Both the role and source of tumor necrosis factor (TNF-α) in lipopolysaccharide (LPS)-induced nasal inflammation were investigated using TNF-α gene deficient (TNF-α -/-) mice and chimeric mice that are TNF-α gene deficient only in bone marrow-derived cells. In the present study, intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) mRNA expression levels in the nasal mucosa were significantly decreased following intranasal instillation of LPS in TNF-α gene deficient mice compared to those in wild type mice. In contrast, ICAM-1 and VCAM-1 mRNA expressions were not significantly decreased although TNF-α mRNA expression was dramatically decreased in TNF-α gene deficient bone marrow-transplanted-chimeric (TNF-α -/-→+/+) mice compared to those in wild type bone marrow-transplanted-control (TNF-α +/+→+/+) mice. These results indicate that the elevation of TNF-α mRNA in the nasal mucosa is mainly originated from bone marrow-derived cells. However, even low expression of TNF-α at local inflammation sites is sufficient to induce the expression of adhesion molecules in acute LPS-induced experimental rhinitis.
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