Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first reported in Wuhan, Hubei Province, China and has subsequently spread to other regions of China and 37 countries, including the United States, Japan, Australia, and France.¹ SARS-CoV-2, which belongs to a unique clade of the sarbecovirus subgenus of the Orthocoronavirinae subfamily, was identified as the pathogen of coronavirus disease 2019 (COVID-19) in January 2020.²

An ongoing outbreak of 2019‐nCoV pneumonia was first identified in Wuhan, Hubei province, China at the end of 2019. With the spread of the new coronavirus accelerating, person‐to‐person transmission in family homes or hospitals, and intercity spread of 2019‐nCoV occurred. At least 40,261 cases confirmed, 23,589 cases suspected, 909 cases death and 3444 cases cured in China and worldwide 24 countries confirmed 383 cases being diagnosed, 1 case death in February 10th, 2020. At present, the mortality of 2019‐nCoV in China is 2.3%, compared with 9.6% of SARS and 34.4% of MERS reported by WHO. It seems the new virus is not as fatal as many people thought. Chinese authorities improved surveillance network, made the laboratory be able to recognize the outbreak within a few weeks and announced the virus genome that provide efficient epidemiological control. More comprehensive information is required to understand 2019‐nCoV feature, the epidemiology of origin and spreading, and the clinical phenomina. According to the current status, blocking transmission, isolation, protection, and alternative medication are the urgent management strategies against 2019‐nCoV.

Background: Particulate matter (PM) is a high risk factor for various respiratory diseases and triggers an inflammatory response in lung tissues. However, the molecular mechanism of the PM-induced inflammatory response is incompletely understood. Methods: Human bronchial epithelial cells (HBECs) were treated with the urban PM 1649b for assessment of the inflammatory response. The intracellular level of reactive oxygen species (ROS) was measured by flow cytometry. PM-activated signaling pathways were addressed with specific inhibitors. In vivo, the C57 mice model of PM-induced acute lung inflammation was established with intratracheal instillation of PM for 2 consecutive days. The oxidant stress in lung tissues was assessed with dihydroethidium (DHE) staining, and malondialdehyde (MDA) activity and hydrogen peroxide (H₂O₂) assays. The histopathologic changes in lung tissues and number of inflammatory cells in bronchoalveolar lavage fluid (BALF) were examined. Expression of pro-inflammatory cytokines in BALF was measured by ELISA. Results: PM increased the expression of interleukin (IL)-1β, IL-6, IL-8, matrix metalloproteinase (MMP)-9 and cyclooxygenase (COX)-2 in a dose-dependent manner. ROS generation and activation of MAPK (ERK, JNK, p38 MAPK) and NF-κB pathways were detected in PM-exposed HBECs. Pretreatment with N-acetylcysteine (NAC) led to the inflammatory response, ROS level and activation of the MAPK and NF-κB pathways to be attenuated. Blockade of ERK, JNK or p38 MAPK pathway with specific inhibitor prevented the release of pro-inflammatory cytokines and activation of the NF-κB pathway. Inhibition of the NF-κB pathway reduced the expression of pro-inflammatory cytokines. In vivo, PM exposure increased oxidant stress in lung tissues, infiltration of inflammatory cells around PM in lung tissues, the number of total cells and inflammatory cells in BALF, and the concentrations of IL-1β, IL-6, IL-8 and MMP-9 in BALF, all of which were reversed partially upon NAC treatment. Conclusions: PM exposure enhanced the airway inflammatory response significantly through ROS-mediated activation of MAPK (ERK, JNK, p38 MAPK) and downstream NF-κB signaling pathways. Oxidative stress appeared to be the key regulator for PM-induced lung inflammation. These results suggested the molecular mechanism of lung inflammation caused by PM.

Background: Acute respiratory distress syndrome (ARDS) is the leading cause of high mortality in intensive care units (ICUs) worldwide. An effective marker for prognosis in ARDS is particularly important given the absence of effective treatment strategies aside from small tidal volume ventilation. Previous studies identified an association between the neutrophil-to-lymphocyte ratio (NLR) and prognosis in critical patients. In this study, we explored the prognostic and predictive value of the NLR in ARDS patients. Methods: We retrospectively included 275 ARDS patients treated at a single institute from 2008 to 2015. After excluding patients with chronic lung disease, acute myocardial infarction and missing data, 247 patients were ultimately included in the analysis. Clinical characteristics and experimental test data, including the NLR, were collected from medical records at 24 hours after the ARDS diagnosis. Independent prognostic factors were determined by multivariate Cox regression analysis. Subgroup stratification was performed according to different factors, and the continuous factors were divided according to the median values. Results: The NLR in survivors was significantly lower than that in non-survivors (P14) and a low NLR group (NLR ≤14). We found that an NLR >14 was associated with a shorter overall survival (OS) (P=0.005). In the multivariate Cox regression model, we further identified an NLR >14 as an independent prognostic factor for OS [hazard ratio (HR) 1.532, (95% CI, 1.095–2.143), P=0.013]. Subgroup analysis showed that the prognostic value of the NLR was higher in hypertensive patients (P=0.009) and in patients with low red blood cell specific volume (P=0.013), high sodium (P=0.002) and high creatinine levels (P=0.017). Conclusions: The NLR is potentially a predictive prognostic biomarker in ARDS patients.

Background: Airborne particulate matter (PM) is associated with increasing susceptibility to respiratory bacterial infection. Tight junctions (TJs) are protein complexes that form airway epithelial barrier against infection. This study aimed to investigate the effects of PM on the airway TJs in response to infection. Methods: The cytotoxicity of PM to BEAS-2B was evaluated. The reactive oxygen species (ROS) production was measured by the flow cytometry. Colony forming units (CFUs) assay and confocal microscopy were utilized to evaluate the number of bacteria. Immunofluorescence and western blot assay were conducted to detect the expressions of TJs proteins. Animal models were used to investigate the role of TJs in PM-induced lung injury upon bacterial infection. Results: In vitro, PM decreased cell viability, increased ROS production, and increased the number of intracellular bacteria accompanying by the degradation of TJs. N-acetylcysteine (NAC) significantly reversed the PM-induced bacterial invasion and PM-induced disruption of TJs. In vivo, PM increases bacteria-infected lung injury, lung bacteria burden and blood bacterial dissemination, which was closely correlated to the degradation of TJs. Conclusions: PM disrupts TJs via oxidative stress to promote bacterial infection.