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Influenza virus-induced type I interferons disrupt alveolar epithelial repair and tight junction integrity in the developing lung

ABSTRACT: Influenza virus-induced type I interferons disrupt alveolar epithelial repair and tight junction integrity in the developing lung

PROVIDER: PRJNA1211121 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32013700_1.fastq.gz	Fastqsanger.gz
	SRR32013700_2.fastq.gz	Fastqsanger.gz
	SRR32013800_1.fastq.gz	Fastqsanger.gz
	SRR32013800_2.fastq.gz	Fastqsanger.gz
	SRR32013701_1.fastq.gz	Fastqsanger.gz

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Influenza virus-induced type I interferons disrupt alveolar epithelial repair and tight junction integrity in the developing lung

Project description:Type I interferons (IFN-I) are key innate immune mediators which control viral infection in adults. Recently, using a neonatal murine model of influenza A infection (IAV), we demonstrated that IAV-infected murine neonates lacking a functional IFN-I receptor (IFNAR-/-) have significantly improved survival and reduced lung pathology relative to wild-type (WT) neonates. However, the opposite is observed in adults, with IAV-infected IFNAR-/- adults exhibiting enhanced morbidity relative to WT adults, indicating an age-specific IFN-I toxicity in neonates. Therefore, we hypothesized that IAV-induced IFN-I signaling in primary neonatal type II alveolar epithelial cells (TIIECs), the main cell type of IAV infection and initiator of host response in the lung, contributed to age-specific viral pathogenesis. To investigate the role of IFN-I signaling in TIIECs, we performed RNA-Seq on purified TIIECs in a multifactorial design, comparing 1. IFNAR-/- and WT genotypes, 2. neonatal and adult ages, 3. IAV-infected and uninfected, 4. over a three-day time course.Analysis of purified TIIECs revealed age, not infection status, as the primary driver of transcriptional differences in TIIECs. Subsequent pathway analysis demonstrated IAV-infected IFNAR-/- neonates significantly upregulate cell proliferation, tissue repair and tight junction genes at 2-days post-infection (dpi), compared to WT neonates. Next, to determine if these growth and repair differences persisted later in infection, targeted analysis of repair gene expression and immunofluorescent quantification of pulmonary sealing tight junction molecules ZO-1 and occludin was performed at 6-dpi. Relative to WT neonates, IFNAR-/- neonates had significantly higher whole lung occludin staining and repair gene expression. Together, our data demonstrates IFN-I signaling is extremely pathogenic in the developing lung because by disrupting alveolar repair and pulmonary barrier integrity.

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Loss of tight junction integrity induces loss of epithelial phenotype: case of Claudin11 knock out in testis.

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Project description:Epithelium barrier integrity is assumed at least in part by the presence of junctions between cells. Tight-junction formation may be necessary for Sertoli cells to cease dividing and to support germ cell development. Microarray analysis of P20 Cldn11 +/- and Cldn11-/- testes confirmed the impact od Cldn11 deficiency on cell cytoskeleton and junction-related genes. Keywords: transcriptomic analysis Two-condition experiment: P20 Cldn11 +/- vs. P20 Cldn11 -/- testes. A pool of RNA from P20 Cldn11 +/- group was used as the reference group. Each P20 Cldn11 -/- was compared to reference group. Three biological replicates were processed in dye swap.

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Clostridioides difficile toxins deregulate tight junction proteins.

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