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Comprehensive Analysis of the Systemic Transcriptomic Alternations and Inflammatory Response during the Occurrence and Progress of COVID-19.

ABSTRACT: The pandemic of the coronavirus disease 2019 (COVID-19) has posed huge threats to healthcare systems and the global economy. However, the host response towards COVID-19 on the molecular and cellular levels still lacks full understanding and effective therapies are in urgent need. Here, we integrate three datasets, GSE152641, GSE161777, and GSE157103. Compared to healthy people, 314 differentially expressed genes were identified, which were mostly involved in neutrophil degranulation and cell division. The protein-protein network was established and two significant subsets were filtered by MCODE: ssGSEA and CIBERSORT, which comprehensively revealed the alternation of immune cell abundance. Weighted gene coexpression network analysis (WGCNA) as well as GO and KEGG analyses unveiled the role of neutrophils and T cells during the progress of the disease. Based on the hospital-free days after 45 days of follow-up and statistical methods such as nonnegative matrix factorization (NMF), submap, and linear correlation analysis, 31 genes were regarded as the signature of the peripheral blood of COVID-19. Various immune cells were identified to be related to the prognosis of the patients. Drugs were predicted for the genes in the signature by DGIdb. Overall, our study comprehensively revealed the relationship between the inflammatory response and the disease course, which provided strategies for the treatment of COVID-19.

SUBMITTER: Mo S

PROVIDER: S-EPMC8397550 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background: Tobacco smoking is known to be involved in the pathogenesis of several cardiopulmonary diseases. Additionally, smokers are highly susceptible to infectious agents due to weakened immunity. However, the progression of lung injury based on SARS-CoV-2-mediated COVID-19 pathogenesis amongst smokers and those with pre-existing pulmonary diseases is not known. We determined the systemic levels and activity of COVID-19 associated proteins, cytokine/chemokines, and lipid mediators (lipidomics) amongst COVID-19 patients with and without a history of smoking to understand the underlying susceptible factor in the pathogenesis of COVID-19. Methods: We obtained serum from healthy (CoV-), COVID-19 positive (CoV+), and COVID-19 recovered (CoV Rec) subjects with and without a history of smoking. We conducted a Luminex multiplex assay (cytokine levels), LC/MS (eicosanoids or oxylipin panel), and ACE2 enzymatic activity assays on the serum samples to determine the systemic changes in COVID-19 patients. Results: On comparing the levels of serum ACE2 amongst COVID-19 (positive and recovered) patients and healthy controls, we found a pronounced increase in serum ACE2 levels in patients with COVID-19 infection. Furthermore, ACE2 enzyme activity was significantly increased amongst COVID-19 patients with a smoking history. Also, we analyzed the levels of Angiotensin 1-7 (Ang1-7) peptide, the product of enzymatic action of ACE2, in the serum samples. We found significantly high levels of Ang1-7 in the serum of both CoV+ and CoV Rec patients. Our data further demonstrated a smoking-induced increase in serum furin and inflammatory cytokine [IFNγ(p = 0.0836), Eotaxin (p < 0.05), MCP-1 (p < 0.05), and IL-9 (p = 0.0991)] levels in COVID-19 patients as compared to non-smoking controls. Overall, our results show that smoking adversely affects the levels of systemic inflammatory markers and COVID-19 associated proteins, thus suggesting that COVID-19 infection may have severe outcomes amongst smokers.

Dataset Information

Comprehensive Analysis of the Systemic Transcriptomic Alternations and Inflammatory Response during the Occurrence and Progress of COVID-19.

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