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Gene signature profiles in lung tisses of wild type mice or Nrf2 deficient mice infected with my nontuberculous mycobacteria

ABSTRACT: Gene signature profiles in lung tisses of wild type mice or Nrf2 deficient mice infected with my nontuberculous mycobacteria

PROVIDER: PRJNA603273 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10969127_1.fastq.gz	Fastqsanger.gz
	SRR10969127_2.fastq.gz	Fastqsanger.gz
	SRR10969128_1.fastq.gz	Fastqsanger.gz
	SRR10969128_2.fastq.gz	Fastqsanger.gz
	SRR10969129_1.fastq.gz	Fastqsanger.gz

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Gene signature profiles in lung tisses of wild type mice or Nrf2 deficient mice infected with my nontuberculous mycobacteria

Project description:Background. Nuclear erythroid 2 p45-related factor 2 (Nrf2) regulates the expression of antioxidant and detoxification genes and are thought to be important in protection against intracellular pathogens. The aim of this study was to determine the role of Nrf2 in the host defense against Mycobacterium avium complex (MAC) infection in mice. Methods. Wild-type mice and Nrf2-deficient mice were infected with MAC via intranasal inoculation with 1x107 CFU of Mycobacterium avium subsp. hominissuis. At 2 months after infection, the bronchoalveolar lavage fluid, lung tissues were collected, then, comprehensive transcriptome analysis in the lungs was performed by RNA-seq. Results. Nrf2-deficient mice were highly susceptible to MAC, compared with wild-type mice. There was no significant changes between genotypes in the level of oxidative stress. In addition, the expression of genes related to Th1 immunity and the proportion of Th1 cells were not changed between genotypes. Comprehensive transcriptome analysis showed that the expression of Nramp1 was much lower in the infected lungs of Nrf2-deficient mice than those of Wild-type mice. The expression of Nramp1 was also much lower in the infected alveolar macrophages of Nrf2-deficient mice than those of Wild-type mice. The result of electron microscopy showed that many infected alveolar macrophages from Nrf2-deficient mice were found to contain a large number of intracellular MAC bacteria compare to alveolar macrophages from wild-type mice, due to inhibition of phagolysosome fusion. Conclusions. This study identified that the Nramp1 regulated by Nrf2 is essential in defining the outcome of MAC disease. Nrf2 is a critical determinant for host resistance to MAC infection as a regulator for the expression of Nramp1.

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Project description:The incidence of pulmonary nontuberculous mycobacterial (PNTM) disease is increasing, but host susceptibility factors are not fully understood. We infected air-liquid interface (ALI) primary respiratory epithelial cell cultures with Mycobacterium avium complex (MAC) or Mycobacterium abscessus (MAB) and performed transcriptome sequencing (RNA-Seq) to identify relevant gene expression differences. We used cells from 4 different donors in order to try to obtain generalizable data. The differentiated respiratory epithelial cells in ALI were infected with MAC or MAB at MOI of 100:1 or 1000:1, and RNA-seq was performed at 1 and 3 days after infection. We found downregulation of ciliary genes, including several identified with polymorphisms in previous PNTM cohorts. The cytokine IL-32, the superpathway of cholesterol biosynthesis and downstream targets within the IL-17 signaling pathway were all elevated. The integrin signaling pathway was more upregulated by MAB than MAC infection. Working with primary respiratory epithelial cells infected with nontuberculous mycobacteria at ALI, we identified ciliary function, cholesterol biosynthesis, chemokine production and the IL-17 pathway as major targets of host responses to infection. Some of these pathways may be amenable to therapeutic manipulation.

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