Host Immune Response to Clinical Hypervirulent Pulmonary Infections via Transcriptome Analysis.

(), especially those with hypervirulence, is becoming a global concern and posing great threat to human health. Studies on individual immune cells or cytokines have partially revealed the function of the host immune defense against pulmonary infection. However, systematic immune response against has not been fully elucidated. Herein, we report a transcriptome analysis of the lungs from a mouse pneumonia model infected with a newly isolated clinical strain YBQ. Total RNA was isolated from the lungs of mice 48 hours post infection to assess transcriptional alteration of genes. Transcriptome data were analyzed with KEGG, GO, and ICEPOP. Results indicated that upregulated transcription level of numerous cytokines and chemokines was coordinated with remarkably activated ribosome and several critical immune signaling pathways, including IL-17 and TNF signaling pathways. Notably, transcription of cysteine cathepsin inhibitor (, , and ) and potential cysteine-type endopeptidase inhibitor (, and ) were upregulated. Results of ICEPOP showed neutrophils functions as the most essential cell type against infection. Critical gene alterations were further validated by rt-PCR. Our findings provided a global transcriptional perspective on the mechanisms of host defense against infection and revealed some unique responding genes.