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Escherichia coli-induced inflammatory responses are temperature-dependent in human whole blood ex vivo

Chaban, Viktoriia (författare)
Univ Oslo, Norway;Oslo Univ Hosp, Norway
de Boer, Eline (författare)
Univ Oslo, Norway;Oslo Univ Hosp, Norway
McAdam, Karin E. (författare)
Univ Oslo, Norway;Oslo Univ Hosp, Norway
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Vaage, Jarle (författare)
Univ Oslo, Norway;Oslo Univ Hosp, Norway
Mollnes, Tom Eirik (författare)
Univ Oslo, Norway;Oslo Univ Hosp, Norway;Nordland Hosp, Norway;Norwegian Univ Sci & Technol, Norway
Nilsson, Per H., 1980- (författare)
Linnéuniversitetet,Institutionen för kemi och biomedicin (KOB),Oslo Univ Hosp, Norway,Linnaeus Ctr Biomat Chem, BMC;HoRB
Piscike, Soren Erik (författare)
Univ Oslo, Norway;Oslo Univ Hosp, Norway
Islam, Rakibul (författare)
Univ Oslo, Norway;Oslo Univ Hosp, Norway
visa färre...
 (creator_code:org_t)
Elsevier, 2023
2023
Engelska.
Ingår i: Molecular Immunology. - : Elsevier. - 0161-5890 .- 1872-9142. ; 157, s. 70-77
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Systemic inflammatory conditions are often associated with hypothermia or hyperthermia. Therapeutic hypothermia is used in post-cardiac arrest and some other acute diseases. There is a need for more knowledge concerning the effect of various temperatures on the acute inflammatory response. The complement system plays a crucial role in initiating the inflammatory response. We hypothesized that temperatures above and below the physiologic 37 & DEG;C affect complement activation and cytokine production ex vivo. Lepirudin-anticoagulated human whole blood from 10 healthy donors was incubated in the presence or absence of Escherichia coli at different temperatures (4 & DEG;C, 12 & DEG;C, 20 & DEG;C, 33 & DEG;C, 37 & DEG;C, 39 & DEG;C, and 41 & DEG;C). Complement activation was assessed by the terminal C5b-9 complement complex (TCC) and the alternative convertase C3bBbP using ELISA. Cytokines were measured using a 27-plex assay. Granulocyte and monocyte activation was evaluated by CD11b surface expression using flow cytometry. A consistent increase in complement activation was observed with rising temperature, reaching a maximum at 41 & DEG;C, both in the absence (C3bBbP p < 0.05) and presence (C3bBbP p < 0.05 and TCC p < 0.05) of E. coli. Temperature alone did not affect cytokine production, whereas incubation with E. coli significantly increased cytokine levels of IL-18, IL-2, IL-6, IL-8, IFN-& gamma;, and TNF at temperatures > 20 & DEG;C. Maximum increase occurred at 39 & DEG;C. However, a consistent decrease was observed at 41 & DEG;C, significant for IL-18 (p = 0.003). Granulocyte CD11b displayed the same temperature-dependent pattern as cytokines, with a corresponding increase in endothelial cell apoptosis and necrosis. Thus, blood temperature differentially determines the degree of complement activation and cytokine release.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Immunology in the medical area (hsv//eng)

Nyckelord

Comblement system
Innate immunity
Cytokine
Temperature
Hypothermia
Hyperthermia
Immunologi
Immunology

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