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Cited by 155Sepsis Diagnosis and TreatmentNosocomial Infections in ICUImmune Response and Inflammation

The DOI matches its Crossref record; 25 of the 26 references it cites were found in a registry or an index.

Cytokines IL-1 β, IL-6, and TNF- α Enhance In Vitro Growth of Bacteria

MEDURI, G. UMBERTO, KANANGAT, SIVA, STEFAN, JENNIFER, TOLLEY, ELIZABETH, SCHABERG, DENNIS·1999·American Journal of Respiratory and Critical Care Medicine
DOI 10.1164/ajrccm.160.3.9807080
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Abstract

We have previously reported that in acute respiratory distress syndrome (ARDS), nonsurvivors have persistent elevation in pulmonary and circulating proinflammatory cytokine levels over time and a high rate of nosocomial infections antemortem. In these patients, none of the proven or suspected nosocomial infections caused a transient or sustained increase in plasma proinflammatory cytokine levels above preinfection values. We hypothesized that cytokines secreted by the host during ARDS may favor the growth of bacteria. We conducted an in vitro study of the growth of three bacteria clinically relevant in nosocomial infections, evaluating their in vitro response to various concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6. We found that all three bacterial species showed concentration-dependent growth enhancement when incubated with one or more tested cytokines and that blockade by specific neutralizing cytokine MoAb significantly inhibited cytokine-induced growth. When compared with control, the 6-h growth response (cfu/ml) was maximal with IL-1beta at 1,000 pg for Staphylococcus aureus (36 +/- 16 versus 377 +/- 16; p = 0.0001) and Acinetobacter spp. (317 +/- 1,147 versus 1,124 +/- 147; p = 0.002) and with IL-6 at 1,000 pg for Pseudomonas aeruginosa (99 +/- 50 versus 509 +/- 50; p = 0.009). The effects of cytokines were seen only with fresh isolates and were lost with passage in vitro on bacteriologic medium without added cytokines. In this study we provide additional evidence for a newly described pathogenetic mechanism for bacterial proliferation in the presence of exaggerated and protracted inflammation.

Overview

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Crossref · 10.1164/ajrccm.160.3.9807080

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Citations

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Research works printed but not linked: 1

  1. Porat, 1992, IL-1β and Escherichia coli [Letter]., Science, 258, 1562, 10.1126/science.258.5088.1562.b · DOI

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Metadata

Authors
MEDURI, G. U., KANANGAT, S., STEFAN, J., TOLLEY, E., & SCHABERG, D.
Affiliations
Memphis VA Medical Center (US)
ORCID
TOLLEY, ELIZABETH
Venue
American Journal of Respiratory and Critical Care Medicine
Publisher
Oxford University Press (OUP)
Published
1999-09-01
Volume
160
Issue
3
Pages
961-967
ISSN
  • 1073-449X (ISSN-L)
  • 1535-4970
DOI
10.1164/ajrccm.160.3.9807080
OpenAlex
W2064610856
Cited by
155
References
26
Citations by year
2026: 3 · 2025: 7 · 2024: 5 · 2023: 5 · 2022: 7 · 2021: 4 · 2020: 8 · 2019: 10 · 2018: 7 · 2017: 4 · 2016: 8 · 2015: 1 · 2014: 5 · 2013: 3 · 2012: 2
FWCI
4.84
Type
journal article
Language
en
Open access
closed
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • American Journal of Respiratory and Critical Care Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Sepsis Diagnosis and Treatment
  • Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Nosocomial Infections in ICU
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
IL-1β, interleukin-6, TNF-α, inflammatory cytokines, bacterial growth enhancement, nosocomial infections, acute respiratory distress syndrome, Staphylococcus aureus, Acinetobacter, Pseudomonas aeruginosa
MeSH terms
Acinetobacter, Analysis of Variance, Antibodies, Monoclonal, Culture Media, Dose-Response Relationship, Drug, Interleukin-1, Pseudomonas aeruginosa, Staphylococcus aureus, Tumor Necrosis Factor-alpha, Interleukin-6, In Vitro Techniques

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