Expression of toll-like receptor 2 and 4 in lipopolysaccharide-induced lung injury in mouse

Pattern recognition receptors, which include the toll-like receptors (TLRs), are considered to play an important role in the response against lipopolysaccharide (LPS). In this study, we performed a reverse transcriptase/polymerase chain reaction (RT-PCR) study, Western analysis, immunohistochemical...

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Bibliographic Details
Published in:Cell and tissue research 2005-07, Vol.321 (1), p.75-88
Main Authors: Saito, Takuma, Yamamoto, Takashi, Kazawa, Toshihiro, Gejyo, Humitake, Naito, Makoto
Format: Article
Language:English
Subjects:
Animals
Blotting, Western
Bronchi - cytology
Epithelium - metabolism
Female
Fluorescein-5-isothiocyanate
Fluorescent Dyes
Immunohistochemistry
In Situ Hybridization
Lipopolysaccharide Receptors - drug effects
Lipopolysaccharide Receptors - metabolism
Lipopolysaccharides - metabolism
Lipopolysaccharides - toxicity
Lung - metabolism
Lung - physiopathology
Macrophages - metabolism
Mice
Mice, Inbred ICR
Microscopy, Confocal
Reverse Transcriptase Polymerase Chain Reaction
Time Factors
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Summary:Pattern recognition receptors, which include the toll-like receptors (TLRs), are considered to play an important role in the response against lipopolysaccharide (LPS). In this study, we performed a reverse transcriptase/polymerase chain reaction (RT-PCR) study, Western analysis, immunohistochemical staining, and RT-PCR-amplified in situ hybridization of TLR2 and TLR4 in the case of LPS-induced lung injury. The expression of TLR2 and TLR4 increased in the lung rapidly after LPS inhalation and peaked at 24 h, followed by a gradual decrease. TLR2 and TLR4 expression was observed on the bronchial epithelium and tissue macrophages. In the early hours after inhalation of fluorescein-isothiocyanate (FITC)-labeled LPS, LPS was detected mainly on the bronchial epithelium and on a few of tissue macrophages. One day after inhalation, the LPS signals disappeared in the lungs of the mice, except for a few alveolar macrophages. The expression of TLR2, TLR4, and CD14 was coincident with the signals of FITC-labeled LPS. Instillation of liposome-encapsulated dichloromethylene diphosphonate induced a significant decrease in alveolar macrophages. In the macrophage-depleted mice, however, expression of TLR2 and TLR4 mRNA or protein was slightly suppressed in the lung after LPS inhalation. These data suggest that the bronchial epithelium and macrophages play crucial roles in LPS-induced lung injury through TLR2 and TLR4.
ISSN:0302-766X
1432-0878
DOI:10.1007/s00441-005-1113-9