Sustained desensitization to bacterial Toll-like receptor ligands after resolution of respiratory influenza infectionCitation formats

  • External authors:
  • Arnaud Didierlaurent
  • John Goulding
  • Seema Patel
  • Robert Snelgrove
  • Lionel Low
  • Magali Bebien
  • Toby Lawrence
  • Leonie S. Van Rijt
  • Bart N. Lambrecht
  • Jean Claude Sirard

Standard

Sustained desensitization to bacterial Toll-like receptor ligands after resolution of respiratory influenza infection. / Didierlaurent, Arnaud; Goulding, John; Patel, Seema; Snelgrove, Robert; Low, Lionel; Bebien, Magali; Lawrence, Toby; Van Rijt, Leonie S.; Lambrecht, Bart N.; Sirard, Jean Claude; Hussell, Tracy.

In: Journal of Experimental Medicine, Vol. 205, No. 2, 18.02.2008, p. 323-329.

Research output: Contribution to journalArticle

Harvard

Didierlaurent, A, Goulding, J, Patel, S, Snelgrove, R, Low, L, Bebien, M, Lawrence, T, Van Rijt, LS, Lambrecht, BN, Sirard, JC & Hussell, T 2008, 'Sustained desensitization to bacterial Toll-like receptor ligands after resolution of respiratory influenza infection', Journal of Experimental Medicine, vol. 205, no. 2, pp. 323-329. https://doi.org/10.1084/jem.20070891

APA

Didierlaurent, A., Goulding, J., Patel, S., Snelgrove, R., Low, L., Bebien, M., ... Hussell, T. (2008). Sustained desensitization to bacterial Toll-like receptor ligands after resolution of respiratory influenza infection. Journal of Experimental Medicine, 205(2), 323-329. https://doi.org/10.1084/jem.20070891

Vancouver

Didierlaurent A, Goulding J, Patel S, Snelgrove R, Low L, Bebien M et al. Sustained desensitization to bacterial Toll-like receptor ligands after resolution of respiratory influenza infection. Journal of Experimental Medicine. 2008 Feb 18;205(2):323-329. https://doi.org/10.1084/jem.20070891

Author

Didierlaurent, Arnaud ; Goulding, John ; Patel, Seema ; Snelgrove, Robert ; Low, Lionel ; Bebien, Magali ; Lawrence, Toby ; Van Rijt, Leonie S. ; Lambrecht, Bart N. ; Sirard, Jean Claude ; Hussell, Tracy. / Sustained desensitization to bacterial Toll-like receptor ligands after resolution of respiratory influenza infection. In: Journal of Experimental Medicine. 2008 ; Vol. 205, No. 2. pp. 323-329.

Bibtex

@article{b116d65a885644418cf0c81764f013a8,
title = "Sustained desensitization to bacterial Toll-like receptor ligands after resolution of respiratory influenza infection",
abstract = "The World Health Organization estimates that lower respiratory tract infections (excluding tuberculosis) account for ∼35{\%} of all deaths caused by infectious diseases. In many cases, the cause of death may be caused by multiple pathogens, e.g., the life-threatening bacterial pneumonia observed in patients infected with influenza virus. The ability to evolve more efficient immunity on each successive encounter with antigen is the hallmark of the adaptive immune response. However, in the absence of cross-reactive T and B cell epitopes, one lung infection can modify immunity and pathology to the next for extended periods of time. We now report for the first time that this phenomenon is mediated by a sustained desensitization of lung sentinel cells to Toll-like receptor (TLR) ligands; this is an effect that lasts for several months after resolution of influenza or respiratory syncytial virus infection and is associated with reduced chemokine production and NF-κB activation in alveolar macrophages. Although such desensitization may be beneficial in alleviating overall immunopathology, the reduced neutrophil recruitment correlates with heightened bacterial load during secondary respiratory infection. Our data therefore suggests that post-viral desensitization to TLR signals may be one possible contributor to the common secondary bacterial pneumonia associated with pandemic and seasonal influenza infection. JEM {\circledC} The Rockefeller University Press.",
author = "Arnaud Didierlaurent and John Goulding and Seema Patel and Robert Snelgrove and Lionel Low and Magali Bebien and Toby Lawrence and {Van Rijt}, {Leonie S.} and Lambrecht, {Bart N.} and Sirard, {Jean Claude} and Tracy Hussell",
year = "2008",
month = "2",
day = "18",
doi = "10.1084/jem.20070891",
language = "English",
volume = "205",
pages = "323--329",
journal = "Journal of Experimental Medicine",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "2",

