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- Title
Elevated IFNA1 and suppressed IL12p40 associated with persistent hyperinflammation in COVID-19 pneumonia.
- Authors
Kyeongseok Jeon; Yuri Kim; Shin Kwang Kang; Uni Park; Jayoun Kim; Nanhee Park; Jaemoon Koh; Man-Shik Shim; Minsoo Kim; Youn Ju Rhee; Hyeongseok Jeong; Siyoung Lee; Donghyun Park; Jinyoung Lim; Hyunsu Kim; Na-Young Ha; Hye-Yeong Jo; Sang Cheol Kim; Ju-Hee Lee; Jiwon Shon
- Abstract
Introduction: Despite of massive endeavors to characterize inflammation in COVID-19 patients, the core network of inflammatory mediators responsible for severe pneumonia stillremain remains elusive. Methods: Here, we performed quantitative and kinetic analysis of 191 inflammatory factors in 955 plasma samples from 80 normal controls (sample n = 80) and 347 confirmed COVID-19 pneumonia patients (sample n =875), including 8 deceased patients. Results: Differential expression analysis showed that 76% of plasmaproteins (145 factors) were upregulated in severe COVID-19 patients comparedwith moderate patients, confirming overt inflammatory responses in severe COVID-19 pneumonia patients. Global correlation analysis of the plasma factorsrevealed two core inflammatory modules, core I and II, comprising mainly myeloid cell and lymphoid cell compartments, respectively, with enhanced impact in a severity-dependent manner. We observed elevated IFNA1 and suppressed IL12p40, presenting a robust inverse correlation in severe patients, which was strongly associated with persistent hyperinflammation in 8.3% of moderate pneumonia patients and 59.4% of severe patients. Discussion: Aberrant persistence of pulmonary and systemic inflammation might be associated with long COVID-19 sequelae. Our comprehensive analysis of inflammatory mediators in plasmarevealed the complexity of pneumonic inflammation in COVID-19 patients anddefined critical modules responsible for severe pneumonic progression.
- Subjects
POST-acute COVID-19 syndrome; COVID-19; COVID-19 pandemic; INFLAMMATION; PNEUMONIA
- Publication
Frontiers in Immunology, 2023, Vol 13, p1
- ISSN
1664-3224
- Publication type
Article
- DOI
10.3389/fimmu.2023.1101808