About: Neues zur Pathophysiologie der Pneumonie

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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	Neues zur Pathophysiologie der Pneumonie
Creator	Battegay, M Hippenstiel, S Opitz, · Rosseau, · Schweiz, Basel Schütte, · Suttorp, · Witzenrath, · Zabel, B
Source	PMC
abstract	Pneumonia can lead to the critical impairment of gas exchange in the lung. Due to the great variability of pneumonia causing pathogens, a large variety of diverse virulence factors act on the lung. Besides stimulation of unspecific defense mechanisms, activation of receptor-dependent cell-mediated innate immune defense mechanisms are critical for the pulmonary immune defense. Pathogen-associated molecules are detected via transmembraneous and cytosolic receptors of the host. This interaction stimulates the expression of immunomodulatory molecules via signal cascades. Of particular importance, in addition to direct pathogen-caused lung damage, is the overwhelming activation of the inflammatory response which can result in lung barrier failure and impairment of pulmonary gas exchange. In addition to the design of new antibiotics, innovative therapeutic strategies should therefore concentrate on the enhancement of antimicrobial mechanisms by concurrent limitation of inflammation.
has issue date	2007-05-04(xsd:dateTime)
bibo:doi	10.1007/s00108-007-1837-6
bibo:pmid	17429589
has license	no-cc
sha1sum (hex)	6dc83f2c5ac88be771ae57478b5315320c1e016d
schema:url	https://doi.org/10.1007/s00108-007-1837-6
resource representing a document's title	Neues zur Pathophysiologie der Pneumonie
has PubMed Central identifier	PMC7079865
has PubMed identifier	17429589
schema:publication	Internist (Berl)
resource representing a document's body	covid:6dc83f2c5ac88be771ae57478b5315320c1e016d#body_text
is schema:about of	named entity 'auch' named entity 'DAS' named entity 'PATHOGEN' named entity 'UND' named entity 'DIE' named entity 'INTERAKTION' named entity '40%' named entity 'PNEUMONIE' named entity 'LUNGE' named entity 'DASS' named entity 'ABER' named entity 'ZUR' named entity 'PNEUMONIE' named entity 'UND' named entity 'DER' named entity '20%' named entity 'IST' named entity 'BCR' named entity 'PROGNOSE' named entity 'DER' named entity 'LAG' named entity 'DEN' named entity 'die' named entity 'stören' named entity 'SP-D' named entity 'Protein' named entity 'PAMPs' named entity 'pulmonary gas exchange' named entity 'monale' named entity 'oder' named entity 'immune defense' named entity 'NOD1' named entity 'SP-A' named entity 'NOD2' named entity 'LL-37' named entity 'gas exchange' named entity 'RIG-I' named entity 'Enzyme' named entity 'Chlamydia pneumoniae' named entity 'severe acute respiratory syndrome' named entity 'Transferrin' named entity 'PRRs' named entity 'TLR1' named entity 'Staphylococcus aureus' named entity 'virulence factors' named entity 'inflammatory response' named entity 'IgG' named entity 'respiratory syncytial virus' named entity 'pneumonia' named entity 'Lactoferrin' named entity 'NOD1' named entity 'Chemotaxis' named entity 'Abb' named entity 'Fibronectin' named entity 'Protein' named entity 'Surfactant' named entity 'angiotensin-converting enzyme' named entity 'Pathogen' named entity 'innate immune defense' named entity 'Innate immunity' named entity 'oder' named entity 'IFNα' named entity 'Chemotaxis' named entity 'Abb' named entity 'TLR2' named entity 'RIG-I' named entity 'gene' named entity 'Pneumonia' named entity 'retinoid acid' named entity 'TLR1' named entity '20%' named entity 'ist' named entity '40%'

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