Linked Life Data

16849492

Source:http://linkedlifedata.com/resource/pubmed/id/16849492

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-7-19
pubmed:abstractText
Influenza A virus pneumonia is characterized by severe lung injury and high mortality. Early infection elicits a strong recruitment of monocytes from the peripheral blood across the endo-/epithelial barrier into the alveolar air space. However, it is currently unclear which of the infected resident lung cell populations, alveolar epithelial cells or alveolar macrophages, elicit monocyte recruitment during influenza A virus infection. In the current study, we investigated whether influenza A virus infection of primary alveolar epithelial cells and resident alveolar macrophages would elicit a basal-to-apical monocyte transepithelial migration in vitro. We found that infection of alveolar epithelial cells with the mouse-adapted influenza A virus strain PR/8 strongly induced the release of monocyte chemoattractants CCL2 and CCL5 followed by a strong monocyte transepithelial migration, and this monocytic response was strictly dependent on monocyte CCR2 but not CCR5 chemokine receptor expression. Analysis of the adhesion molecule pathways demonstrated a role of ICAM-1, VCAM-1, integrin-associated protein (CD47), and junctional adhesion molecule-c on the epithelial cell surface interacting with monocyte beta(1) and beta(2) integrins and integrin-associated protein in the monocyte transmigration process. Importantly, addition of influenza A virus-infected alveolar macrophages further enhanced monocyte transmigration across virus-infected epithelium in a TNF-alpha-dependent manner. Collectively, the data show an active role for virus-infected alveolar epithelium in the regulation of CCL2/CCR2-dependent monocyte transepithelial migration during influenza infection that is essentially dependent on both classical beta(1) and beta(2) integrins but also junctional adhesion molecule pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
177
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1817-24
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:16849492-Animals, pubmed-meshheading:16849492-Cell Adhesion Molecules, pubmed-meshheading:16849492-Cell Communication, pubmed-meshheading:16849492-Cell Movement, pubmed-meshheading:16849492-Cells, Cultured, pubmed-meshheading:16849492-Chemokine CCL2, pubmed-meshheading:16849492-Chemokines, pubmed-meshheading:16849492-Epithelial Cells, pubmed-meshheading:16849492-Female, pubmed-meshheading:16849492-Influenza A Virus, H1N1 Subtype, pubmed-meshheading:16849492-Mice, pubmed-meshheading:16849492-Mice, Inbred BALB C, pubmed-meshheading:16849492-Mice, Inbred C57BL, pubmed-meshheading:16849492-Mice, Knockout, pubmed-meshheading:16849492-Monocytes, pubmed-meshheading:16849492-Nucleoproteins, pubmed-meshheading:16849492-Pulmonary Alveoli, pubmed-meshheading:16849492-RNA-Binding Proteins, pubmed-meshheading:16849492-Receptors, CCR2, pubmed-meshheading:16849492-Receptors, Chemokine, pubmed-meshheading:16849492-Up-Regulation, pubmed-meshheading:16849492-Viral Core Proteins
pubmed:year
2006
pubmed:articleTitle
Alveolar epithelial cells direct monocyte transepithelial migration upon influenza virus infection: impact of chemokines and adhesion molecules.
pubmed:affiliation
University of Giessen Lung Center, Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine and Infectious Diseases, Justus-Liebig-University, Giessen, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't