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Suppression of pattern-recognition receptor TLR4 sensing does not alter lung responses to pneumovirus infection.

Abstract
Toll-like receptors (TLR) are an important component in the innate immune response to a wide variety of pathogens. Recently, a series of studies has addressed the hypothesis that TLR4 also participates in the host innate response against respiratory syncytial virus (RSV), the leading cause of lower respiratory tract infections in infants and young children. In most of the studies available, RSV, which is not a natural pathogen of mice, has been systematically used in mouse models of human bronchiolitis, with conflicting results. Pneumonia virus of mice (PVM), a member of the pneumovirus genus, shares many similarities with RSV. The serological and structural relationships that exist between them suggest that the immune response to these viruses may be similar in their respective natural hosts. To determine the role of TLR4 in host defense against PVM, TLR4-competent and TLR4-deficient mice were intranasally infected with PVM. Variation of body weight, pulmonary function values, histopathology, and pulmonary viral loads were analyzed. None of the investigated clinical, functional, histological and virological parameters was different between strains, which demonstrates that the sensitivity of the mouse to its natural pneumovirus infection is independent of the presence or absence of TLR4 sensing.
AuthorsPedro Faisca, Dao Bui Tran Anh, Anne Thomas, Daniel Desmecht
JournalMicrobes and infection (Microbes Infect) Vol. 8 Issue 3 Pg. 621-7 (Mar 2006) ISSN: 1286-4579 [Print] France
PMID16458035 (Publication Type: Journal Article)
Chemical References
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
Topics
  • Animals
  • Body Weight
  • Female
  • Gene Expression Regulation
  • Lung (metabolism, pathology, virology)
  • Mice
  • Pneumovirus Infections (metabolism)
  • Respiration
  • Respirovirus (physiology)
  • Toll-Like Receptor 4 (genetics, metabolism)

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