Bioinformatics analysis of potential common pathogenic mechanisms for COVID-19 infection and primary Sjogren’s syndrome

Luo, Hong; Zhou, Xin

doi:10.3389/fimmu.2022.938837

Cited by 13 publications

(5 citation statements)

References 73 publications

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“…Moreover, we unveiled a tight co-expression relationship among these hub genes for the first time. Other studies have revealed shared hub genes between COVID-19 and primary Sjogren's syndrome (Luo and Zhou 2022 ) or rheumatoid arthritis (Hu et al 2022 ), such as MX1 and RSAD2, consistent with this study, indicating that the identified hub genes and their co-expression relations might be promising biomarkers for pan-ADs and COVID-19.…”

Section: Discussionsupporting

confidence: 90%

Multi-omics analysis uncovered systemic lupus erythematosus and COVID-19 crosstalk

Nian,

Mao,

et al. 2024

Mol Med

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Background Studies have highlighted a possible crosstalk between the pathogeneses of COVID-19 and systemic lupus erythematosus (SLE); however, the interactive mechanisms remain unclear. We aimed to elucidate the impact of COVID-19 on SLE using clinical information and the underlying mechanisms of both diseases. Methods RNA-seq datasets were used to identify shared hub gene signatures between COVID-19 and SLE, while genome-wide association study datasets were used to delineate the interaction mechanisms of the key signaling pathways. Finally, single-cell RNA-seq datasets were used to determine the primary target cells expressing the shared hub genes and key signaling pathways. Results COVID-19 may affect patients with SLE through hematologic involvement and exacerbated inflammatory responses. We identified 14 shared hub genes between COVID-19 and SLE that were significantly associated with interferon (IFN)-I/II. We also screened and obtained four core transcription factors related to these hub genes, confirming the regulatory role of the IFN-I/II-mediated Janus kinase/signal transducers and activators of transcription (JAK-STAT) signaling pathway on these hub genes. Further, SLE and COVID-19 can interact via IFN-I/II and IFN-I/II receptors, promoting the levels of monokines, including interleukin (IL)-6/10, tumor necrosis factor-α, and IFN-γ, and elevating the incidence rate and risk of cytokine release syndrome. Therefore, in SLE and COVID-19, both hub genes and core TFs are enriched within monocytes/macrophages. Conclusions The interaction between SLE and COVID-19 promotes the activation of the IFN-I/II-triggered JAK-STAT signaling pathway in monocytes/macrophages. These findings provide a new direction and rationale for diagnosing and treating patients with SLE–COVID-19 comorbidity.

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Section: Discussionsupporting

confidence: 90%

Multi-omics analysis uncovered systemic lupus erythematosus and COVID-19 crosstalk

Nian,

Mao,

et al. 2024

Mol Med

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“…Contemporary, the rapid advances in bioinformatics approaches allow us to delve deeper into the molecularlevel investigation of disease-disease interactions and co-pathogenesis [23][24][25][26]. To discover the biological mechanisms of LUAD and PAH, we used the weighted gene co-expression network analysis (WGCNA) to discover the co-expression cluster and connected shared genes in these two diseases and explored potential drug molecules using molecular docking.…”

Section: Introductionmentioning

confidence: 99%

G6PD is a prognostic biomarker correlated with immune infiltrates in lung adenocarcinoma and pulmonary arterial hypertension

Ding,

Sang,

et al. 2024

Aging

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Background: Lung adenocarcinoma (LUAD) with Pulmonary arterial hypertension (PAH) shows a poor prognosis. Detecting related genes is imperative for prognosis prediction. Methods: The gene expression profiles of LUAD and PAH were acquired from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) database, respectively. The co-expression modules associated with LUAD and PAH were evaluated using the Weighted Gene Co-Expression Network Analysis (WGCNA). The relationship between key gene expression with immune-cell infiltration and the tumor immune microenvironment (TIME) was evaluated. We confirmed the mRNA and protein levels in vivo and vitro. G6PD knockdown was used to conduct the colony formation assay, transwell invasion assay, and scratch wound assay of A549 cells. EDU staining and CCK8 assay were performed on G6PD knockdown HPASMCs. We identified therapeutic drug molecules and performed molecular docking between the key gene and small drug molecules. Results: Three major modules and 52 overlapped genes were recognized in LUAD and PAH. We identified the key gene G6PD, which was significantly upregulated in LUAD and PAH. In addition, we discovered a significant difference in infiltration for most immune cells between high-and low-G6PD expression groups. The mRNA and protein expressions of G6PD were significantly upregulated in LUAD and PAH. G6PD knockdown decreased proliferation, cloning, and migration of A549 cells and cell proliferation in HPASMCs. We screened five potential drug molecules against G6PD and targeted glutaraldehyde by molecular docking. Conclusions: This study reveals that G6PD is an immune-related biomarker and a possible therapeutic target for LUAD and PAH patients.

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“…Sjogren’s syndrome (SS) is a systemic autoimmune chronic disease characterized by marked exocrine glandular dysfunction such as salivary and lachrymal glands, presenting a persistent dryness of mouth and eyes 1 . In some areas like China, the prevalence can reach as high as 5.6%, with a female-to-male ratio of 9:1 due to an association with hormonal changes 2 . SS process can also extend to several other organs and tissues including lungs, kidneys, blood vessels, skin, and nervous system, which may impair patients’ quality of life.…”

Section: Introductionmentioning

confidence: 99%

Effect of adipose tissue-derived stem cells therapy on clinical response in patients with primary Sjogren’s syndrome

Li,

Lu,

Shi

et al. 2023

Sci Rep

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The purpose of this trial was to clinically assess the effect and safety of Adipose Tissue-derived Stem Cells (ADSCs) treatment on primary Sjogren’s Syndrome (pSS). In this 6-month randomized, triple-blind, placebo-controlled clinical trial, pSS patients were randomly assigned to two groups. After demographic characteristics and clinical examination were achieved, local injection of ADSCs into bilateral glands was performed with patients in ADSCs group (n = 35) and placebo solution was used for another group (n = 39) at three time points. Patients were followed up at 1-, 3- and 6-month. At each visit, studies of clinical and laboratory outcomes, as well as subjective symptoms, were conducted. A total of 74 subjects who met the including criteria were allocated in two groups and eventually 64 subjects (86.5%) completed the treatments and the follow-up assessments. Secretion of salivary and lachrymal glands were significantly improved in 3-month (P < 0.05). A great improvement of European League Against Rheumatism Sjögren’s Syndrome Disease Activity Index (ESSDAI) was found after ADSCs treatment with intergroup comparison from baseline to follow-up (P < 0.05). There is also a significant difference of European Alliance of Associations for Rheumatology SS Patient Reported Index (ESSPRI) between the two groups in the follow-up (P < 0.05). A significant abatement of IgG, IgM, C3, C4 and ESR between two groups was observed in part of follow-up time points (P < 0.05). The ADSCs therapy can provide relief of oral and eye’s dryness in our trial in a short time and has potential improvement of subjective and systemic syndromes of pSS.

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Bioinformatics analysis of potential common pathogenic mechanisms for COVID-19 infection and primary Sjogren’s syndrome

Cited by 13 publications

References 73 publications

Multi-omics analysis uncovered systemic lupus erythematosus and COVID-19 crosstalk

Multi-omics analysis uncovered systemic lupus erythematosus and COVID-19 crosstalk

G6PD is a prognostic biomarker correlated with immune infiltrates in lung adenocarcinoma and pulmonary arterial hypertension

Effect of adipose tissue-derived stem cells therapy on clinical response in patients with primary Sjogren’s syndrome

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