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About:
Concurrent Immune Suppression and Hyperinflammation in Patients With Community-Acquired Pneumonia
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An Entity of Type :
schema:ScholarlyArticle
, within Data Space :
covidontheweb.inria.fr
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document(s)
Type:
Academic Article
research paper
schema:ScholarlyArticle
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type
Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
has title
Concurrent Immune Suppression and Hyperinflammation in Patients With Community-Acquired Pneumonia
Creator
Lutter, René
Van Der Poll, Tom
Chousterman, Benjamin
Scicluna, Brendon
Brands, Xanthe
Faber, Daniël
Haak, Bastiaan
Joost Wiersinga, W
Klarenbeek, Augustijn
Lariboisière, Hôpital
Man, Chaoxin
Otto, Natasja
Yang, France
Source
Medline; PMC
abstract
BACKGROUND: The nature and timing of the host immune response during infections remain uncertain and most knowledge is derived from critically ill sepsis patients. We aimed to test the hypothesis that community-acquired pneumonia (CAP) is associated with concurrent immune suppression and systemic inflammation. METHODS: Blood was collected from 79 CAP patients within 24 h after hospitalization and 1 month after discharge; 42 age- and sex-matched subjects without acute infection served as controls. Blood leukocytes were stimulated with lipopolysaccharide (LPS) or Klebsiella pneumoniae, and cytokines were measured in supernatants. Fifteen plasma biomarkers reflective of key host response pathways were compared between CAP patients with the strongest immune suppression (lowest 25% blood leukocyte tumor necrosis factor (TNF)-α production in response to LPS) and those with the least immune suppression (highest 25% of LPS-induced TNF-α production). RESULTS: Blood leukocytes of CAP patients (relative to control subjects) showed a reduced capacity to release TNF-α, interleukin (IL)-1β, IL-6 and IL-10 upon stimulation with LPS or K. pneumoniae, with a concurrently enhanced ability to release the anti-inflammatory mediator IL-1 receptor antagonist, irrespective of the presence of sepsis (18.9% of cases). Low (relative to high) TNF-α producers displayed higher plasma levels of biomarkers reflecting systemic inflammation, neutrophil degranulation, endothelial cell activation, a disturbed vascular barrier function and coagulation activation. CONCLUSION: CAP replicates a common feature of immune suppression in sepsis. The coexistence of immune suppression and hyperinflammation in CAP argues against the theory of two distinct phases during the host response to sepsis.
has issue date
2020-05-06
(
xsd:dateTime
)
bibo:doi
10.3389/fimmu.2020.00796
bibo:pmid
32477337
has license
cc-by
sha1sum (hex)
e2c21564edcbfe29fcced2a826404badbef89c3b
schema:url
https://doi.org/10.3389/fimmu.2020.00796
resource representing a document's title
Concurrent Immune Suppression and Hyperinflammation in Patients With Community-Acquired Pneumonia
has PubMed Central identifier
PMC7232566
has PubMed identifier
32477337
schema:publication
Front Immunol
resource representing a document's body
covid:e2c21564edcbfe29fcced2a826404badbef89c3b#body_text
is
schema:about
of
named entity 'sepsis'
named entity 'SYSTEMIC INFLAMMATION'
named entity 'CRITICALLY ILL'
named entity 'IMMUNE SUPPRESSION'
named entity 'NATURE'
named entity 'CONCURRENT'
named entity 'HOST IMMUNE RESPONSE'
named entity 'hypothesis'
named entity 'systemic inflammation'
named entity 'concurrent'
named entity 'community-acquired pneumonia'
named entity 'systemic inflammation'
named entity 'critically ill'
named entity 'Immune Suppression'
named entity 'Hyperinflammation'
named entity 'K. pneumoniae'
named entity 'detecting danger'
named entity 'PD1'
named entity 'tumor necrosis factor (TNF)-α'
named entity 'BioRad'
named entity 'TNF-α'
named entity 'IL-10'
named entity 'sputum production'
named entity 'CAP'
named entity 'vascular cell adhesion molecule'
named entity 'COPD'
named entity 'immune suppression'
named entity 'Staphylococcus aureus'
named entity 'LPS'
named entity 'fever'
named entity 'immune suppression'
named entity 'plasma'
named entity 'cytokines'
named entity 'computed tomography scan'
named entity 'community-acquired pneumonia'
named entity 'leukocyte'
named entity 'Vienna'
named entity 'respiratory tract'
named entity 'endothelial cell'
named entity 'Life Technologies'
named entity 'plasma levels'
named entity 'plasma'
named entity 'fever'
named entity 'critically ill patients'
named entity 'COPD'
named entity 'COPD'
named entity 'CAP'
named entity 'lipopolysaccharide'
named entity 'immune suppression'
named entity 'leukocytosis'
named entity 'sepsis'
named entity 'TNF-α'
named entity 'informed consent'
named entity 'France'
named entity 'TNF'
named entity 'TNF-α'
named entity 'LPS'
named entity 'red blood cell'
named entity 'CAP'
named entity 'sepsis'
named entity 'leukocyte'
named entity 'CAP'
named entity 'PSI'
named entity 'MPO'
named entity 'TFF3'
named entity 'sepsis'
named entity 'mortality rate'
named entity '0.01'
named entity 'control subjects'
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