Anti-IFN-γ therapy alleviates acute lung injury induced by severe influenza A (H1N1) pdm09 infection in mice

Liu, Bo; Bao, Linlin; Wang, Li; Li, Fengdi; Wen, Mingjie; Li, Hui; Deng, Wei; Zhang, Xulong; Cao, Bin

doi:10.1016/j.jmii.2019.07.009

Cited by 46 publications

(43 citation statements)

References 25 publications

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“…IL-6, IFN-γ, IP-10 and MCP-1 have been shown to be elevated in people infected with influenza [40] , [41] , [42] , [43] . In experimental models, blockade of IFN-γ and IP-10 with monoclonal antibodies ameliorates virus-induced lung injury [ 44 , 45 ].…”

Section: Discussionmentioning

confidence: 99%

Intranasal Bifidobacterium longum protects against viral-induced lung inflammation and injury in a murine model of lethal influenza infection

Groeger

Schiavi

Grant³

et al. 2020

EBioMedicine

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Background Prophylactic strategies are urgently needed for prevention of severe inflammatory responses to respiratory viral infections. Bacterial-host interactions may modify the immune response to viral infections. Methods We examined the contribution of Intranasal administration of two different Bifidobacterium longum strains or its isolated cell wall in controlling viral induced inflammation using a murine model of influenza infection. We monitored mortality and morbidity over a 10-day period and viral load, differential broncho alveolar lavage (BAL) fluid inflammatory cell counts, Lung tissue histology, BAL and serum cytokines, markers of vascular damage and cell death were quantified. Findings Intranasal administration of Bifidobacterium longum 35624® or its isolated cell wall prior to virus inoculation significantly reduced viral load within the lungs and significantly improved survival. Reduced viral load was associated with reduced lung injury as suggested by cell death and vascular leakage markers, a shift from neutrophil to macrophage recruitment, reduced inflammatory cytokine levels (including IL-6), reduced type 1 and 2 interferon levels, but increased levels of interferon-λ and surfactant protein D. These protective effects were maintained when the bifidobacterial cell wall preparation was administered 24 h after viral inoculation. The protective effects were also observed for the Bifidobacterium longum PB-VIR™ strain. Interpretation Exposure to these bifidobacterial strains protect against the inflammatory sequelae and damage associated with uncontrolled viral replication within the lung. Funding This work has been funded, in part, by a research grant from GlaxoSmithKline, PrecisionBiotics Group Ltd., Swiss National Science Foundation grants (project numbers CRSII3_154488, 310030_144219, 310030_127356 and 310030_144219) and Christine Kühne – Center for Allergy Research and Education (CK-CARE).

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Section: Discussionmentioning

confidence: 99%

Intranasal Bifidobacterium longum protects against viral-induced lung inflammation and injury in a murine model of lethal influenza infection

Groeger

Schiavi

Grant³

et al. 2020

EBioMedicine

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“…The late phase, from day 6 to day 28, may be the product of incoming antigen-specific T cells. Importantly, simply neutralizing INFg in a mouse model of infection with influenza A virus strain A/California/07/2009 (H1N1v; "Swine Flu") is sufficient to not only alleviate acute lung injury but also to increase weight and survival rate 19 . Reduced IFNg is associated with reduced TNFa and NFkB activation.…”

Section: Discussionmentioning

confidence: 99%

Classical drug digitoxin inhibits influenza cytokine storm, with implications for COVID-19 therapy

Pollard¹,

Blanco

Pollard

et al. 2020

Preprint

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Influenza viruses, corona viruses and related pneumotropic viruses cause sickness anddeath partly by inducing a hyper-proinflammatory response by immune cells and cytokines in the host airway. Here we show that the cardiac glycoside digitoxin suppresses this response induced by influenza virus strain A/Wuhan/H3N2/359/95 in the cotton rat lung. The cytokines TNFa, GRO/KC, MIP2, MCP1, TGFb, and IFNg. are significantly reduced. Since the hyperproinflammatory overproduction of cytokines is a host response, we suggest that digitoxin may have therapeutic potential for not only influenza and but also for coronovirus infections.

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“…8 21 36 94 Additionally, IFNγ enhances IL-6 production in monocytes 95 and an IFNγ-related cytokine storm syndrome was reported in some patients during the 2003 SARS coronavirus outbreak. 96 Anti-IFN antibodies have been demonstrated to alleviate acute lung injury induced by severe H1N1 influenza infection in murine models, 97 and a trial of the human monoclonal anti-IFNγ emapalumab in combination with the IL-1 receptor antagonist anakinra for COVID-19 is ongoing. 98 Anti-interferon therapy is approved in the US for the treatment of primary HLH.…”

Section: Interferon Gammamentioning

confidence: 99%

The Society for Immunotherapy of Cancer perspective on regulation of interleukin-6 signaling in COVID-19-related systemic inflammatory response

Arnaldez

O’Day

Drake

et al. 2020

J Immunother Cancer

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The pandemic caused by the novel coronavirus SARS-CoV-2 has placed an unprecedented burden on healthcare systems around the world. In patients who experience severe disease, acute respiratory distress is often accompanied by a pathological immune reaction, sometimes referred to as ‘cytokine storm’. One hallmark feature of the profound inflammatory state seen in patients with COVID-19 who succumb to pneumonia and hypoxia is marked elevation of serum cytokines, especially interferon gamma, tumor necrosis factor alpha, interleukin 17 (IL-17), interleukin 8 (IL-8) and interleukin 6 (IL-6). Initial experience from the outbreaks in Italy, China and the USA has anecdotally demonstrated improved outcomes for critically ill patients with COVID-19 with the administration of cytokine-modulatory therapies, especially anti-IL-6 agents. Although ongoing trials are investigating anti-IL-6 therapies, access to these therapies is a concern, especially as the numbers of cases worldwide continue to climb. An immunology-informed approach may help identify alternative agents to modulate the pathological inflammation seen in patients with COVID-19. Drawing on extensive experience administering these and other immune-modulating therapies, the Society for Immunotherapy of Cancer offers this perspective on potential alternatives to anti-IL-6 that may also warrant consideration for management of the systemic inflammatory response and pulmonary compromise that can be seen in patients with severe COVID-19.

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Anti-IFN-γ therapy alleviates acute lung injury induced by severe influenza A (H1N1) pdm09 infection in mice

Cited by 46 publications

References 25 publications

Intranasal Bifidobacterium longum protects against viral-induced lung inflammation and injury in a murine model of lethal influenza infection

Intranasal Bifidobacterium longum protects against viral-induced lung inflammation and injury in a murine model of lethal influenza infection

Classical drug digitoxin inhibits influenza cytokine storm, with implications for COVID-19 therapy

The Society for Immunotherapy of Cancer perspective on regulation of interleukin-6 signaling in COVID-19-related systemic inflammatory response

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