Characterization of a novel mouse model with genetic deletion of CD177

Qing Xie; Julia Klesney-Tait; Kathy Keck; Corey Parlet; Nicholas Borcherding; Ryan Kolb; Lorraine Tygrett; Wei Li; Thomas Waldschmidt; Alicia Olivier; Songhai Chen; Guang-Hui Liu; Xiangrui Li; Weizhou Zhang

doi:10.1007/s13238-014-0109-1

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Characterization of a novel mouse model with genetic deletion of CD177

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Characterization of a novel mouse model with genetic deletion of CD177

Qing Xie, Julia Klesney-Tait, Kathy Keck, Corey Parlet, Nicholas Borcherding, Ryan Kolb, Lorraine Tygrett, Wei Li, Thomas Waldschmidt, Alicia Olivier, …

Protein & cell, Vol.6(2), pp.117-126

02/2015

DOI: 10.1007/s13238-014-0109-1

PMCID: PMC4312768

PMID: 25359465

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Abstract

Neutrophils play an essential role in the innate immune response to infection. Neutrophils migrate from the vasculature into the tissue in response to infection. Recently, a neutrophil cell surface receptor, CD177, was shown to help mediate neutrophil migration across the endothelium through interactions with PECAM1. We examined a publicly available gene array dataset of CD177 expression from human neutrophils following pulmonary endotoxin instillation. Among all 22,214 genes examined, CD177 mRNA was the most upregulated following endotoxin exposure. The high level of CD177 expression is also maintained in airspace neutrophils, suggesting a potential involvement of CD177 in neutrophil infiltration under infectious diseases. To determine the role of CD177 in neutrophils in vivo, we constructed a CD177-genetic knockout mouse model. The mice with homozygous deletion of CD177 have no discernible phenotype and no significant change in immune cells, other than decreased neutrophil counts in peripheral blood. We examined the role of CD177 in neutrophil accumulation using a skin infection model with Staphylococcus aureus. CD177 deletion reduced neutrophil counts in inflammatory skin caused by S. aureus. Mechanistically we found that CD177 deletion in mouse neutrophils has no significant impact in CXCL1/KC- or fMLP-induced migration, but led to significant cell death. Herein we established a novel genetic mouse model to study the role of CD177 and found that CD177 plays an important role in neutrophils.

Genetic Therapy

Inflammation - pathology

Inflammation - microbiology

Isoantigens - genetics

Humans

Transcriptional Activation

Gene Expression Regulation

Immunity, Innate - genetics

Staphylococcus aureus - pathogenicity

Mice, Knockout

Animals

Platelet Endothelial Cell Adhesion Molecule-1 - metabolism

Inflammation - genetics

Mice

Neutrophils - metabolism

Disease Models, Animal

GPI-Linked Proteins - genetics

Neutrophils - pathology

Receptors, Cell Surface - genetics

Details

Title: Subtitle: Characterization of a novel mouse model with genetic deletion of CD177
Creators: Qing Xie - College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, China
Julia Klesney-Tait
Kathy Keck
Corey Parlet
Nicholas Borcherding
Ryan Kolb
Lorraine Tygrett
Wei Li
Thomas Waldschmidt
Alicia Olivier
Songhai Chen
Guang-Hui Liu
Xiangrui Li
Weizhou Zhang
Resource Type: Journal article
Publication Details: Protein & cell, Vol.6(2), pp.117-126
DOI: 10.1007/s13238-014-0109-1
PMID: 25359465
PMCID: PMC4312768
NLM abbreviation: Protein Cell
ISSN: 1674-800X
eISSN: 1674-8018
Publisher: Germany
Grant note: R00 CA158055 / NCI NIH HHS K99 CA158055 / NCI NIH HHS CA158055 / NCI NIH HHS R01 GM094255 / NIGMS NIH HHS T32 GM007337 / NIGMS NIH HHS R01 HL121105 / NHLBI NIH HHS
Language: English
Date published: 02/2015
Academic Unit: Dermatology; Pulmonary, Critical Care, and Occupational Medicine; Microbiology and Immunology; Pathology; Iowa Neuroscience Institute; Radiation Oncology; Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology; Internal Medicine
Record Identifier: 9984040279502771

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