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In Frontiers in immunology ; h5-index 100.0

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.

Jeon Kyeongseok, Kim Yuri, Kang Shin Kwang, Park Uni, Kim Jayoun, Park Nanhee, Koh Jaemoon, Shim Man-Shik, Kim Minsoo, Rhee Youn Ju, Jeong Hyeongseok, Lee Siyoung, Park Donghyun, Lim Jinyoung, Kim Hyunsu, Ha Na-Young, Jo Hye-Yeong, Kim Sang Cheol, Lee Ju-Hee, Shon Jiwon, Kim Hoon, Jeon Yoon Kyung, Choi Youn-Soo, Kim Hye Young, Lee Won-Woo, Choi Murim, Park Hyun-Young, Park Woong-Yang, Kim Yeon-Sook, Cho Nam-Hyuk


COVID-19, IFNa, IL-12p40, SARS-CoV-2, inflammation, pneumonia