Ion transport mechanisms for smoke inhalation–injured airway epithelial barrier

Chang, Jianjun; Chen, Zaixing; Zhao, Runzhen; Nie, Hongguang; Ji, Hong‐Long

doi:10.1007/s10565-020-09545-1

Cited by 4 publications

(2 citation statements)

References 45 publications

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“…For drug treatments, HBECs were basally treated with tezacaftor, JCI Insight 2023;8(14):e170022 https://doi.org/10.1172/jci.insight.170022 and ivacaftor or CFTR inhibitor 172 with time course and concentration indicated in figure legends. The dose of CFTR inhibitor 172 was selected based on previously published research (58). CFTR potentiator and corrector doses were selected based on preliminary data indicating maximal efficacy and minimal cytotoxicity at these doses (data not shown).…”

Section: Methodsmentioning

confidence: 99%

Influenza A–induced cystic fibrosis transmembrane conductance regulator dysfunction increases susceptibility to Streptococcus pneumoniae

Earnhardt,

Tipper,

D’Mello

et al. 2023

JCI Insight

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Influenza A virus (IAV) infection is commonly complicated by secondary bacterial infections that lead to increased morbidity and mortality. Our recent work demonstrates that IAV disrupts airway homeostasis, leading to airway pathophysiology resembling cystic fibrosis disease through diminished cystic fibrosis transmembrane conductance regulator (CFTR) function. Here, we use human airway organotypic cultures to investigate how IAV alters the airway microenvironment to increase susceptibility to secondary infection with Streptococcus pneumoniae ( Spn ). We observed that IAV-induced CFTR dysfunction and airway surface liquid acidification is central to increasing susceptibility to Spn . Additionally, we observed that IAV induced profound transcriptional changes in the airway epithelium and proteomic changes in the airway surface liquid in both CFTR-dependent and -independent manners. These changes correspond to multiple diminished host defense pathways and altered airway epithelial function. Collectively, these findings highlight both the importance of CFTR function during infectious challenge and demonstrate a central role for the lung epithelium in secondary bacterial infections following IAV.

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Section: Methodsmentioning

confidence: 99%

Influenza A–induced cystic fibrosis transmembrane conductance regulator dysfunction increases susceptibility to Streptococcus pneumoniae

Earnhardt,

Tipper,

D’Mello

et al. 2023

JCI Insight

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“…Smoke exposure seemed to damage the tight junctions and impair the airway epithelial barrier, which was mediated by disturbed transcellular Na, K-ATPase ion transport. 185 …”

Section: Experimental Lung Injury - Acute Lung Inflammatory Modelsmentioning

confidence: 99%

Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques

Keskinidou¹,

Vassiliou²,

Dimopoulou³

et al. 2022

JIR

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Acute respiratory distress syndrome (ARDS) is a life-threatening lung injury characterized by an acute inflammatory response in the lung parenchyma. Hence, it is considered as the most appropriate clinical syndrome to study pathogenic mechanisms of lung inflammation. ARDS is associated with increased morbidity and mortality in the intensive care unit (ICU), while no effective pharmacological treatment exists. It is very important therefore to fully characterize the underlying pathobiology and the related mechanisms, in order to develop novel therapeutic approaches. In vivo and in vitro models are important pre-clinical tools in biological and medical research in the mechanistic and pathological understanding of the majority of diseases. In this review, we will present data from selected experimental models of lung injury/acute lung inflammation, which have been based on clinical disorders that can lead to the development of ARDS and related inflammatory lung processes in humans, including ventilation-induced lung injury (VILI), sepsis, ischemia/reperfusion, smoke, acid aspiration, radiation, transfusion-related acute lung injury (TRALI), influenza, Streptococcus ( S .) pneumoniae and coronaviruses infection. Data from the corresponding clinical conditions will also be presented. The mechanisms related to lung inflammation that will be covered are oxidative stress, neutrophil extracellular traps, mitogen-activated protein kinase (MAPK) pathways, surfactant, and water and ion channels. Finally, we will present a brief overview of emerging techniques in the field of omics research that have been applied to ARDS research, encompassing genomics, transcriptomics, proteomics, and metabolomics, which may recognize factors to help stratify ICU patients at risk, predict their prognosis, and possibly, serve as more specific therapeutic targets.

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Regulatory roles of NAT10 in airway epithelial cell function and metabolism in pathological conditions

et al. 2022

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Ion transport mechanisms for smoke inhalation–injured airway epithelial barrier

Cited by 4 publications

References 45 publications

Influenza A–induced cystic fibrosis transmembrane conductance regulator dysfunction increases susceptibility to Streptococcus pneumoniae

Influenza A–induced cystic fibrosis transmembrane conductance regulator dysfunction increases susceptibility to Streptococcus pneumoniae

Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques

Regulatory roles of NAT10 in airway epithelial cell function and metabolism in pathological conditions

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