About: Influenza induces IL-8 and GM-CSF secretion by human alveolar epithelial cells through HGF/c-Met and TGF-α/EGFR signaling

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About: Influenza induces IL-8 and GM-CSF secretion by human alveolar epithelial cells through HGF/c-Met and TGF-α/EGFR signaling Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Influenza induces IL-8 and GM-CSF secretion by human alveolar epithelial cells through HGF/c-Met and TGF-α/EGFR signaling
Creator	Ito, Yoko Correll, Kelly Mason, Robert Zemans, Rachel Leslie, Christina Murphy, Robert
Source	PMC
abstract	The most severe complication of influenza is viral pneumonia, which can lead to the acute respiratory distress syndrome. Alveolar epithelial cells (AECs) are the first cells that influenza virus encounters upon entering the alveolus. Infected epithelial cells produce cytokines that attract and activate neutrophils and macrophages, which in turn induce damage to the epithelial-endothelial barrier. Hepatocyte growth factor (HGF)/c-Met and transforming growth factor-α (TGF-α)/epidermal growth factor receptor (EGFR) are well known to regulate repair of damaged alveolar epithelium by stimulating cell migration and proliferation. Recently, TGF-α/EGFR signaling has also been shown to regulate innate immune responses in bronchial epithelial cells. However, little is known about whether HGF/c-Met signaling alters the innate immune responses and whether the innate immune responses in AECs are regulated by HGF/c-Met and TGF-α/EGFR. We hypothesized that HGF/c-Met and TGF-α/EGFR would regulate innate immune responses to influenza A virus infection in human AECs. We found that recombinant human HGF (rhHGF) and rhTGF-α stimulated primary human AECs to secrete IL-8 and granulocyte macrophage colony-stimulating factor (GM-CSF) strongly and IL-6 and monocyte chemotactic protein 1 moderately. Influenza infection stimulated the secretion of IL-8 and GM-CSF by AECs plated on rat-tail collagen through EGFR activation likely by TGF-α released from AECs and through c-Met activated by HGF secreted from lung fibroblasts. HGF secretion by fibroblasts was stimulated by AEC production of prostaglandin E(2) during influenza infection. We conclude that HGF/c-Met and TGF-α/EGFR signaling enhances the innate immune responses by human AECs during influenza infections.
has issue date	2015-04-10(xsd:dateTime)
bibo:doi	10.1152/ajplung.00290.2014
bibo:pmid	26033355
has license	cc-by
schema:url	https://doi.org/10.1152/ajplung.00290.2014
resource representing a document's title	Influenza induces IL-8 and GM-CSF secretion by human alveolar epithelial cells through HGF/c-Met and TGF-α/EGFR signaling
has PubMed Central identifier	PMC4451400
has PubMed identifier	26033355
schema:publication	Am J Physiol Lung Cell Mol Physiol
resource representing a document's body	covid:PMC4451400#body_text
is schema:about of	named entity 'TGF' named entity 'GM-CSF' named entity 'alveolar' named entity 'HGF' named entity 'HGF' named entity 'ALVEOLAR EPITHELIAL CELLS' named entity 'CSF SECRETION' named entity 'SIGNALING' named entity 'MET' named entity 'IL-8' named entity 'INFLUENZA' named entity 'HUMAN' named entity 'c-Met' named entity 'GM-CSF' named entity 'alveolar epithelial cells' named entity 'HGF' named entity 'terminal differentiation' named entity 'oncogene protein' named entity 'PGE2' named entity 'cell culture' named entity 'pathogenesis' named entity 'AECs' named entity 'c-Met' named entity 'inflammation' named entity 'ARDS' named entity 'secretion' named entity 'AECs' named entity 'MIP-1β' named entity 'innate immune defense' named entity 'indomethacin' named entity 'DMEM' named entity 'AECs' named entity 'granulocyte macrophage colony-stimulating factor' named entity 'bronchial epithelial cells' named entity 'cytokines' named entity 'viral pneumonia' named entity 'IL-6' named entity 'GM-CSF' named entity 'EGFR family' named entity 'human lung' named entity 'IL-1β' named entity 'eotaxin' named entity 'influenza' named entity 'TGF-α' named entity 'infection' named entity 'rat' named entity 'GM-CSF' named entity 'IL-8' named entity 'human lung' named entity 'Toll-like receptor 4' named entity 'secretion' named entity 'HGF' named entity 'EGFR' named entity 'IAV' named entity 'AECs' named entity 'c-Met' named entity 'PGE2' named entity 'AREG' named entity '5-HETE' named entity 'EGFR' named entity 'K.C.' named entity 'HGF' named entity 'c-Met' named entity 'EGFR' named entity 'Madin-Darby canine kidney cells' named entity 'LTB4' named entity 'IL-8' named entity 'neutrophils' named entity 'influenza infection' named entity 'HGF' named entity 'KGF' named entity 'host defense' named entity 'AECs' named entity 'secretion' named entity 'medical research' named entity 'organ donors' named entity 'viral pneumonia'

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