scholarly journals Blockade of endothelial, but not epithelial, cell expression of PD-L1 following severe shock attenuates the development of indirect acute lung injury in mice

2020 ◽  
Vol 318 (4) ◽  
pp. L801-L812 ◽  
Author(s):  
Shumin Xu ◽  
Qian Yang ◽  
Jianwen Bai ◽  
Tianzhu Tao ◽  
Lunxian Tang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Critical Role ◽  
Lavage Fluid ◽  
Protein Levels ◽  
Pulmonary Endothelial Cells ◽  
Junction Protein ◽  
Cell Expression ◽  
Intratracheal Delivery

This study sets out to establish the comparative contribution of PD-L1 expression by pulmonary endothelial cells (ECs) and/or epithelial cells (EpiCs) to the development of indirect acute lung injury (iALI) by taking advantage of the observation that treatment with naked siRNA by intratracheal delivery in mice primarily affects lung EpiCs, but not lung ECs, while intravenous delivery of liposomal-encapsulated siRNA largely targets vascular ECs including the lung, but not pulmonary EpiCs. We showed that using a mouse model of iALI [induced by hemorrhagic shock followed by septic challenge (Hem-CLP)], PD-L1 expression on pulmonary ECs or EpiCs was significantly upregulated in the iALI mice at 24 h post–septic insult. After documenting the selective ability of intratracheal versus intravenous delivery of PD-L1 siRNA to inhibit PD-L1 expression on EpiCs versus ECs, respectively, we observed that the iALI-induced elevation of cytokine/chemokine levels (in the bronchoalveolar lavage fluid, lung lysates, or plasma), lung myeloperoxidase and caspase-3 activities could largely only be inhibited by intravenous, but not intratracheal, delivery of PD-L1 siRNA. Moreover, intravenous, but not intratracheal, delivery led to a preservation of normal tissue architecture, lessened pulmonary edema, and reduced neutrophils influx induced by iALI. In addition, in vitro mouse endothelial cell line studies showed that PD-L1 gene knockdown by siRNA or knockout by CRISPR/Cas9-mediated gene manipulation, reduced monolayer permeability, and maintained tight junction protein levels upon recombinant IFN-γ stimulation. Together, these data imply a critical role for pulmonary vascular ECs in mediating PD-1:PD-L1–driven pathological changes resulting from systemic stimuli such as Hem-CLP.

scholarly journals Natural Antioxidant Betanin Protects Rats from Paraquat-Induced Acute Lung Injury Interstitial Pneumonia

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Junyan Han ◽  
Deshun Ma ◽  
Miao Zhang ◽  
Xuelian Yang ◽  
Dehong Tan
Keyword(s):  
Body Weight ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Weight Ratio ◽  
Lavage Fluid ◽  
Dependent Manner ◽  
Sod Activity ◽  
Protein Levels ◽  
Injury Characteristic ◽  
Dose Dependent

The effect of betanin on a rat paraquat-induced acute lung injury (ALI) model was investigated. Paraquat was injected intraperitoneally at a single dose of 20 mg/kg body weight, and betanin (25 and 100 mg/kg/d) was orally administered 3 days before and 2 days after paraquat administration. Rats were sacrificed 24 hours after the last betanin dosage, and lung tissue and bronchoalveolar lavage fluid (BALF) were collected. In rats treated only with paraquat, extensive lung injury characteristic of ALI was observed, including histological changes, elevation of lung : body weight ratio, increased lung permeability, increased lung neutrophilia infiltration, increased malondialdehyde (MDA) and myeloperoxidase (MPO) activity, reduced superoxide dismutase (SOD) activity, reduced claudin-4 and zonula occluden-1 protein levels, increased BALF interleukin (IL-1) and tumor necrosis factor (TNF)-αlevels, reduced BALF IL-10 levels, and increased lung nuclear factor kappa (NF-κB) activity. In rats treated with betanin, paraquat-induced ALI was attenuated in a dose-dependent manner. In conclusion, our results indicate that betanin attenuates paraquat-induced ALI possibly via antioxidant and anti-inflammatory mechanisms. Thus, the potential for using betanin as an auxilliary therapy for ALI should be explored further.

