About: The endotoxin-induced pulmonary inflammatory response is enhanced during the acute phase of influenza infection

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	The endotoxin-induced pulmonary inflammatory response is enhanced during the acute phase of influenza infection
Creator	Koch, R Ferwerda, G De Jonge, M Diavatopoulos, D Kox, M Pickkers, P
Source	PMC
abstract	BACKGROUND: Influenza infections are often complicated by secondary infections, which are associated with high morbidity and mortality, suggesting that influenza profoundly influences the immune response towards a subsequent pathogenic challenge. However, data on the immunological interplay between influenza and secondary infections are equivocal, with some studies reporting influenza-induced augmentation of the immune response, whereas others demonstrate that influenza suppresses the immune response towards a subsequent challenge. These contrasting results may be due to the use of various types of live bacteria as secondary challenges, which impedes clear interpretation of causal relations, and to differences in timing of the secondary challenge relative to influenza infection. Herein, we investigated whether influenza infection results in an enhanced or suppressed innate immune response upon a secondary challenge with bacterial lipopolysaccharide (LPS) in either the acute or the recovery phase of infection. METHODS: Male C57BL/6J mice were intranasally inoculated with 5 × 10(3) PFU influenza virus (pH1N1, strain A/Netherlands/602/2009) or mock treated. After 4 (acute phase) or 10 (recovery phase) days, 5 mg/kg LPS or saline was administered intravenously, and mice were sacrificed 90 min later. Cytokine levels in plasma and lung tissue, and lung myeloperoxidase (MPO) content were determined. RESULTS: LPS administration 4 days after influenza infection resulted in a synergistic increase in TNF-α, IL-1β, and IL-6 concentrations in lung tissue, but not in plasma. This effect was also observed 10 days after influenza infection, albeit to a lesser extent. LPS-induced plasma levels of the anti-inflammatory cytokine IL-10 were enhanced 4 days after influenza infection, whereas a trend towards increased pulmonary IL-10 concentrations was found. LPS-induced increases in pulmonary MPO content tended to be enhanced as well, but only at 4 days post-infection. CONCLUSIONS: An LPS challenge in the acute phase of influenza infection results in an enhanced pulmonary pro-inflammatory innate immune response. These data increase our insight on influenza-bacterial interplay. Combing data of the present study with previous findings, it appears that this enhanced response is not beneficial in terms of protection against secondary infections, but rather damaging by increasing immunopathology.
has issue date	2018-07-05(xsd:dateTime)
bibo:doi	10.1186/s40635-018-0182-5
bibo:pmid	29978355
has license	cc-by
sha1sum (hex)	bd63f19c8f62b5d7db463a04492c27242b0791ff
schema:url	https://doi.org/10.1186/s40635-018-0182-5
resource representing a document's title	The endotoxin-induced pulmonary inflammatory response is enhanced during the acute phase of influenza infection
has PubMed Central identifier	PMC6033844
has PubMed identifier	29978355
schema:publication	Intensive Care Med Exp
resource representing a document's body	covid:bd63f19c8f62b5d7db463a04492c27242b0791ff#body_text
is schema:about of	named entity 'IL-1β' named entity 'influenza' named entity 'influenza' named entity 'recovery' named entity 'immune response' named entity 'secondary' named entity 'interplay' named entity 'content' named entity 'studies' named entity 'inoculated' named entity 'acute' named entity 'inflammatory response' named entity 'IMMUNOLOGICAL' named entity 'STUDIES' named entity 'INFLAMMATORY' named entity 'PRO-' named entity 'BACTERIA ' named entity 'COMPLICATED BY' named entity 'SUBSEQUENT' named entity 'INDUCED' named entity 'infection' named entity 'timing' named entity 'Combing' named entity 'PFU' named entity 'phase' named entity 'tissue' named entity 'virus' named entity 'levels' named entity 'insight' named entity 'Male' named entity 'immune response' named entity 'mice' named entity 'data' named entity 'data' named entity 'intravenously' named entity 'LPS' named entity 'influenza' named entity 'Cytokine' named entity 'mortality' named entity 'influenza infection' named entity 'inoculated' named entity 'IL-1β' named entity 'LPS' named entity 'saline' named entity 'intranasally' named entity 'immune response' named entity 'immune response' named entity 'TNF-α' named entity 'morbidity' named entity 'immunological' named entity 'influenza' named entity 'causal relations' named entity 'LPS' named entity 'anti-inflammatory' named entity 'MPO' named entity 'influenza infection' named entity 'Netherlands' named entity 'plasma levels' named entity 'immunopathology' named entity 'LPS' named entity 'synergistic' named entity 'mice' named entity 'acute phase' named entity 'influenza infection' named entity 'Aspergillus fumigatus' named entity 'LPS' named entity 'LPS' named entity 'inoculation' named entity 'data reporting' named entity 'lung' named entity 'mice' named entity 'pro-inflammatory cytokines' named entity 'influenza infection' named entity 'innate immune' named entity 'lethargy' named entity 'vasculature'

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