Table_1_Elevated IFNA1 and suppressed IL12p40 associated with persistent hyperinflammation in COVID-19 pneumonia.xlsx (169.35 kB)

Table_1_Elevated IFNA1 and suppressed IL12p40 associated with persistent hyperinflammation in COVID-19 pneumonia.xlsx

dataset

posted on 2023-01-27, 04:15 authored by 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, Hoon Kim, Yoon Kyung Jeon, Youn-Soo Choi, Hye Young Kim, Won-Woo Lee, Murim Choi, Hyun-Young Park, Woong-Yang Park, Yeon-Sook Kim, Nam-Hyuk Cho

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.