Diammonium glycyrrhizinate lipid ligand ameliorates lipopolysaccharide-induced acute lung injury by modulating vascular endothelial barrier function

2020 ◽  
Author(s):  
Mei-Mei Liu ◽  
Jin Zhou ◽  
Dan Ji ◽  
Jun Yang ◽  
Yan-Ping Huang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Protein Concentration ◽  
Weight Ratio ◽  
Dry Weight ◽  
Lavage Fluid ◽  
Inhibitory Effect ◽  
Vascular Endothelial ◽  
Junction Protein

Abstract Background: The present study investigated the attenuating effect of diammonium glycyrrhizinate lipid ligand (DGLL) on acute lung injury (ALI) and pulmonary edema induced by lipopolysaccharide (LPS) in rats.Methods: Rat ALI model was established by LPS (10 mg/kg) intraperitoneal injection, and DGLL (30, 60, 120 mg/kg) was administrated orall 1 hour before LPS infusion. Six hours after LPS stimulation, lung injury was evaluated by histological staining. Pulmonary edema was evaluated by lung wet-dry weight ratio, the protein concentration of bronchoalveolar lavage fluid (BALF), and the evans blue (EB) extravasation in lung tissues. The expression of cytokines and adhesion molecules in lung tissues were detected by ELISA method. The myeloperoxidase (MPO) expression was detected by immunohistochemical staining. Western blot was used to detect the expression changes of the proteins associated with pulmonary inflammation and microvascular permeability.Results: DGLL significantly inhibited LPS induced ALI, manifested as attenuation of MPO positive cells and TNF-α, IL-6, ICAM-1 expression in rat lung tissue. In addition, DGLL abrogated LPS-induced pulmonary edema, decreased the protein concentration in BALF and EB extravasation. Meanwhile, DGLL inhibited the degradation of vascular endothelial cadherin (VE-Cadherin) and tight junction protein, including ZO-1, Occludin, and JAM-1.Conclusions: DGLL has an inhibitory effect on LPS-induced rat ALI, which is related to the inhibition of inflammatory cell infiltration and microvascular barrier disruption. These results provide a theoretical basis for DGLL in the potential clinical treatment of ALI.

scholarly journals Inhibition of ERRα Aggravates Sepsis-Induced Acute Lung Injury in Rats via Provoking Inflammation and Oxidative Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Wenfang Xia ◽  
Zhou Pan ◽  
Huanming Zhang ◽  
Qingshan Zhou ◽  
Yu Liu
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Cecal Ligation ◽  
Endothelial Permeability ◽  
Inflammatory Factors ◽  
Inflammatory Factor ◽  
Junction Protein ◽  
And Oxidative Stress

Inflammation and oxidative stress are critical pathologies that contribute to sepsis-induced acute lung injury (ALI). This study investigated the regulatory role of estrogen-related receptor alpha (ERRα) in an experimental model of sepsis-induced ALI. In vivo, a cecal ligation and puncture- (CLP-) induced ALI model was established in anesthetized rats. Animals were then randomly assigned to receive an intraperitoneal injection of vehicle or ERRα inverse agonist (XCT-790, 2.5 mg/kg). Administration of XCT-790 significantly aggravated a sepsis-induced increase in pathological damage of lung tissues, lung endothelial permeability, myeloperoxidase (MPO) activity in lung tissues, production of serum inflammatory factors, and inflammatory cell accumulation in bronchoalveolar lavage fluid. In addition, XCT-790 treatment exacerbated a CLP-induced decrease in lung superoxide dismutase and an increase in lung malondialdehyde levels. In vitro, the exposure of rat pulmonary microvascular endothelial cells (PMVECs) to lipopolysaccharide (LPS) resulted in increased endothelial permeability and reduced expression of tight junction protein ZO-1, Occludin, JAM-A, and adherens junction protein VE-cadherin, which were further deteriorated by knockdown of ERRα. In addition, LPS-triggered inflammatory factor production and increase in the expression of phosphorylated IκBα and NF-κB p65 were also exacerbated by silencing ERRα gene. Meanwhile, knockdown of ERRα dramatically promoted LPS-activated mitochondrial reactive oxygen species production and LPS-induced downregulation of Sirt3 protein levels in rat PMVECs. Taken together, our present study provides evidences that ERRα functions as a novel negative modulator of sepsis-induced ALI in rats. The underlying mechanisms responsible for ERRα-elicited effects are largely dependent on the regulation of inflammatory response and oxidative stress.

