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Eur J Clin Invest. 2018 Jan;48(1). doi: 10.1111/eci.12865. Epub 2017 Dec 7.

Cytokine responses, microbial aetiology and short-term outcome in community-acquired pneumonia.

Siljan WW1,2,3, Holter JC1,2,3, Nymo SH1,2,3, Husebye E1,3, Ueland T2,3,4, Aukrust P2,3,4,5, Mollnes TE4,6,7,8,9, Heggelund L1,3.

Author information

1
Department of Internal Medicine, Drammen Hospital, Vestre Viken Hospital Trust, Drammen, Norway.
2
Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
3
Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
4
K.G. Jebsen Inflammatory Research Center, University of Oslo, Oslo, Norway.
5
Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Oslo, Norway.
6
Department of Immunology, Faculty of Medicine, University of Oslo, Oslo, Norway.
7
Research Laboratory, Nordland Hospital, Bodø, Norway.
8
Faculty of Health Sciences, K.G. Jebsen TREC, University of Tromsø, Tromsø, Norway.
9
Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway.

Abstract

BACKGROUND:

The inflammatory response to community-acquired pneumonia (CAP) is orchestrated through activation of cytokine networks and the complement system. We examined the association of multiple cytokines and the terminal complement complex (TCC) with microbial aetiology, disease severity and short-term outcome.

MATERIALS AND METHODS:

Plasma levels of 27 cytokines and TCC were analysed in blood samples obtained at hospital admission, clinical stabilization and 6-week follow-up from 247 hospitalized adults with CAP. Fourteen mediators were included in final analyses. Adverse short-term outcome was defined as intensive care unit (ICU) admission and 30-day mortality.

RESULTS:

Cytokine and TCC levels were dynamic in the clinical course of CAP, with highest levels seen at admission for most mediators. Admission levels of cytokines and TCC did not differ between groups of microbial aetiology. High admission levels of IL-6 (odds ratio [OR] 1.47, 95% confidence interval [CI] 1.18-1.84, P = .001), IL-8 (OR 1.79, 95% CI 1.26-2.55, P = .001) and MIP-1β (OR 2.28, 95% CI 1.36-3.81, P = .002) were associated with a CURB-65 severity score of ≥3, while IL-6 (OR 1.37, 95% CI 1.07-1.74, P = .011) and MIP-1β (OR 1.86, 95% CI 1.03-3.36, P = .040) were associated with a high risk of an adverse short-term outcome.

CONCLUSIONS:

In this CAP cohort, admission levels of IL-6, IL-8 and MIP-1β were associated with disease severity and/or adverse short-term outcome. Still, for most mediators, only nonsignificant variations in inflammatory responses were observed for groups of microbial aetiology, disease severity and short-term outcome.

KEYWORDS:

aetiology; complement activation; cytokines; mortality; pneumonia

PMID:
29171871
PMCID:
PMC5767742
DOI:
10.1111/eci.12865
[Indexed for MEDLINE]
Free PMC Article

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