About: Inflammatory Responses Regulating Alveolar Ion Transport during Pulmonary Infections

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Inflammatory Responses Regulating Alveolar Ion Transport during Pulmonary Infections
Creator	Herold, Susanne Peteranderl, Christin Lecuona, Emilia Lucas, Rudolf Sznajder, Jacob Langhans, Sigrid Pittet, Jean-Francois
topic	covid:720d81cbf900cfce68db61398f8c41f92f798314#this
Source	Medline; PMC
abstract	The respiratory epithelium is lined by a tightly balanced fluid layer that allows normal O(2) and CO(2) exchange and maintains surface tension and host defense. To maintain alveolar fluid homeostasis, both the integrity of the alveolar–capillary barrier and the expression of epithelial ion channels and pumps are necessary to establish a vectorial ion gradient. However, during pulmonary infection, auto- and/or paracrine-acting mediators induce pathophysiological changes of the alveolar–capillary barrier, altered expression of epithelial Na,K-ATPase and of epithelial ion channels including epithelial sodium channel and cystic fibrosis membrane conductance regulator, leading to the accumulation of edema and impaired alveolar fluid clearance. These mediators include classical pro-inflammatory cytokines such as TGF-β, TNF-α, interferons, or IL-1β that are released upon bacterial challenge with Streptococcus pneumoniae, Klebsiella pneumoniae, or Mycoplasma pneumoniae as well as in viral infection with influenza A virus, pathogenic coronaviruses, or respiratory syncytial virus. Moreover, the pro-apoptotic mediator TNF-related apoptosis-inducing ligand, extracellular nucleotides, or reactive oxygen species impair epithelial ion channel expression and function. Interestingly, during bacterial infection, alterations of ion transport function may serve as an additional feedback loop on the respiratory inflammatory profile, further aggravating disease progression. These changes lead to edema formation and impair edema clearance which results in suboptimal gas exchange causing hypoxemia and hypercapnia. Recent preclinical studies suggest that modulation of the alveolar–capillary fluid homeostasis could represent novel therapeutic approaches to improve outcomes in infection-induced lung injury.
has issue date	2017-04-18(xsd:dateTime)
bibo:doi	10.3389/fimmu.2017.00446
bibo:pmid	28458673
has license	cc-by
sha1sum (hex)	720d81cbf900cfce68db61398f8c41f92f798314
schema:url	https://doi.org/10.3389/fimmu.2017.00446
resource representing a document's title	Inflammatory Responses Regulating Alveolar Ion Transport during Pulmonary Infections
has PubMed Central identifier	PMC5394420
has PubMed identifier	28458673
schema:publication	Front Immunol
resource representing a document's body	covid:720d81cbf900cfce68db61398f8c41f92f798314#body_text
is http://vocab.deri.ie/void#inDataset of	https://covidontheweb.inria.fr:4443/about/id/http/ns.inria.fr/covid19/720d81cbf900cfce68db61398f8c41f92f798314
is schema:about of	named entity 'MEDIATORS' named entity 'LIGAND' named entity 'CO2' named entity 'OUTCOMES' named entity 'RESPIRATORY EPITHELIUM' named entity 'CONDUCTANCE' named entity 'SUGGEST' named entity 'CAPILLARY' named entity 'EXCHANGE' named entity 'BALANCED' named entity 'PRO-' named entity 'ESTABLISH' named entity 'REACTIVE OXYGEN SPECIES' named entity 'BARRIER' named entity 'HYPERCAPNIA' named entity 'INFECTION' named entity 'CLEARANCE' named entity 'AUTO' named entity 'BACTERIAL INFECTION' named entity 'SUBOPTIMAL' named entity 'CHALLENGE' named entity 'FORMATION' named entity 'PARACRINE' named entity 'BACTERIAL' named entity 'ADDITIONAL' named entity 'edema' named entity 'preclinical studies' named entity 'ion' named entity 'normal' named entity 'hypercapnia' named entity 'pro-apoptotic' named entity 'surface tension' named entity 'Recent' named entity 'transport' named entity 'However' named entity 'TNF-' named entity 'INFLAMMATORY RESPONSES' named entity 'INDUCED' named entity 'VIRAL INFECTION' named entity 'PULMONARY INFECTION' named entity 'ION TRANSPORT' named entity 'GRADIENT' named entity 'FEEDBACK LOOP' named entity 'REGULATOR' named entity 'CLASSICAL' named entity 'FUNCTION' named entity 'LEADING' named entity 'RESULTS' named entity 'LEAD' named entity 'PROFILE' named entity 'CYSTIC FIBROSIS' named entity 'INCLUDE' named entity 'DISEASE PROGRESSION' named entity 'NOVEL' named entity 'HOMEOSTASIS' named entity 'LUNG INJURY' named entity 'EXTRACELLULAR' named entity 'IMPAIRED' named entity 'SERVE' named entity 'PULMONARY INFECTIONS' named entity 'REGULATING' named entity 'ION TRANSPORT' named entity 'ALVEOLAR' named entity 'THERAPEUTIC' named entity 'ALTERATIONS' named entity 'TRANSPORT FUNCTION' named entity 'RESPIRATORY' named entity 'ALTERED' named entity 'CHANGES' named entity 'MYCOPLASMA PNEUMONIAE' named entity 'EXPRESSION' named entity 'LINED' named entity 'ION CHANNELS'

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