scholarly journals Lung protective effect of Punicalagin on LPS-induced acute lung injury in mice

2022 ◽  
Author(s):  
Yibin Zeng ◽  
Hongying Zhao ◽  
Tong Zhang ◽  
Chao Zhang ◽  
Yanni He ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protective Effect ◽  
Lung Tissue ◽  
White Blood Cells ◽  
Weight Ratio ◽  
Dry Weight ◽  
Lavage Fluid ◽  
Protein Levels ◽  
Anti Inflammation

Background: Punicalagin (Pun) is one of the main bioactive compounds in pomegranate peel, it possesses many properties, including antioxidant, anti-inflammation, and immunosuppressive activities. The study was aimed to investigate the protective effect and mechanisms of Pun on lipopolysaccharide (LPS) induced acute lung injury (ALI) in mice. Methods and Results: Forty-eight BALB/c male mice were used to establish ALI by intratracheal-instilled 2.4 mg/kg LPS, the mice were randomly divided into model and Pun (10, 20, 40 mg/kg) groups. The other twelve mice were intratracheal-instilled same volume of water as control. After 2 h of receiving LPS, mice were administrated drug through intraperitoneal injection. Lung index, histopathological changes, white blood cells and biomarkers in bronchoalveolar lavage fluid (BALF) were analyzed. The protein expression of total and phosphor p65, IκBα, ERK1/2, JNK and p38 in lung tissue was detected. The result showed that Pun could reduce the lung index and wet/dry weight ratio, improve lung histopathological injury. In addition, Pun decreased the inflammation cells and regulated the biomarkers in BALF. Furthermore, Pun dose-dependently reduced the phosphor protein levels of p65, IκBα, ERK1/2, JNK and p38 in lung tissue, which exhibited that the effect of Pun related to MAPKs pathway. More importantly, there is no toxicity was observed in the acute toxicity study of Pun. Conclusion: Pun improves LPS-induced ALI mainly through its anti-inflammatory properties, which is associated with NF-κB and MAPKs signaling pathways. The study implied that Pun maybe a potent agent against ALI in future clinic.

scholarly journals Resveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells’ maturation and function

2021 ◽  
Vol 16 (1) ◽  
pp. 1064-1081
Author(s):  
Bingnan Guo ◽  
Yigen Peng ◽  
Yuting Gu ◽  
Yi Zhong ◽  
Chenglei Su ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Enhanced Recovery ◽  
Lavage Fluid ◽  
Protective Role ◽  
High Morbidity ◽  
And Function

Abstract Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe syndrome lacking efficient therapy and resulting in high morbidity and mortality. Although resveratrol (RES), a natural phytoalexin, has been reported to protect the ALI by suppressing the inflammatory response, the detailed mechanism of how RES affected the immune system is poorly studied. Pulmonary conventional dendritic cells (cDCs) are critically involved in the pathogenesis of inflammatory lung diseases including ALI. In this study, we aimed to investigate the protective role of RES via pulmonary cDCs in lipopolysaccharide (LPS)-induced ALI mice. Murine ALI model was established by intratracheally challenging with 5 mg/kg LPS. We found that RES pretreatment could mitigate LPS-induced ALI. Additionally, proinflammatory-skewed cytokines decreased whereas anti-inflammatory-related cytokines increased in bronchoalveolar lavage fluid by RES pretreatment. Mechanistically, RES regulated pulmonary cDCs’ maturation and function, exhibiting lower level of CD80, CD86, major histocompatibility complex (MHC) II expression, and IL-10 secretion in ALI mice. Furthermore, RES modulated the balance between proinflammation and anti-inflammation of cDCs. Moreover, in vitro RES pretreatment regulated the maturation and function of bone marrow derived dendritic cells (BMDCs). Finally, the adoptive transfer of RES-pretreated BMDCs enhanced recovery of ALI. Thus, these data might further extend our understanding of a protective role of RES in regulating pulmonary cDCs against ALI.

