Distinct Inflammatory Profiles Distinguish COVID-19 from Influenza with Limited Contributions from Cytokine Storm

Mudd, Philip A.; Crawford, Jeremy Chase; Turner, Jackson S.; Souquette, Aisha; Reynolds, Daniel B.; Bender, Diane; Bosanquet, James P.; Anand, Nitin; Striker, David A.; Martin, R. Scott; Boon, Adrianus C. M.; House, Stacey L.; Remy, Kenneth E.; Hotchkiss, Richard S.; Presti, Rachel; O’Halloran, Jane A.; Powderly, William; Ellebedy, Ali H.

doi:10.9734/bpi/mono/978-81-19039-63-0/ch3

Cited by 4 publications

(8 citation statements)

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“…The exact mechanisms by which IL‐17 may contribute to inflammation and lung injury in SARS‐CoV‐2 infection are incompletely understood, but IL‐17 response is known to mediate acute lung injury induced by viral infection 46 . Furthermore, we found relative abundance of Bifidobacterium in the salivary microbiome was negatively correlated with plasma concentrations of MCP‐1, another biomarker of severity in COVID‐19 patients 47 . Indeed, some strains of Bifidobacterium have been shown to downregulate MCP‐1 levels in vitro and in vivo, suggesting an anti‐inflammatory effect of certain Bifidobacterium strains 48,49 .…”

Section: Discussionmentioning

confidence: 70%

“…46 Furthermore, we found relative abundance of Bifidobacterium in the salivary microbiome was negatively correlated with plasma concentrations of MCP-1, another biomarker of severity in COVID-19 patients. 47 Indeed, some strains of Bifidobacterium have been shown to downregulate MCP-1 levels in vitro and in vivo, suggesting an anti-inflammatory effect of certain Bifidobacterium F I G U R E 4 (See caption on next page) strains. 48,49 Further work is needed to confirm these associations and elucidate any potential role of Bifidobacterium SARS-CoV-2 infection.…”

Section: Discussionmentioning

confidence: 99%

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The salivary and nasopharyngeal microbiomes are associated with SARS‐CoV‐2 infection and disease severity

Kim

Rauseo

et al. 2023

Journal of Medical Virology

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Emerging evidence suggests the oral and upper respiratory microbiota may play important roles in modulating host immune responses to viral infection. As the host microbiome may be involved in the pathophysiology of coronavirus disease 2019 , we investigated associations between the oral and nasopharyngeal microbiome and COVID-19 severity. We collected saliva (n = 78) and nasopharyngeal swab (n = 66) samples from a COVID-19 cohort and characterized the microbiomes using 16S ribosomal RNA gene sequencing. We also examined associations between the salivary and nasopharyngeal microbiome and age, COVID-19 symptoms, and blood cytokines. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection status, but not COVID-19 severity, was associated with community-level differences in the oral and nasopharyngeal microbiomes. Salivary and nasopharyngeal microbiome alpha diversity negatively correlated with age and were associated with fever and diarrhea. Oral Bifidobacterium, Lactobacillus, and Solobacterium were depleted in patients with severe COVID-19. Nasopharyngeal Paracoccus was depleted while nasopharyngeal Proteus, Cupravidus, and Lactobacillus were increased in patients with severe COVID-19.Further analysis revealed that the abundance of oral Bifidobacterium was negatively associated with plasma concentrations of known COVID-19 biomarkers interleukin 17F and monocyte chemoattractant protein-1. Our results suggest COVID-19 disease severity is associated with the relative abundance of certain bacterial taxa.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

The salivary and nasopharyngeal microbiomes are associated with SARS‐CoV‐2 infection and disease severity

Kim

Rauseo

et al. 2023

Journal of Medical Virology

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“…Mean interleukin-6 concentrations were nearly 100 times higher in patients with cytokine release syndrome (3110.5pg/mL, 632.3-15 302.9 pg/mL; p<0•0001), 27 times higher in patients with sepsis (983.6 pg/mL, 550.1-1758.4 pg/mL; p<0•0001), and 12 times higher in patients with acute respiratory distress syndrome unrelated to COVID-19 (460 pg/mL, 216•3-978•7 pg/mL; p<0•0001). Furthermore, a recent study demonstrated that only a small proportion of COVID-19 patients exhibited a cytokine profile considered by the authors to be consistent with cytokine storm and though several cytokines (including IL-6) were associated with mortality, the levels of these cytokines were in a similar range as patients with seasonal influenza (15). However, data from iMCD demonstrate that the level of circulating IL-6 is not a reliable predictor of response to IL-6 inhibition with some patients with low IL-6 levels benefitting from siltuximab and others with very elevated IL-6 levels not responding (16,17).…”

Section: Cytokine Levels In Covid-19mentioning

confidence: 97%

“…These antibodies were only detected in 4 (0.3%) of 1227 unexposed, healthy individuals (49). Additionally, single cell transcriptional profiling revealed profound suppression of interferon signalling among patients with COVID-19 compared with seasonal influenza (15). Finally, a recent study found that interferon-stimulated gene expressing cells were systemically absent in patients with severe COVID-19 compared to mild disease (50).…”

Section: Other Mechanisms Influencing Severity In Covid-19mentioning

confidence: 99%

Is severe COVID-19 a cytokine storm syndrome: a hyperinflammatory debate

Mehta

Fajgenbaum

2021

Current Opinion in Rheumatology

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The COVID-19 pandemic is a global public health crisis with considerable mortality and morbidity. A role for cytokine storm and therapeutic immunomodulation in a subgroup of patients with severe COVID-19 was proposed early in the pandemic. The concept of cytokine storm in COVID-19 has been criticised, given the lack of clear definition and relatively modest cytokinaemia (which may be necessary for viral clearance) compared with acute respiratory distress syndrome and bacterial sepsis.Here we consider the argument for and against the concept of cytokine storm in COVID-19. Recent findings:Several criteria have been proposed to identify the subgroup of COVID-19 patients exhibiting a cytokine storm. The beneficial effect of corticosteroids and interleukin (IL)-6 inhibition suggest that inflammation is a modifiable pathogenic component of severe COVID-19. The presence of genetic polymorphisms and pathogenic auto-autoantibodies in severe COVID-19 also suggests a significant contribution of immune dysregulation to poor outcomes.

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“…Most flow and mass cytometry-based studies of COVID-19 that analyzed PBMCs from patients with COVID-19 report reduced frequencies or abundances of circulating basophils [10][11][12] , monocytes [13][14][15] (especially CD14 lo CD16 hi non-classical monocytes 16 ), dendritic cells (DCs) 10,14,15,17 and natural killer (NK) cells 14,15,[17][18][19] when compared with those from healthy donors, with greater reductions in individuals with severe COVID-19 than in those with mild COVID-19 (refs. [15][16][17][18][19] ).…”

Section: Innate Immune Responsesmentioning

confidence: 99%