Study of the role of CCR5 in a mouse model of intranasal challenge with Yersinia pestis

Katie L. Styer; Eva M. Click; Gregory W. Hopkins; Richard Frothingham; Alejandro Aballay

doi:10.1016/j.micinf.2007.04.012

Study of the role of CCR5 in a mouse model of intranasal challenge with Yersinia pestis

Katie L. Styer
, Eva M. Click
, Gregory W. Hopkins
, Richard Frothingham
, Alejandro Aballay

Research output: Contribution to journal › Article › peer-review

10 Scopus citations

Abstract

CCR5 is a chemokine receptor used by HIV-1 to enter cells and has recently been found to act as a pathogen associated molecule pattern receptor. Current positive selection for the high frequency of a CCR5-Δ32 allele in humans has been attributed to resistance to HIV, smallpox, and plague infections. Using an intranasal mouse model of Y. pestis infection, we have found that lack of CCR5 does not enhance host resistance to Y. pestis infection and that CCR5-mediated responses might have a protective role. CCR5-/- mice exhibited higher levels of circulating RANTES and MIP-1α than those exhibited by wild-type mice at the baseline and throughout the course of Y. pestis infection. High levels of RANTES and MIP-1α, which are CCR5 ligands that mediate Natural Killer cell migration, may reflect compensation for the absence of CCR5 signaling.

Original language	English (US)
Pages (from-to)	1135-1138
Number of pages	4
Journal	Microbes and Infection
Volume	9
Issue number	9
DOIs	https://doi.org/10.1016/j.micinf.2007.04.012
State	Published - Jul 2007
Externally published	Yes

Funding

We thank Jeffrey Hale of the DUMC Immune Reconstitution Core Facility for assistance in cytokine/chemokine data collection. R.F. is funded by Duke Center for Translational Research (NIH P30 AI51445), Southeast Regional Center of Excellence for Emerging Infections and Biodefense (U54 AI057157), and NIH grant R21 AI59689. A.A. is funded by The Whitehead Scholars Program, Duke Center for Translational Research (NIH P30 AI51445), Southeast Regional Center of Excellence for Emerging Infections and Biodefense (U54 AI057157), and NIH grants GM070977 and AI065641.

Funders	Funder number
Duke Center for Translational Research
Whitehead Scholars Program	AI065641, GM070977
Author National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health The Bev Hartig Huntington's Disease Foundation National Institutes of Health	P30 AI51445
National Institute of Allergy and Infectious Diseases	U54AI057157
Great Lakes Regional Center of Excellence for Biodefense and Emerging Infectious Diseases Research	R21 AI59689, U54 AI057157

Keywords

CCR5
Host resistance
Plague
Yersinia pestis

ASJC Scopus subject areas

Microbiology
Immunology
Infectious Diseases

Access to Document

10.1016/j.micinf.2007.04.012

Cite this

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title = "Study of the role of CCR5 in a mouse model of intranasal challenge with Yersinia pestis",

abstract = "CCR5 is a chemokine receptor used by HIV-1 to enter cells and has recently been found to act as a pathogen associated molecule pattern receptor. Current positive selection for the high frequency of a CCR5-Δ32 allele in humans has been attributed to resistance to HIV, smallpox, and plague infections. Using an intranasal mouse model of Y. pestis infection, we have found that lack of CCR5 does not enhance host resistance to Y. pestis infection and that CCR5-mediated responses might have a protective role. CCR5-/- mice exhibited higher levels of circulating RANTES and MIP-1α than those exhibited by wild-type mice at the baseline and throughout the course of Y. pestis infection. High levels of RANTES and MIP-1α, which are CCR5 ligands that mediate Natural Killer cell migration, may reflect compensation for the absence of CCR5 signaling.",

keywords = "CCR5, Host resistance, Plague, Yersinia pestis",

author = "Styer, \{Katie L.\} and Click, \{Eva M.\} and Hopkins, \{Gregory W.\} and Richard Frothingham and Alejandro Aballay",

note = "Funding Information: We thank Jeffrey Hale of the DUMC Immune Reconstitution Core Facility for assistance in cytokine/chemokine data collection. R.F. is funded by Duke Center for Translational Research (NIH P30 AI51445), Southeast Regional Center of Excellence for Emerging Infections and Biodefense (U54 AI057157), and NIH grant R21 AI59689. A.A. is funded by The Whitehead Scholars Program, Duke Center for Translational Research (NIH P30 AI51445), Southeast Regional Center of Excellence for Emerging Infections and Biodefense (U54 AI057157), and NIH grants GM070977 and AI065641.",

year = "2007",

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language = "English (US)",

volume = "9",

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N1 - Funding Information: We thank Jeffrey Hale of the DUMC Immune Reconstitution Core Facility for assistance in cytokine/chemokine data collection. R.F. is funded by Duke Center for Translational Research (NIH P30 AI51445), Southeast Regional Center of Excellence for Emerging Infections and Biodefense (U54 AI057157), and NIH grant R21 AI59689. A.A. is funded by The Whitehead Scholars Program, Duke Center for Translational Research (NIH P30 AI51445), Southeast Regional Center of Excellence for Emerging Infections and Biodefense (U54 AI057157), and NIH grants GM070977 and AI065641.

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Study of the role of CCR5 in a mouse model of intranasal challenge with Yersinia pestis

Abstract

Funding

Keywords

ASJC Scopus subject areas

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