scholarly journals Interactions of Cardiopulmonary Bypass and Erythrocyte Transfusion in the Pathogenesis of Pulmonary Dysfunction in Swine

2013 ◽  
Vol 119 (2) ◽  
pp. 365-378 ◽  
Author(s):  
Nishith N. Patel ◽  
Hua Lin ◽  
Ceri Jones ◽  
Graham Walkden ◽  
Paramita Ray ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Cardiopulmonary Bypass ◽  
Lung Injury ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Endothelial Activation ◽  
Surgical Patients ◽  
Pulmonary Dysfunction ◽  
Erythrocyte Transfusion ◽  
Protein Levels

Abstract Background: Allogeneic erythrocyte transfusion in cardiac surgical patients is associated with a fourfold increase in pulmonary complications. Our understanding of the processes underlying these observations is poor and there is no experimental model of transfusion-related acute lung injury that shows homology to cardiac surgical patients. Our objective was to develop a novel swine recovery model to determine how two clinical risk factors, allogenic erythrocyte transfusion and cardiopulmonary bypass, interact in the genesis of postcardiac surgery acute lung injury. Methods: Thirty-six pigs were infused with allogeneic 14- or 42-day-old erythrocytes or they underwent cardiopulmonary bypass with or without transfusion of 42-day erythrocyte. Controls received saline. All pigs were recovered and assessed for pulmonary dysfunction, inflammation, and endothelial activation at 24 h. Results: Transfusion of stored allogeneic erythrocytes in pigs compared with sham caused pulmonary dysfunction characterized by reduced lung compliance (mean difference −3.36 [95% CI, −5.31 to −1.42] ml/cm H2O), an increase in protein levels in bronchoalveolar lavage fluid, histological lung injury inflammation, and endothelial activation. Transfusion of blood stored for up to 42 days resulted in greater protein levels in bronchoalveolar lavage fluid, macrophage infiltration, platelet activation, and depletion of T-lymphocytes in recipient lungs versus 14-day-old blood. Transfusion interacted with cardiopulmonary bypass to increase lung injury in the absence of platelet activation. Conclusions: In this novel large animal model of allogeneic erythrocyte transfusion, pulmonary dysfunction occurs in the absence of any priming event, is increased when combined with other inflammatory stimuli, and is mediated by monocyte activation and T-lymphocyte depletion.

scholarly journals Mesenchymal stem cells alleviate LPS-induced acute lung injury by inhibiting the proinflammatory function of Ly6C+ CD8+ T cells

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Jiaqi Zhu ◽  
Bing Feng ◽  
Yanping Xu ◽  
Wenyi Chen ◽  
Xinyu Sheng ◽  
...  
Keyword(s):  
Stem Cells ◽  
T Cells ◽  
Mesenchymal Stem Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Intratracheal Instillation ◽  
Lavage Fluid ◽  
Mass Cytometry ◽  
Neutrophil Accumulation ◽  
Protein Levels

