Mendelian randomization analysis identified tumor necrosis factor as being associated with severe COVID-19

Song, Hongfei; Lei, Na; Zeng, Lei; Li, Xiuyan; Jiang, Cen; Qian, Feng; Su, Yue; Liu, Ji‐Bin; Mu, Jie

doi:10.3389/fphar.2023.1171404

Cited by 3 publications

(2 citation statements)

References 41 publications

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“…Using the same filter (q<0.05) 528 DEGs were identified and were analysed as above ( Supplementary Table 6 ). A number of proinflammatory cytokine IPA USR signatures were up-regulated ( Figure 4 , Proinflammatory cytokines), all are associated with increased COVID-19 severity; TNF ( 100 , 101 ), IL1B ( 102 ), IL1A ( 103 ), OSM ( 104 ), IL17A ( 105 ), and IL6 ( 106 ). Upregulated activity of the transcription factor EPHAS is also associated with pulmonary inflammatory responses in lethal COVID-19 ( 107 ).…”

Section: Resultsmentioning

confidence: 99%

Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung

Bishop,

Yan,

Nguyen

et al. 2024

Front. Immunol.

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IntroductionGlobal microplastic (MP) pollution is now well recognized, with humans and animals consuming and inhaling MPs on a daily basis, with a growing body of concern surrounding the potential impacts on human health.MethodsUsing a mouse model of mild COVID-19, we describe herein the effects of azide-free 1 μm polystyrene MP beads, co-delivered into lungs with a SARS-CoV-2 omicron BA.5 inoculum. The effect of MPs on the host response to SARS-CoV-2 infection was analysed using histopathology and RNA-Seq at 2 and 6 days post-infection (dpi).ResultsAlthough infection reduced clearance of MPs from the lung, virus titres and viral RNA levels were not significantly affected by MPs, and overt MP-associated clinical or histopathological changes were not observed. However, RNA-Seq of infected lungs revealed that MP exposure suppressed innate immune responses at 2 dpi and increased pro-inflammatory signatures at 6 dpi. The cytokine profile at 6 dpi showed a significant correlation with the ‘cytokine release syndrome’ signature observed in some COVID-19 patients.DiscussionThe findings are consistent with the recent finding that MPs can inhibit phagocytosis of apoptotic cells via binding of Tim4. They also add to a growing body of literature suggesting that MPs can dysregulate inflammatory processes in specific disease settings.

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Section: Resultsmentioning

confidence: 99%

Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung

Bishop,

Yan,

Nguyen

et al. 2024

Front. Immunol.

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“…A number of proinflammatory cytokine IPA USR signatures were up-regulated (Fig. 4, Proinflammatory cytokines), all are associated with increased COVID-19 severity; TNF (Kokkotis et al, 2022;Song et al, 2023), IL1B (Labzin et al, 2023), IL1A (Sanchez-de Prada et al, 2022), OSM (Arunachalam et al, 2020), IL17A (Yin et al, 2023a), and IL6 (Avdeev et al, 2021). Upregulated activity of the transcription factor EPHAS is also associated with pulmonary inflammatory responses in lethal COVID-19 (Lopez-Cortes et al, 2022).…”

Section: Some Anti-inflammatory Signatures Increased By Mps At 2 Dpimentioning

confidence: 99%

Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung

Bishop,

Yan,

Nguyen

et al. 2023

Preprint

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Global microplastic (MP) pollution is now well recognized, with humans and animals consuming and inhaling MPs on a daily basis. Herein we described the effects of azide-free, 1 µm polystyrene MP beads co-delivered into lungs with a SARS-CoV-2 omicron BA.5 inoculum using a mouse model of mild COVID-19. Lung virus titres and viral RNA levels were not significantly affected by MPs, with overt clinical or histopathological changes also not observed. However, RNA-Seq of infected lungs revealed that MP exposure suppressed innate immune responses at 2 days post infection (dpi) and increased pro-inflammatory signatures at 6 dpi. The cytokine profile at 6 dpi showed a significant correlation with the ‘cytokine release syndrome’ signature seen in some severe COVID-19 patients. This study adds to a growing body of literature suggesting that MPs can dysregulate inflammation in specific disease settings.Graphical AbstractHIGHLIGHTSA single inoculation of microplastics dysregulated SARS-CoV-2 lung inflammationAt the peak of SARS-CoV-2 infection microplastics decreased early innate responsesLater post infection microplastics promoted a “cytokine release syndrome” signatureA key mechanism may involve the inhibition of the phagocytosis of infected cellsAzide-free microplastics were used, with no elevated ROS responses identifiedPostulated mechanisms whereby microplastics might decrease the proinflammatory responses 2 days after SARS-CoV-2 infection, yet promote the proinflammatory ‘cytokine release syndrome’ signature at 6 days post infection.

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COVID-19, vaccination and migraine: Causal association or epiphenomenon?

Jiang,

Zhang,

Meng

et al. 2024

PLoS ONE

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Background Diverse studies have revealed discrepant evidence concerning the causal association between Corona Virus Disease 2019 (COVID-19) and COVID-19 vaccination in relation to migraines. Investigating the correlation between the former two factors and migraines can facilitate policymakers in the precise formulation of comprehensive post-pandemic interventions while urging the populace to adopt a judicious perspective on COVID-19 vaccination. Methods We undertook a Mendelian randomization (MR) study. The primary assessment of the causal relationship between the three different COVID-19 exposures and migraine was conducted using the standard inverse variance weighted (IVW) approach. In the supplementary analysis, we also employed two methodologies: the weighted median estimator (WME) and the MR-Egger regression. Ultimately, the reliability and stability of the outcomes were assessed via Cochran’s Q test, the leave-one-out method, the MR-Egger intercept test, and the MR pleiotropy residual sum and outlier (MR-PRESSO) test. Results The results indicate an absence of correlation between genetically predicted COVID-19 (①Very severe respiratory confirmed COVID-19: odds ratio [OR], 1.0000881; 95%CI, 0.999748–1.000428; p = 0.6118; ②Hospitalized COVID-19: OR, 1.000024; 95%CI, 0.9994893–1.000559; p = 0.931;③SARS-CoV-2 infection: OR, 1.000358; 95%CI, 0.999023–1.001695; p = 0.5993) and the risk of migraine. Furthermore, the MR-Egger regression and WME also yielded no evidence of COVID-19 elevating the risk of migraine occurrence. Sensitivity analysis affirmed the robustness and consistency of all outcomes. Conclusions The results of this study do not offer genetic evidence to substantiate a causal relationship between COVID-19 and migraines. Thus, the deduction drawn from COVID-19 genetic data is that COVID-19 vaccination is unlikely to exert an impact on the occurrence of migraines, though this conclusion warrants further investigation.

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Mendelian randomization analysis identified tumor necrosis factor as being associated with severe COVID-19

Cited by 3 publications

References 41 publications

Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung

Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung

Microplastics dysregulate innate immunity in the SARS-CoV-2 infected lung

COVID-19, vaccination and migraine: Causal association or epiphenomenon?

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