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. 2003 Oct 31;89(2-3):201-6.
doi: 10.1016/s0165-2478(03)00138-x.

Toll-like receptor 4 is not involved in host defense against respiratory tract infection with Sendai virus

Koenraad F van der Sluijs  1 , Leontine van Elden, Monique Nijhuis, Rob Schuurman, Sandrine Florquin, Henk M Jansen, René Lutter, Tom van der Poll
Affiliations

Toll-like receptor 4 is not involved in host defense against respiratory tract infection with Sendai virus

Koenraad F van der Sluijs et al. Immunol Lett. .

Abstract

Toll-like receptors (TLR) induce innate immune responses upon stimulation by a wide variety of pathogens. TLR4 has been implicated in innate immunity against respiratory syncytial virus (RSV) by an interaction with the viral envelope fusion (F) protein. Sendai virus (mouse parainfluenza type 1) shares many features with RSV, including a structurally and functionally similar F protein. To determine the role of TLR4 in host defense against Sendai virus respiratory tract infection, TLR4 mutant and wildtype mice were intranasally infected with Sendai virus. Sendai infection resulted in an increase in viral RNA copies in lung homogenates peaking on day 4. Pulmonary viral loads, histopathology, cytokine levels and leukocyte influx were similar in TLR4 mutant and wildtype mice. In spite of the structural similarities shared by the F proteins of Sendai virus and RSV, TLR4 is not involved in host defense against respiratory tract infection with Sendai virus.

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Figures

Fig. 1
Fig. 1
Viral kinetics by wildtype and TLR4 mutant mice for Sendai (A) and influenza (B). Viral load is expressed as RNA copies per lung (mean±S.E.) as determined by real-time PCR (six to eight mice per group, similar results were obtained in three independent experiments).
Fig. 2
Fig. 2
Cytokine levels in the lungs of Sendai-infected mice (left panels) and influenza-infected mice (right panels): IL-6 (A, B), IL-12 p40 (C, D) and IFN-γ (E, F). Data are expressed in pg/g lung tissue (mean±S.E., six to eight mice per group, similar results were obtained in three independent experiments). BD, below detection level, i.e. <1000 pg/g lung tissue. No differences were found between wildtype (filled bars) and TLR4 mutant mice (open bars) at any time-point for these cytokines.
Fig. 3
Fig. 3
Inflammatory response upon Sendai virus infection and influenza virus infection on day 4 (figure A and B resp.) and day 8 (figure C and D resp.) post-infection. Lung slides (six mice per group) were stained by hematoxylin and eosin (original magnification 33×). Representative slides are shown.
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