Abstract Systemic inflammatory processes, including alveolar injury, cytokine induction, and neutrophil accumulation, play key roles in the pathophysiology of acute lung injury (ALI). The immunomodulatory effects of mesenchymal stem cells (MSCs) can contribute to the treatment of inflammatory disorders. In previous studies, the focus was on innate immune cells and the effects of MSCs on ALI through CD8+ T cells remain unclear. In the present study, lipopolysaccharide (LPS) was used to induce ALI in mice. ALI mice were treated with MSCs via intratracheal instillation. Survival rate, histopathological changes, protein levels, total cell count, cytokine levels, and chemokine levels in alveolar lavage fluid were used to determine the efficacy of MSCs. Mass cytometry and single-cell RNA sequencing (scRNA-seq) were used to characterize the CD8+ T cells in the lungs. Ly6C− CD8+ T cells are prevalent in normal mice, whereas a specialized effector phenotype expressing a high level of Ly6C is predominant in advanced disease. MSCs significantly mitigated ALI and improved survival. MSCs decreased the infiltration of CD8+ T cells, especially Ly6C+ CD8+ T cells into the lungs. Mass cytometry revealed that CD8+ T cells expressing high Ly6C and CXCR3 levels caused tissue damage in the lungs of ALI mice, which was alleviated by MSCs. The scRNA-seq showed that Ly6C+ CD8+ T cells exhibited a more activated phenotype and decreased expression of proinflammatory factors that were enriched the most in immune chemotaxis after treatment with MSCs. We showed that CD8+ T cells play an important role in MSC-mediated ALI remission, and both infiltration quantity and proinflammatory function were inhibited by MSCs, indicating a potential mechanism for therapeutic intervention.

ID: 109: PARKIN MEDIATES ENDOTHELIAL PRO-INFLAMMATORY RESPONSES IN ACUTE LUNG INJURY

2016 ◽  
Vol 64 (4) ◽  
pp. 963.1-963
Author(s):  
E Letsiou ◽  
H Wang ◽  
P Belvitch ◽  
S Dudek ◽  
S Sammani
Keyword(s):  
Acute Lung Injury ◽  
Endothelial Dysfunction ◽  
Lung Injury ◽  
Kinase Inhibitor ◽  
Inflammatory Responses ◽  
Neutrophil Adhesion ◽  
Protein Levels ◽  
Cell Counts

IntroductionAcute lung injury (ALI) and its more severe form, the Acute Respiratory Distress Syndrome (ARDS), are serious conditions resulting from direct or indirect lung injury that occur in critically ill patients and are associated with an unacceptable mortality of up to 40%. A key biological event in the pathogenesis of ALI/ARDS is the dysfunction of the lung endothelium (EC), which is triggered by a variety of inflammatory insults leading to damaged EC, vascular leak, and excessive inflammation. Recently, we demonstrated that an Abl family tyrosine kinase inhibitor, imatinib, protects against LPS-induced endothelial dysfunction by inhibiting c-Abl kinase through mechanisms that remain largely unknown. In the present study, we identified parkin, a novel c-Abl substrate, as a critical mediator of endothelial dysfunction in ALI.MethodsIn vitro Human pulmonary artery endothelial cells (EC) were transfected with siRNA for parkin and then challenged with LPS (1 µg/ml, 3 hrs). Inflammatory mediators were determined in cell lysates and supernatants by Western blotting and ELISA respectively. In vivo C57BL/6 (WT) and parkin deficient (PARK2 KO) male mice (8–12 wks, n=5–8) were subjected to LPS (intratracheally, 1 mg/kg) or PBS (controls), and allowed to recover prior to harvest 18 hrs later. Leakage of proteins into the alveolar space was assessed by measuring the protein levels in the bronchoalveolar lavage (BAL). To assess lung inflammation, neutrophil cell counts, myeloperoxidase (MPO) activity, and IL-6 levels were determined in BAL.ResultsIn human lung EC, down-regulation of parkin by siRNA reduces LPS-induced VCAM-1 expression (adhesion molecule involved in neutrophil adhesion to EC) (by 35%, p<0.05), IL-8 (neutrophil chemoattractant) (by 59%, p<0.01), and IL-6 (inflammatory cytokine) release (by 79%, p<0.01). PARK2 KO mice exhibit less ALI after LPS compared to WT. In PARK2 KO, BAL protein levels were reduced by 27% (p=0.0024) compared to WT mice. LPS-induced neutrophil recruitment into the alveoli of PARK2 KO was attenuated by 47% compared to WT (p=0.0019). BAL MPO activity (marker of neutrophil activation) and BAL IL-6 levels were also significantly lower in PARK2 KO by 52% (p=0.03) and 28% (p=0.0061) respectively.ConclusionThese results suggest that endothelial parkin mediates EC activation and neutrophil adhesion/migration after LPS, and therefore it may represent a new potential therapeutic target in ALI/ARDS.