}

RIS

TY - JOUR

T1 - Sustained desensitization to bacterial Toll-like receptor ligands after resolution of respiratory influenza infection

AU - Didierlaurent, Arnaud

AU - Goulding, John

AU - Patel, Seema

AU - Snelgrove, Robert

AU - Low, Lionel

AU - Bebien, Magali

AU - Lawrence, Toby

AU - Van Rijt, Leonie S.

AU - Lambrecht, Bart N.

AU - Sirard, Jean Claude

AU - Hussell, Tracy

PY - 2008/2/18

Y1 - 2008/2/18

N2 - The World Health Organization estimates that lower respiratory tract infections (excluding tuberculosis) account for ∼35% of all deaths caused by infectious diseases. In many cases, the cause of death may be caused by multiple pathogens, e.g., the life-threatening bacterial pneumonia observed in patients infected with influenza virus. The ability to evolve more efficient immunity on each successive encounter with antigen is the hallmark of the adaptive immune response. However, in the absence of cross-reactive T and B cell epitopes, one lung infection can modify immunity and pathology to the next for extended periods of time. We now report for the first time that this phenomenon is mediated by a sustained desensitization of lung sentinel cells to Toll-like receptor (TLR) ligands; this is an effect that lasts for several months after resolution of influenza or respiratory syncytial virus infection and is associated with reduced chemokine production and NF-κB activation in alveolar macrophages. Although such desensitization may be beneficial in alleviating overall immunopathology, the reduced neutrophil recruitment correlates with heightened bacterial load during secondary respiratory infection. Our data therefore suggests that post-viral desensitization to TLR signals may be one possible contributor to the common secondary bacterial pneumonia associated with pandemic and seasonal influenza infection. JEM © The Rockefeller University Press.

AB - The World Health Organization estimates that lower respiratory tract infections (excluding tuberculosis) account for ∼35% of all deaths caused by infectious diseases. In many cases, the cause of death may be caused by multiple pathogens, e.g., the life-threatening bacterial pneumonia observed in patients infected with influenza virus. The ability to evolve more efficient immunity on each successive encounter with antigen is the hallmark of the adaptive immune response. However, in the absence of cross-reactive T and B cell epitopes, one lung infection can modify immunity and pathology to the next for extended periods of time. We now report for the first time that this phenomenon is mediated by a sustained desensitization of lung sentinel cells to Toll-like receptor (TLR) ligands; this is an effect that lasts for several months after resolution of influenza or respiratory syncytial virus infection and is associated with reduced chemokine production and NF-κB activation in alveolar macrophages. Although such desensitization may be beneficial in alleviating overall immunopathology, the reduced neutrophil recruitment correlates with heightened bacterial load during secondary respiratory infection. Our data therefore suggests that post-viral desensitization to TLR signals may be one possible contributor to the common secondary bacterial pneumonia associated with pandemic and seasonal influenza infection. JEM © The Rockefeller University Press.

U2 - 10.1084/jem.20070891

DO - 10.1084/jem.20070891

M3 - Article

VL - 205

SP - 323

EP - 329

JO - Journal of Experimental Medicine

JF - Journal of Experimental Medicine

SN - 0022-1007

IS - 2

ER -