald I Byrne,

C57BL/6J mice were 10(5)-fold more resistant to Chlamydia psittaci infection than DBA/2J mice by LD(100) determinations. Linkage analysis using BXD recombinant inbred strains revealed a single effector locus at a 1.5-Mbp region on chromosome 11 encoding a cluster of three p47 GTPases (Irgb10, Igtp, and Iigp2). Western blots of infected tissue showed that Irgb10 was elevated in resistant mice and one of the two possible Iigp2 protein isoforms was preferentially expressed in susceptible mice. The BXD39 strain, susceptible at Irgb10 and resistant at Iigp2, had an intermediate phenotype implicating the nonredundant role of these p47 GTPases. C57BL/6J and DBA/2J exhibited a difference in IFN-gamma-dependent chlamydial control, which was reversible by Iigp2 small interfering RNA knockdown. Microarrays of infected peritoneal lavage revealed >10-fold up-regulation of neutrophil-recruiting chemokines in susceptible mice and >100-fold increase in macrophage differentiation genes in resistant mice, indicating that the susceptibility pattern involves the stimulation of different inflammatory cell-recruiting pathways. Massive neutrophil recruitment was seen in susceptible mice by histology and flow cytometry, and neutrophil chemokine receptor (CXCR2) knockout mice on a susceptible background survived a lethal challenge, confirming that neutrophil recruitment was required for susceptibility. Congenic Igtp knockout mice also susceptible at Irgb10 and Iigp2 on a resistant background recruited neutrophils and succumbed to infection. We conclude that Irgb10 and Iigp2 act together to confer differential susceptibility against murine chlamydial infection. Data indicate that these p47 GTPases have cell-autonomous effects that result in vastly different inflammatory stimulations, leading to either recovery or death.

The p47 GTPases Iigp2 and Irgb10 regulate innate immunity and inflammation to murine Chlamydia psittaci infection. Publishing Authors By Initials

I Miyairi,VR Tatireddigari,OS Mahdi,LA Rose,RJ Belland,L Lu,RW Williams,GI Byrne,

For similar bacterial infections and mycoses: bacterial infections: gram-negative bacterial infections: chlamydiaceae infections: chlamydophila infections: psittacosis research abstracts see: bacterial infections and mycoses: bacterial infections: gram-negative bacterial infections: chlamydiaceae infections: chlamydophila infections: psittacosis research

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The p47 GTPases Iigp2 and Irgb10 regulate innate immunity and inflammation to murine Chlamydia psittaci infection. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 179

Page Numbers: 1814-24

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 1

MONTH: Aug

YEAR: 2007

The p47 GTPases Iigp2 and Irgb10 regulate innate immunity and inflammation to murine Chlamydia psittaci infection. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985117

The p47 GTPases Iigp2 and Irgb10 regulate innate immunity and inflammation to murine Chlamydia psittaci infection. Keywords Mesh Terms:

KEYWORDS: Psittacosis

MESH TERMS: prevention & control

Chemical & Substance for Abstract: The p47 GTPases Iigp2 and Irgb10 regulate innate immunity and inflammation to murine Chlamydia psittaci infection. Information

Substance Name: Irgb10 protein, mouse

Registry Number: EC 3.6.1.-.

Grant and Affiliation Information for The p47 GTPases Iigp2 and Irgb10 regulate innate immunity and inflammation to murine Chlamydia psittaci infection.

AFFILIATION: Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38163, USA.

Country: United States

AGENCY: United States NINR

GRANT: U01NR105417

ACRONYM: NR

MEDLINETA: J Immunol

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