scholarly journals Aging exacerbates acute lung injury-induced changes of the air-blood barrier, lung function, and inflammation in the mouse

2017 ◽  
Vol 312 (1) ◽  
pp. L1-L12 ◽  
Author(s):  
Katharina Maria Kling ◽  
Elena Lopez-Rodriguez ◽  
Christiane Pfarrer ◽  
Christian Mühlfeld ◽  
Christina Brandenberger
Keyword(s):  
Acute Lung Injury ◽  
Lung Function ◽  
Lung Injury ◽  
The Elderly ◽  
Lavage Fluid ◽  
Ultrastructural Level ◽  
Saline Control ◽  
Age Related ◽  
Junction Protein ◽  
Old Mice

Acute lung injury (ALI) is characterized by hypoxemia, enhanced permeability of the air-blood barrier, and pulmonary edema. Particularly in the elderly, ALI is associated with increased morbidity and mortality. The reasons for this, however, are poorly understood. We hypothesized that age-related changes in pulmonary structure, function, and inflammation lead to a worse prognosis in ALI. ALI was induced in young (10 wk old) and old (18 mo old) male C57BL/6 mice by intranasal application of 2.5 mg lipopolysaccharide (LPS)/kg body wt or saline (control mice). After 24 h, lung function was assessed, and lungs were either processed for stereological or inflammatory analysis, such as bronchoalveolar lavage fluid (BALF) cytometry and qPCR. Both young and old mice developed severe signs of ALI, including alveolar and septal edema and enhanced inflammatory BALF cells. However, the pathology of ALI was more pronounced in old compared with young mice with nearly sixfold higher BALF protein concentration, twice the number of neutrophils, and significantly higher expression of neutrophil chemokine Cxcl1, adhesion molecule Icam-1, and metalloprotease-9, whereas the expression of tight junction protein occludin significantly decreased. The old LPS mice had thicker alveolar septa attributable to higher volumes of interstitial cells and extracellular matrix. Tissue resistance and elastance reflected observed changes at the ultrastructural level in the lung parenchyma in ALI of young and old mice. In summary, the pathology of ALI with advanced age in mice is characterized by a greater neutrophilic inflammation, leakier air-blood barrier, and altered lung function, which is in line with findings in elderly patients.

scholarly journals DNaseI Protects against Paraquat-Induced Acute Lung Injury and Pulmonary Fibrosis Mediated by Mitochondrial DNA

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Guo Li ◽  
Li Yuzhen ◽  
Chen Yi ◽  
Chen Xiaoxiang ◽  
Zhou Wei ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Alveolar Epithelial Cell ◽  
Disease Model ◽  
Lavage Fluid ◽  
Alveolar Epithelial ◽  
Fast Tracking ◽  
Lung Injury Model

Background. Paraquat (PQ) poisoning is a lethal toxicological challenge that served as a disease model of acute lung injury and pulmonary fibrosis, but the mechanism is undetermined and no effective treatment has been discovered.Methods and Findings. We demonstrated that PQ injures mitochondria and leads to mtDNA release. The mtDNA mediated PBMC recruitment and stimulated the alveolar epithelial cell production of TGF-β1 in vitro. The levels of mtDNA in circulation and bronchial alveolar lavage fluid (BALF) were elevated in a mouse of PQ-induced lung injury. DNaseI could protect PQ-induced lung injury and significantly improved survival. Acute lung injury markers, such as TNFα, IL-1β, and IL-6, and marker of fibrosis, collagen I, were downregulated in parallel with the elimination of mtDNA by DNaseI. These data indicate a possible mechanism for PQ-induced, mtDNA-mediated lung injury, which may be shared by other causes of lung injury, as suggested by the same protective effect of DNaseI in bleomycin-induced lung injury model. Interestingly, increased mtDNA in the BALF of patients with amyopathic dermatomyositis-interstitial lung disease can be appreciated.Conclusions. DNaseI targeting mtDNA may be a promising approach for the treatment of PQ-induced acute lung injury and pulmonary fibrosis that merits fast tracking through clinical trials.

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