The coronavirus disease 19 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic since the first report in Wuhan. COVID-19 is a zoonotic disease and the natural reservoir of SARS-CoV-2 seems to be bats. However, the intermediate host explaining the transmission and evolvement is still unclear. In addition to the wildlife which has access to contact with bats in the natural ecological environment and then infects humans in wildlife market, domestic animals are also able to establish themselves as the intermediate host after infected by SARS-CoV-2. Although recent studies related to SARS-CoV-2 have made a lot of progress, many critical issues are still unaddressed. Here, we reviewed findings regarding the investigations of the intermediate host, which may inspire future investigators and provide them with plenty of information. The results demonstrate the critical role of the intermediate host in the transmission chain of SARS-CoV-2, and the efficient intervention on this basis may be useful to prevent further deterioration of COVID-19.

Acute respiratory distress syndrome (ARDS) threatens the survival of critically ill patients, the mechanisms of which are still unclear. Neutrophil extracellular traps (NETs) released by activated neutrophils play a critical role in inflammatory injury. We investigated the role of NETs and the underlying mechanism involved in acute lung injury (ALI). We found a higher expression of NETs and cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) in the airways, which was reduced by Deoxyribonuclease I (DNase I) in ALI. The administration of the STING inhibitor H-151 also significantly relieved inflammatory lung injury, but failed to affect the high expression of NETs in ALI. We isolated murine neutrophils from bone marrow and acquired human neutrophils by inducing HL-60 to differentiate. After the PMA interventions, exogenous NETs were obtained from such extracted neutrophils. Exogenous NETs intervention in vitro and in vivo resulted in airway injury, and such inflammatory lung injury was reversed upon degrading NETs with or inhibiting cGAS-STING with H-151 as well as siRNA STING. In conclusion, cGAS-STING participates in regulating NETs-mediated inflammatory pulmonary injury, which is expected to be a new therapeutic target for ARDS/ALI.

Neutrophil extracellular traps (NETs) are essential for immune defense and have been increasingly recognized for their role in infection and inflammation. In the context of airway inflammatory diseases, there is growing evidence suggesting the involvement and significance of NETs. This review aims to provide an overview of the formation mechanisms and components of NETs and their impact on various airway inflammatory diseases, including acute lung injury/ARDS, asthma, chronic obstructive pulmonary disease (COPD) and cystic fibrosis. By understanding the role of NETs in airway inflammation, we can gain valuable insights into the underlying pathogenesis of these diseases and identify potential targets for future therapeutic strategies that either target NETs formation or modulate their harmful effects. Further research is warranted to elucidate the complex interactions between NETs and airway inflammation and to develop targeted therapies that can effectively mitigate their detrimental effects while preserving their beneficial functions in host defense.

Neurogenic pulmonary edema (NPE) following acute stroke is an acute respiratory distress syndrome (ARDS) with clinical characteristics that include acute onset, apparent pulmonary interstitial fluid infiltration and rapid resolution. The pathological process of NPE centers on sympathetic stimulation and fulminant release of catecholamines, which cause contraction of resistance vessels. Elevated systemic resistance forces fluid into pulmonary circulation, while pulmonary circulation overload induces pulmonary capillary pressure that elevates, and in turn damages the alveolar capillary barrier. Damage to the alveolar capillary barrier leads to pulmonary ventilation disorder, blood perfusion disorder and oxygenation disorder. Eventually, NPE will cause post-stroke patients' prognosis to further deteriorate. At present, we lack specific biological diagnostic indicators and a meticulously unified diagnostic criterion, and this results in a situation in which many patients are not recognized quickly and/or diagnosed accurately. There are no drugs that are effective against NPE. Therefore, understanding how to diagnose NPE early by identifying the risk factors and how to apply appropriate treatment to avoid a deteriorating prognosis are important scientific goals. We will elaborate the progress of NPE after acute stroke in terms of its pathophysiological mechanisms, etiology, epidemiology, clinical diagnosis and early prediction, comprehensive treatment strategies, and novel drug development. We also propose our own thinking and prospects regarding NPE.

Background: Probiotic treatments might contribute to the prevention of ventilator-associated pneumonia (VAP). Due to its unclear clinical effects, here we intend to assess the preventive effect and safety of probiotics on intensive care unit (ICU) patients.Methods: Eligible randomised controlled trials were selected in databases until 30 September 2019. The characteristics of the studies were extracted, including study design, definition of VAP, probiotics intervention, category of included patients, incidence of VAP, mortality, duration of mechanical ventilation (MV) and ICU stay. Heterogeneity was evaluated by Chi-squared and I²tests.Results: 15 studies involving 2039 patients were identified for analysis. The pooled analysis suggests significant reduction on VAP (risk ratio, 0.68; 95% Cl, 0.60 to 0.77; p<0.00001) in a fixed-effects model. Subgroup analyses performed on the category of clinical and microbiological criteria both support the above conclusion; however, there were no significant differences in duration of MV or length of ICU stay in a random-effects model. Also, no significant differences in total mortality, overall mortality, 28-day mortality or 90-day mortality were found in the fixed-effects model.Conclusions: The probiotics helped to prevent VAP without impacting the duration of MV, length of ICU stay or mortality.