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Lung type II alveolar epithelial cells collaborate with CCR2+ inflammatory monocytes in host defense against acute viral infection

ABSTRACT: Lung type II alveolar epithelial cells collaborate with CCR2+ inflammatory monocytes in host defense against acute viral infection

PROVIDER: PRJNA664698 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12681700_1.fastq.gz	Fastqsanger.gz
	SRR12681700_2.fastq.gz	Fastqsanger.gz
	SRR12681701_1.fastq.gz	Fastqsanger.gz
	SRR12681701_2.fastq.gz	Fastqsanger.gz
	SRR12681702_1.fastq.gz	Fastqsanger.gz

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Lung type II alveolar epithelial cells collaborate with CCR2+ inflammatory monocytes in host defense against acute viral infection

Project description:The pulmonary immune system consists of a network of tissue-resident cells as well as immune cells that are recruited to the lungs during infection and/or inflammation. How these immune components communicate during an acute DNA viral infection is not well understood. Intranasal infection of mice with vaccinia virus causes lethal pneumonia and systemic dissemination. Here we report that vaccinia host range protein C7 is a critical virulence factor. We provide evidence that lung type II alveolar epithelial cells (AECIIs) provide first-line of defense against viral infection by inducing IFN-b and IFN-stimulated genes via the activation of the MDA5 and STING-mediated nucleic acid-sensing pathways and the type I IFN positive feedback loop. This leads to the recruitment and activation of CCR2+ inflammatory monocytes in the lungs, which are indispensable to fight against viral dissemination. Our data provide novel insights into how the lung AECIIs orchestrate innate immune responses to defend pulmonary viral infection.

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Transcriptome comparison between CCR2+ and CCR2- classical monocytes in SIV-infected Macaca nemestrina

Project description:Monocytes have been categorized in three main subpopulations based on CD14 and CD16 surface expression. Classical monocytes are the most abundant subset in the blood. They express a CD14+CD16-CCR2+ phenotype, which confers on them the ability to migrate to inflammatory sites by quickly responding to CCL2 signaling. Here we identified and characterized the surge and expansion of a novel monocyte subset during SIV and HIV infection. They were undistinguishable from classical monocytes regarding CD14 and CD16 expression, but did not express surface CCR2. Transcriptome analysis of sorted cells confirmed that they represent a distinct subpopulation that expresses lower levels of inflammatory cytokines and activation markers than their CCR2+ counterparts. They exhibited impaired phagocytosis and deficient chemotaxis in response to CCL2 and CCL7, besides being refractory to SIV infection. We named these cells atypical CCR2- classical (ACC) monocytes, and believe they play an important role in AIDS pathogenesis, possibly reflecting an anti-inflammatory response against the extreme immune activation observed during SIV and HIV infection. Antiretroviral therapy caused this population to decline in both macaque and human subjects, suggesting that this atypical phenotype may be induced by viral replication. Expression profiling by NanoString nCounter gene expression system. Classical monocytes (CD14++CD16-) from six SIV-infected macaques (day 14 post inoculation) were sorted in two groups according to CCR2 expression.

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Lung type II alveolar epithelial cells collaborate with CCR2<sup>+</sup> inflammatory monocytes in host defense against poxvirus infection.

Project description: Not available

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Transcriptome comparison between CCR2+ and CCR2- classical monocytes in SIV-infected Macaca nemestrina

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