Sera proteomic features of active and recovered COVID-19 patients: potential diagnostic and prognostic biomarkers

Leng, Ling; Li, Mansheng; Li, Wei; Mou, Danny; Liu, Guopeng; Ma, Jie; Zhang, Shuyang; Zhang, Dongliang; Cao, Ruiyuan; Zhong, Wu

doi:10.1038/s41392-021-00612-5

Cited by 25 publications

(21 citation statements)

References 5 publications

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“…SAAs and SERPINAs are important for proper neutrophil functionality [56,[65][66][67], which might play an additional role in the impairment we observed. Moreover, recent reports linked plasma proteomic changes of COVID-19 patients to different degrees of disease severity, with special emphasis on tissue repair and coagulation proteins, such as the SERPINAs, inflammatory markers and regulators, like CRP and TSKU, macrophage trafficking markers, like SELENOP, as well as immune cell markers such as LBP and CD14 [68][69][70][71][72][73][74][75]. These findings in our cohort further strengthens our hypothesis on myeloid cell dysregulation and it is in line with the reported COVID-19 proteomic data [71,74,75].…”

Section: Plos Pathogensmentioning

confidence: 99%

Hyperinflammatory environment drives dysfunctional myeloid cell effector response to bacterial challenge in COVID-19

et al. 2022

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COVID-19 displays diverse disease severities and symptoms including acute systemic inflammation and hypercytokinemia, with subsequent dysregulation of immune cells. Bacterial superinfections in COVID-19 can further complicate the disease course and are associated with increased mortality. However, there is limited understanding of how SARS-CoV-2 pathogenesis and hypercytokinemia impede the innate immune function against bacterial superinfections. We assessed the influence of COVID-19 plasma hypercytokinemia on the functional responses of myeloid immune cells upon bacterial challenges from acute-phase COVID-19 patients and their corresponding recovery (rec)-phase. We show that a severe hypercytokinemia status in COVID-19 patients correlates with the development of bacterial superinfections. Neutrophils and monocytes derived from COVID-19 patients in their acute-phase showed an impaired intracellular microbicidal capacity upon bacterial challenges. The impaired microbicidal capacity was reflected by abrogated MPO and reduced NETs production in neutrophils along with reduced ROS production in both neutrophils and monocytes. Moreover, we observed a distinct pattern of cell surface receptor expression on both neutrophils and monocytes, in line with suppressed autocrine and paracrine cytokine signaling. This phenotype was characterized by a high expression of CD66b, CXCR4 and low expression of CXCR1, CXCR2 and CD15 in neutrophils and low expression of HLA-DR, CD86 and high expression of CD163 and CD11b in monocytes. Furthermore, the impaired antibacterial effector function was mediated by synergistic effect of the cytokines TNF-α, IFN-γ and IL-4. COVID-19 patients receiving dexamethasone showed a significant reduction of overall inflammatory markers in the plasma as well as exhibited an enhanced immune response towards bacterial challenge ex vivo. Finally, broad anti-inflammatory treatment was associated with a reduction in CRP, IL-6 levels as well as length of ICU and hospital stay in critically ill COVID-19 patients. Our data provides insights into the transient functional dysregulation of myeloid immune cells against subsequent bacterial infections in COVID-19 patients and describe a beneficial role for the use of dexamethasone in these patients.

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Section: Plos Pathogensmentioning

confidence: 99%

Hyperinflammatory environment drives dysfunctional myeloid cell effector response to bacterial challenge in COVID-19

et al. 2022

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“…While most published studies analyzed in this research area have focused on the following specimen types: blood samples, including serum [11][12][13][14][15][16][17][18][19][20][21] , plasma 12,13,[22][23][24][25][26][27][28][29][30][31][32] , and peripheral blood mononuclear cells (PBMC) 33,34 , there are also studies analyzing FFPE tissue 35,36 , urine [37][38][39][40][41] , fecal 42 , sputum 23 , extracellular vesicle 43,44 , cerebrospinal fluid 21 , semen 45 , colostrum 46 , colostrum 47 and nasopharynx swabs samples 48 . All these studies have provided proteomic snapshots of different aspects of tissues from COVID-19 patients.…”

