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Cited by 111Influenza Virus Research StudiesPneumonia and Respiratory InfectionsTryptophan and brain disorders

Influenza‐Induced Expression of Indoleamine 2,3‐Dioxygenase Enhances Interleukin‐10 Production and Bacterial Outgrowth during Secondary Pneumococcal Pneumonia

van der Sluijs, Koenraad F., Nijhuis, Monique, Levels, Johannes H. M., Florquin, Sandrine, Mellor, Andrew L., Jansen, Henk M., der Poll, Tom van, Lutter, René·2006·The Journal of Infectious Diseases
DOI 10.1086/498911
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Abstract

BACKGROUND: Airway infection with influenza virus induces local expression of the tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase (IDO), which has been shown to enhance inflammatory mediator responses in vitro. Because secondary pneumococcal infections occurring shortly after recovery from influenza are associated with enhanced inflammatory responses, we hypothesized that IDO activity contributes to the enhanced response to bacterial challenges in mice previously infected with influenza virus. METHODS: On day 14 after influenza virus infection (with strain A/PR/8/34), C57Bl/6 mice were intranasally inoculated with 1 x 10(4) colony-forming units of S. pneumoniae (serotype 3). Matrix-driven delivery pellets that contained 70 mg of the IDO inhibitor 1-methyl-DL-tryptophan (MeTrp) released over a period of 7 days were subcutaneously implanted 48 h before pneumococcal infection. RESULTS: MeTrp treatment resulted in a 20-fold reduction in pneumococcal outgrowth 48 h after bacterial inoculation. Remarkably, pulmonary levels of interleukin-10 and tumor necrosis factor-alpha were significantly reduced in mice treated with MeTrp. CONCLUSIONS: Our data suggest that IDO expression during influenza virus infection alters the inflammatory response and facilitates the outgrowth of pneumococci during secondary bacterial pneumonia.

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  • A body of experimental research over the last three decades has identified possible mechanisms by which influenza virus and bacterial coinfection might affect pathogenicity, including viral neuraminidase-induced exposure of bacterial adherence receptors, bacterial neuraminidase-induced upregulation of influenza infection, interleukin 10-induced susceptibility to pneumococci and possibly staphyloc

    “As reviewed recently by McCullers [75], a body of experimental research during the last 3 decades has identified possible mechanisms by which coinfection with the influenza virus and bacteria might affect pathogenicity. These include viral neuraminidase (NA)–induced exposure of bacterial adherence receptors; bacterial NA-induced upregulation of influenza infection; interleukin 10–induced suscept”

    From Predominant Role of Bacterial Pneumonia as a Cause of Death in Pandemic Influenza: Implications for Pandemic Influenza Preparedness (2008) · cites this paper as [76]

    The introduction (p. 1) says excessive IL-10 was critically involved in bacterial outgrowth during postinfluenza pneumococcal pneumonia in mice; the Discussion (p. 6) also reports that neutralizing IL-10 reduced bacterial loads. The paper does not establish the claimed neuraminidase mechanisms or IL-10-induced susceptibility to staphylococci, although it mentions staphylococci as a cause of postinfluenza pneumonia. (LLM, conf=0.86)

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Research works printed but not linked: 2

  1. [3]3. Zhang WJ, Sarawar S, Nguyen P, et al. Lethal synergism between influenza and staphylococcal enterotoxin B in mice. J Immunol 1996 ; 157:5049-60.
  2. [20]20. Von Bubnoff D, Matz H, Frahnert C, et al. Fc 𝛆 RI induces the tryptophan degradation pathway involved in regulating T cell responses. J Immunol 2002 ; 169:1810-6.

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Authors
van der Sluijs, K. F., Nijhuis, M., Levels, J. H. M., Florquin, S., Mellor, A. L., Jansen, H. M., der Poll, T. V., & Lutter, R.
Affiliations
  • University Medical Center Utrecht (NL)
  • Augusta University (US)
  • Amsterdam UMC Location University of Amsterdam (NL)
ORCID
Venue
The Journal of Infectious Diseases
Publisher
Oxford University Press (OUP)
Published
2006-01-15
Volume
193
Issue
2
Pages
214-222
ISSN
  • 0022-1899 (ISSN-L)
  • 1537-6613
DOI
10.1086/498911
OpenAlex
W2116742245
Cited by
111
References
31
Citations by year
2026: 1 · 2025: 5 · 2024: 2 · 2023: 3 · 2022: 3 · 2021: 9 · 2020: 2 · 2019: 4 · 2018: 5 · 2017: 7 · 2016: 6 · 2015: 5 · 2014: 5 · 2013: 10 · 2012: 7
FWCI
3.58
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Infectious Diseases (publishedVersion)
  • PubMed (publishedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
  • Pure Amsterdam UMC (submittedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
  • Health Sciences › Medicine › Epidemiology › Pneumonia and Respiratory Infections
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
indoleamine 2,3-dioxygenase, influenza virus, Streptococcus pneumoniae, IL-10, TNF-α, tryptophan catabolism, airway infection, IDO inhibition
MeSH terms
Animals, Bronchoalveolar Lavage Fluid, Delayed-Action Preparations, Disease Models, Animal, Enzyme Inhibitors, Female, Lung, Mice, Inbred C57BL, Orthomyxoviridae Infections, Influenza A virus, Pneumonia, Pneumococcal, Streptococcus pneumoniae, Tryptophan, Tumor Necrosis Factor-alpha, Survival Analysis, Interleukin-10, Indoleamine-Pyrrole 2,3,-Dioxygenase, Mice

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