Differential expression of toll-like receptor 13 and ribosomal protein L29 in inflammatory lung and brain.

Viral dsRNA acts as the paramount pathogen-associated molecular pattern on infection and orchestrates inflammation or immune cascades of the host's tissues. The comparative effects or mechanisms of inflammation or immunity in different organs on viral infections are critical in immunology or virology. To outline the organ-based molecular mechanisms of inflammation or immunity on viral infection, we challenged mice with the viral mimic poly(I:C) and quantified inflammatory cytokines Il-1b and TNF-α in the brain and lung tissues. As cytokines showed differential expression, transcriptome screenings of mouse lung and brain tissues were analyzed. We identified 629 differentially expressed genes (DEGs) in lung and 137 DEGs in brain tissues with a few overlapping genes. Most of those DEGs were interferon-stimulated genes (ISGs) that are involved in the anti-viral defense mechanisms. The expression patterns of viral dsRNA stimulated genes, and consequently, their association with different molecular mechanisms of inflammation and immunity were specific to the organs. The effects of viral mimic were higher in the lung than in the brain in terms of the number of DEGs and ISGs. Interestingly ribosomal protein L29 (Rpl29), a cell surface heparin-binding protein, was upregulated in the brain and downregulated in the lung. The contrasting expression of Rpl29 gene might be responsible for tissue-specific inflammatory responses in lung and brain tissue on virus infection. In addition, the upregulation of Tlr13, a dsRNA and bacterial 23s rRNA receptor, in the poly(I:C)-stimulated mouse lungs suggests its important role in lung inflammatory responses. It is likely that the combined effects of these genes orchestrate the organ-specific inflammatory or immune responses. Our findings would be beneficial to explore new insights in inflammation and immunity against many critical viral diseases.