Section: Introductionmentioning

confidence: 99%

COVIDpro: Database for mining protein dysregulation in patients with COVID-19

Zhang

Luna

Tan

et al. 2022

Preprint

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Background: The ongoing pandemic of the coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) still has limited treatment options partially due to our incomplete understanding of the molecular dysregulations of the COVID-19 patients. We aimed to generate a repository and data analysis tools to examine the modulated proteins underlying COVID-19 patients for the discovery of potential therapeutic targets and diagnostic biomarkers. Methods: We built a web server containing proteomic expression data from COVID-19 patients with a toolset for user-friendly data analysis and visualization. The web resource covers expert-curated proteomic data from COVID-19 patients published before May 2022. The data were collected from ProteomeXchange and from select publications via PubMed searches and aggregated into a comprehensive dataset. Protein expression by disease subgroups across projects was compared by examining differentially expressed proteins. We also visualize differentially expressed pathways and proteins. Moreover, circulating proteins that differentiated severe cases were nominated as predictive biomarkers. Findings: We built and maintain a web server COVIDpro (https://www.guomics.com/covidPro/) containing proteomics data generated by 41 original studies from 32 hospitals worldwide, with data from 3077 patients covering 19 types of clinical specimens, the majority from plasma and sera. 53 protein expression matrices were collected, for a total of 5434 samples and 14,403 unique proteins. Our analyses showed that the lipopolysaccharide-binding protein, as identified in the majority of the studies, was highly expressed in the blood samples of patients with severe disease. A panel of significantly dysregulated proteins was identified to separate patients with severe disease from non-severe disease. Classification of severe disease based on these proteomic signatures on five test sets reached a mean AUC of 0.87 and ACC of 0.80. Interpretation: COVIDpro is an online database with an integrated analysis toolkit. It is a unique and valuable resource for testing hypotheses and identifying proteins or pathways that could be targeted by new treatments of COVID-19 patients.

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“…The severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection affects multiple organs such as the lungs, gut, kidney, brain, and skin. [ 1 , 2 , 3 , 4 ] Previous reports have shown that coronavirus disease 2019 (COVID‐19) patients developed acral areas of erythema with vesicles or pustules (pseudochilblain), acral areas with erythematous rash, widespread urticaria, chickenpox‐like vesicles, and maculopapular eruptions. [ 5 , 6 ] In addition, it has been reported that depending on the clinical severity of the disease COVID‐19 patients experienced hair loss on their scalp.…”

Section: Introductionmentioning

confidence: 99%

Establishment of Human Pluripotent Stem Cell‐Derived Skin Organoids Enabled Pathophysiological Model of SARS‐CoV‐2 Infection

Liu

Gao

et al. 2021

Advanced Science

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Coronavirus disease 2019 (COVID‐19) patients with impact on skin and hair loss are reported. Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is detected in the skin of some patients; however, the detailed pathological features of skin tissues from patients infected with SARS‐CoV‐2 at a molecular level are limited. Especially, the ability of SARS‐CoV‐2 to infect skin cells and impact their function is not well understood. A proteome map of COVID‐19 skin is established here and the susceptibility of human‐induced pluripotent stem cell (hiPSC)‐derived skin organoids with hair follicles and nervous system is investigated, to SARS‐CoV‐2 infection. It is shown that KRT17+ hair follicles can be infected by SARS‐CoV‐2 and are associated with the impaired development of hair follicles and epidermis. Different types of nervous system cells are also found to be infected, which can lead to neuron death. Findings from the present work provide evidence for the association between COVID‐19 and hair loss. hiPSC‐derived skin organoids are also presented as an experimental model which can be used to investigate the susceptibility of skin cells to SARS‐CoV‐2 infection and can help identify various pathological mechanisms and drug screening strategies.

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Sera proteomic features of active and recovered COVID-19 patients: potential diagnostic and prognostic biomarkers

Cited by 25 publications

References 5 publications

Hyperinflammatory environment drives dysfunctional myeloid cell effector response to bacterial challenge in COVID-19

Hyperinflammatory environment drives dysfunctional myeloid cell effector response to bacterial challenge in COVID-19

COVIDpro: Database for mining protein dysregulation in patients with COVID-19

Establishment of Human Pluripotent Stem Cell‐Derived Skin Organoids Enabled Pathophysiological Model of SARS‐CoV‐2 Infection

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