Differential Expression of Mitosis and Cell Cycle Regulatory Genes during Recovery from an Acute Respiratory Virus Infection

Abstract

Acute respiratory virus infections can have profound and long-term effects on lung function that persist even after the acute responses have fully resolved. In this study, we examined gene expression by RNA sequencing in the lung tissue of wild-type BALB/c mice that were recovering from a sublethal infection with the pneumonia virus of mice (PVM), a natural rodent pathogen of the same virus family and genus as the human respiratory syncytial virus. We compared these responses to gene expression in PVM-infected mice treated with Lactobacillus plantarum, an immunobiotic agent that limits inflammation and averts the negative clinical sequelae typically observed in response to acute infection with this pathogen. Our findings revealed prominent differential expression of inflammation-associated genes as well as numerous genes and gene families implicated in mitosis and cell-cycle regulation, including cyclins, cyclin-dependent kinases, cell division cycle genes, E2F transcription factors, kinesins, centromere proteins, and aurora kinases, among others. Of particular note was the differential expression of the cell division cycle gene Cdc20b, which was previously identified as critical for the ex vivo differentiation of multi-ciliated cells. Collectively, these findings provided us with substantial insight into post-viral repair processes and broadened our understanding of the mechanisms underlying Lactobacillus-mediated protection.

Tumor-promoting inflammation in lung cancer: A literature review

“…Tumor cells that have been formed can escape from the patient's immune system by expressing PDL-1 (Programmed Cell-Death-1 Ligand) so that tumor cells look like normal cells. These modulators are usually desctibed in 40%–50% of NSCLC cells [ [25] , [26] , [27] ].…”

“…One of the promotional factors that cause tumor cells to experience excessive/abnormal proliferation is EGFR (Epidermal Growth Factor Receptor). It is a transmembrane factor with intrinsic tyrosine kinase activity that triggers instability of cell genes and DNA mismatches at several nucleotide levels in lung cancer cells [ [25] , [26] , [27] ].…”

“…For example, MMP can activate insoluble TNF-α into soluble TNF-α. MMP-9 also controls the IL-12-dependent proliferation of T lymphocytes [ [25] , [26] , [27] , [28] ].…”