Document Detail

Murine lung eosinophil activation and chemokine production in allergic airway inflammation.
MedLine Citation:
PMID:  20622891     Owner:  NLM     Status:  MEDLINE    
Eosinophils play important roles in asthma and lung infections. Murine models are widely used for assessing the functional significance and mechanistic basis for eosinophil involvements in these diseases. However, little is known about tissue eosinophils in homeostasis. In addition, little data on eosinophil chemokine production during allergic airway inflammation are available. In this study, the properties and functions of homeostatic and activated eosinophils were compared. Eosinophils from normal tissues expressed costimulation and adhesion molecules B7-1, B7-2 and ICAM-1 for Ag presentation but little major histocompatibility complex (MHC) class II, and were found to be poor stimulators of T-cell proliferation. However, these eosinophils expressed high levels of chemokine mRNA including C10, macrophage inflammatory protein (MIP)-1alpha, MIP-1gamma, MIP-2, eotaxin and monocyte chemoattractant protein-5 (MCP-5), and produced chemokine proteins. Eosinophil intracellular chemokines decreased rapidly with concomitant surface marker downregulation upon in vitro culturing consistent with piecemeal degranulation. Lung eosinophils from mice with induced allergic airway inflammation exhibited increased chemokines mRNA expression and chemokines protein production and upregulated MHC class II and CD11c expression. They were also found to be the predominant producers of the CCR1 ligands CCL6/C10 and CCL9/MIP-1gamma in inflamed lungs. Eosinophil production of C10 and MIP-1gamma correlated with the marked influx of CD11b(high) lung dendritic cells during allergic airway inflammation and the high expression of CCR1 on these dendritic cells (DCs). The study provided baseline information on tissue eosinophils, documented the upregulation of activation markers and chemokine production in activated eosinophils, and indicated that eosinophils were a key chemokine-producing cell type in allergic lung inflammation.
C Edward Rose; Joanne A Lannigan; Paul Kim; James J Lee; Shu Man Fu; Sun-sang J Sung
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-07-12
Journal Detail:
Title:  Cellular & molecular immunology     Volume:  7     ISSN:  2042-0226     ISO Abbreviation:  Cell. Mol. Immunol.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-06     Completed Date:  2010-10-08     Revised Date:  2014-09-21    
Medline Journal Info:
Nlm Unique ID:  101242872     Medline TA:  Cell Mol Immunol     Country:  China    
Other Details:
Languages:  eng     Pagination:  361-74     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Antigens, Surface / immunology
Asthma / immunology*,  metabolism
Cell Proliferation
Chemokines / biosynthesis,  immunology*
Eosinophils / immunology*
Mice, Inbred BALB C
Spleen / immunology
T-Lymphocytes / cytology,  immunology
Grant Support
AI079906/AI/NIAID NIH HHS; AR047988/AR/NIAMS NIH HHS; AR049449/AR/NIAMS NIH HHS; HL065228/HL/NHLBI NIH HHS; HL065344/HL/NHLBI NIH HHS; HL070065/HL/NHLBI NIH HHS; K26 RR019709/RR/NCRR NIH HHS; K26 RR019709-03/RR/NCRR NIH HHS; K26 RR019709-04/RR/NCRR NIH HHS; K26 RR019709-05/RR/NCRR NIH HHS; K26-RR019709/RR/NCRR NIH HHS; R01 HL065228/HL/NHLBI NIH HHS; R01 HL065228-09A1/HL/NHLBI NIH HHS; R01 HL065228-10/HL/NHLBI NIH HHS; R01 HL065228-11/HL/NHLBI NIH HHS; R01 HL065344-02/HL/NHLBI NIH HHS; R01 HL065344-03/HL/NHLBI NIH HHS; R01 HL065344-04/HL/NHLBI NIH HHS; R21 AI079906/AI/NIAID NIH HHS; R21 AI079906-01/AI/NIAID NIH HHS; R21 AI079906-01S1/AI/NIAID NIH HHS; R21 AI079906-02/AI/NIAID NIH HHS
Reg. No./Substance:
0/Antigens, Surface; 0/Chemokines

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Restoration of dysregulated CC chemokine signaling for monocyte/macrophage chemotaxis in head and ne...
Next Document:  The impact of the microbiota on the pathogenesis of IBD: lessons from mouse infection models.