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Pre-existing interferon gamma conditions the lung to mediate early control of SARS-CoV-2

ABSTRACT: Pre-existing interferon gamma conditions the lung to mediate early control of SARS-CoV-2

PROVIDER: PRJNA991639 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25153463_1.fastq.gz	Fastqsanger.gz
	SRR25153463_2.fastq.gz	Fastqsanger.gz
	SRR25153464_1.fastq.gz	Fastqsanger.gz
	SRR25153464_2.fastq.gz	Fastqsanger.gz
	SRR25153465_1.fastq.gz	Fastqsanger.gz

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Pre-existing interferon gamma conditions the lung to mediate early control of SARS-CoV-2

Project description:Interferons (IFNs) are critical for anti-viral host defence. Type-1 and type-3 IFNs are typically associated with early control of viral replication and promotion of inflammatory immune responses; however, less is known about the role of IFNγ in anti-viral immunity, particularly in the context of SARS-CoV-2. We have previously observed that lung infection with attenuated bacteria M. bovis BCG achieved though intravenous (iv) administration provides strong protection against SARS-CoV-2 (SCV2) infection and disease in two mouse models. Assessment of the pulmonary cytokine milieu revealed that iv BCG induces a robust IFNγ response and low levels of IFNβ. Here we examined the role of ongoing IFNγ responses due to concurrent bacterial infection on SCV2 disease outcomes in two murine models. We report that IFNγ is required for iv BCG induced reduction in pulmonary viral loads and that this outcome is dependent on IFNγ receptor expression by non-hematopoietic cells. Further analysis revealed that BCG infection promotes the upregulation of ISGs with reported anti-viral activity by pneumocytes and bronchial epithelial cells in an IFNγ dependent manner, suggesting a possible mechanism for the observed protection. Finally, we confirmed the importance of IFNγ in these anti-viral effects by demonstrating that the recombinant cytokine itself provides strong protection against SCV2 challenge when administered intranasally. Together, our data show that a pre-established IFNγ response within the lung is protective against SCV2 infection, suggesting that concurrent or recent infections that drive IFNγ may limit the pathogenesis of this virus and supporting possible prophylactic uses of this cytokine in COVID-19 management.

2023-11-01 | GSE236601 | GEO

RNA-seq of monocyte derived macrophages exposed to arachidonic acid, interferon beta, or interferon gamma

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Project description:Human fibroblasts were infected or not with Toxoplasma gondii (Pru strain) for 18 h at a nominal MOI of 3. Cells were subsequently treated with human recombinant interferon gamma (0.5 ng/ml = 30 pM) for 0, 2, 4 and 8 h before RNA was harvested for cDNA microarray experiments. Uninfected samples were named N0, N2, N4 and N8 (i.e., N2 indicated uninfected cells treated with interferon gamma for 2 h); infected samples were named P0, P2, P4 and P8. Duplicate cultures were analyzed for each condition (indicated as "a" and "b"). The reference channel (ch1, green) contained Universal Human Reference RNA. Using a genome-wide microarray analysis we show here a complete dysregulation of interferon-gamma-inducible gene expression in human fibroblasts infected with Toxoplasma. Notably, 46 of the 127 interferon-gamma-responsive genes were induced and 19 were suppressed in infected cells before they were exposed to interferon gamma, indicating that other stimuli produced during infection may also regulate these genes. Following interferon-gamma treatment, none of the 127 interferon-gamma-responsive genes could be significantly induced in infected cells.

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