tetano
Editor, Senior Moderator
Ann Intensive Care
. 2024 May 12;14(1):72.
doi: 10.1186/s13613-024-01293-3. Pulmonary redox imbalance drives early fibroproliferative response in moderate/severe coronavirus disease-19 acute respiratory distress syndrome and impacts long-term lung abnormalities
Chun Yang[SUP] #[/SUP][SUP] 1 [/SUP], Yuanyuan Tan[SUP] #[/SUP][SUP] 1 [/SUP], Zihao Li[SUP] 1 [/SUP], Lei Hu[SUP] 1 [/SUP], Yuanyuan Chen[SUP] 1 [/SUP], Shouliang Zhu[SUP] 1 [/SUP], Jiawei Hu[SUP] 1 [/SUP], Tingting Huai[SUP] 1 [/SUP], Mingqing Li[SUP] 1 [/SUP], Guobin Zhang[SUP] 1 [/SUP], Dewang Rao[SUP] 2 [/SUP], Guanghe Fei[SUP] 3 [/SUP], Min Shao[SUP] 4 [/SUP], Zhenxing Ding[SUP] 5 [/SUP]
Affiliations
Background: COVID-19-associated pulmonary fibrosis remains frequent. This study aimed to investigate pulmonary redox balance in COVID-19 ARDS patients and possible relationship with pulmonary fibrosis and long-term lung abnormalities.
Methods: Baseline data, chest CT fibrosis scores, N-terminal peptide of alveolar collagen III (NT-PCP-III), transforming growth factor (TGF)-β1, superoxide dismutase (SOD), reduced glutathione (GSH), oxidized glutathione (GSSG) and malondialdehyde (MDA) in bronchoalveolar lavage fluid (BALF) were first collected and compared between SARS-CoV-2 RNA positive patients with moderate to severe ARDS (n = 65, COVID-19 ARDS) and SARS-CoV-2 RNA negative non-ARDS patients requiring mechanical ventilation (n = 63, non-ARDS). Then, correlations between fibroproliferative (NT-PCP-III and TGF-β1) and redox markers were analyzed within COVID-19 ARDS group, and comparisons between survivor and non-survivor subgroups were performed. Finally, follow-up of COVID-19 ARDS survivors was performed to analyze the relationship between pulmonary abnormalities, fibroproliferative and redox markers 3 months after discharge.
Results: Compared with non-ARDS group, COVID-19 ARDS group had significantly elevated chest CT fibrosis scores (p < 0.001) and NT-PCP-III (p < 0.001), TGF-β1 (p < 0.001), GSSG (p < 0.001), and MDA (p < 0.001) concentrations on admission, while decreased SOD (p < 0.001) and GSH (p < 0.001) levels were observed in BALF. Both NT-PCP-III and TGF-β1 in BALF from COVID-19 ARDS group were directly correlated with GSSG (p < 0.001) and MDA (p < 0.001) and were inversely correlated with SOD (p < 0.001) and GSH (p < 0.001). Within COVID-19 ARDS group, non-survivors (n = 28) showed significant pulmonary fibroproliferation (p < 0.001) with more severe redox imbalance (p < 0.001) than survivors (n = 37). Furthermore, according to data from COVID-19 ARDS survivor follow-up (n = 37), radiographic residual pulmonary fibrosis and lung function impairment improved 3 months after discharge compared with discharge (p < 0.001) and were associated with early pulmonary fibroproliferation and redox imbalance (p < 0.01).
Conclusions: Pulmonary redox imbalance occurring early in COVID-19 ARDS patients drives fibroproliferative response and increases the risk of death. Long-term lung abnormalities post-COVID-19 are associated with early pulmonary fibroproliferation and redox imbalance.
Keywords: Acute respiratory distress syndrome; COVID-19; Long COVID; Oxidative stress; Pulmonary fibrosis.
. 2024 May 12;14(1):72.
doi: 10.1186/s13613-024-01293-3. Pulmonary redox imbalance drives early fibroproliferative response in moderate/severe coronavirus disease-19 acute respiratory distress syndrome and impacts long-term lung abnormalities
Chun Yang[SUP] #[/SUP][SUP] 1 [/SUP], Yuanyuan Tan[SUP] #[/SUP][SUP] 1 [/SUP], Zihao Li[SUP] 1 [/SUP], Lei Hu[SUP] 1 [/SUP], Yuanyuan Chen[SUP] 1 [/SUP], Shouliang Zhu[SUP] 1 [/SUP], Jiawei Hu[SUP] 1 [/SUP], Tingting Huai[SUP] 1 [/SUP], Mingqing Li[SUP] 1 [/SUP], Guobin Zhang[SUP] 1 [/SUP], Dewang Rao[SUP] 2 [/SUP], Guanghe Fei[SUP] 3 [/SUP], Min Shao[SUP] 4 [/SUP], Zhenxing Ding[SUP] 5 [/SUP]
Affiliations
- PMID: 38735020
- DOI: 10.1186/s13613-024-01293-3
Background: COVID-19-associated pulmonary fibrosis remains frequent. This study aimed to investigate pulmonary redox balance in COVID-19 ARDS patients and possible relationship with pulmonary fibrosis and long-term lung abnormalities.
Methods: Baseline data, chest CT fibrosis scores, N-terminal peptide of alveolar collagen III (NT-PCP-III), transforming growth factor (TGF)-β1, superoxide dismutase (SOD), reduced glutathione (GSH), oxidized glutathione (GSSG) and malondialdehyde (MDA) in bronchoalveolar lavage fluid (BALF) were first collected and compared between SARS-CoV-2 RNA positive patients with moderate to severe ARDS (n = 65, COVID-19 ARDS) and SARS-CoV-2 RNA negative non-ARDS patients requiring mechanical ventilation (n = 63, non-ARDS). Then, correlations between fibroproliferative (NT-PCP-III and TGF-β1) and redox markers were analyzed within COVID-19 ARDS group, and comparisons between survivor and non-survivor subgroups were performed. Finally, follow-up of COVID-19 ARDS survivors was performed to analyze the relationship between pulmonary abnormalities, fibroproliferative and redox markers 3 months after discharge.
Results: Compared with non-ARDS group, COVID-19 ARDS group had significantly elevated chest CT fibrosis scores (p < 0.001) and NT-PCP-III (p < 0.001), TGF-β1 (p < 0.001), GSSG (p < 0.001), and MDA (p < 0.001) concentrations on admission, while decreased SOD (p < 0.001) and GSH (p < 0.001) levels were observed in BALF. Both NT-PCP-III and TGF-β1 in BALF from COVID-19 ARDS group were directly correlated with GSSG (p < 0.001) and MDA (p < 0.001) and were inversely correlated with SOD (p < 0.001) and GSH (p < 0.001). Within COVID-19 ARDS group, non-survivors (n = 28) showed significant pulmonary fibroproliferation (p < 0.001) with more severe redox imbalance (p < 0.001) than survivors (n = 37). Furthermore, according to data from COVID-19 ARDS survivor follow-up (n = 37), radiographic residual pulmonary fibrosis and lung function impairment improved 3 months after discharge compared with discharge (p < 0.001) and were associated with early pulmonary fibroproliferation and redox imbalance (p < 0.01).
Conclusions: Pulmonary redox imbalance occurring early in COVID-19 ARDS patients drives fibroproliferative response and increases the risk of death. Long-term lung abnormalities post-COVID-19 are associated with early pulmonary fibroproliferation and redox imbalance.
Keywords: Acute respiratory distress syndrome; COVID-19; Long COVID; Oxidative stress; Pulmonary fibrosis.