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Background: CXCL3 (C-X-C motif chemokine ligand 3) is a member of chemokines family, which binds to the receptor to recruit neutrophils to lungs, thus participating in the pathogenesis of asthmatic lung. The role of CXCL3 in sepsis-induced acute lung injury is investigated here. Methods: Human lung epithelial cell line (BEAS-2B) and human pulmonary artery endothelial cell line (HPAEC) were treated with lipopolysaccharides (LPS). MTT and flow cytometry were performed to detect cell viability and apoptosis, respectively. Enzyme-linked immunosorbent assay (ELISA) and real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) were used to assess the levels of inflammatory factors. Results: Treatment with LPS resulted in the decrease of cell viability in BEAS-2B and HPAEC. CXCL3 was particularly upregulated in LPS-treated BEAS-2B and HPAE cells. Knockdown of CXCL3 enhanced viability and suppressed apoptosis i006E LPS-treated BEAS-2B and HPAE cells. Knockdown of CXCL3 also upregulated TNF-α, IL-1β, and IL-18 in LPS-treated BEAS-2B and HPAE cells. Moreover, knockdown of CXCL3 suppressed the activation of mitogen-activated protein kinases (MAPKs) signaling in LPS-treated BEAS-2B and HPAE cells through downregulation of p-ERK1/2, p-p38, and p-JNK. On the other hand, overexpression of CXCL3 caused completely opposite results in LPS-treated BEAS-2B and HPAE cells. Conclusion: Knockdown of CXCL3 exerted antiapoptotic and anti-inflammatory effects against LPS-treated BEAS-2B and HPAE cells, at least partially, through inactivation of MAPKs signaling, suggesting a potential strategy for the intervention of sepsis-induced acute lung injury.

Spatio-temporal dynamics of riverine nitrogen (N) and phosphorus (P) in karst regions are closely linked to hydrological conditions, human activities and karst features in upstream catchments. From October 2017 to September 2019, we undertook 22 sampling campaigns in 11 nested catchments ranging from 21.00 to 373.37 km2 in Huixian karst wetland to quantify forms, concentrations, and fluxes of riverine total nitrogen (TN) and total phosphorus (TP), and to identify spatial and temporal variations of nutrients transfer from upstream to downstream, tributaries (Mudong River and Huixian River) to the main stem (Xiangsi River) in the dry and wet seasons. Considering the hydrological conditions, human activities and karst features within upstream catchments, the following three spatial and temporal variations of riverine nutrients were found over the monitoring period: (1) the dynamics of riverine nitrogen and phosphorus varied seasonally with hydrological conditions; (2) the spatial disparities of riverine nitrogen and phosphorus were induced by different human activities within catchment scales; (3) the dynamics of riverine nitrogen and phosphorus varied similarly at spatial scale restricted by karst features. The findings from this study may improve our understanding of the influence of hydrological conditions, human activities and karst features on nitrogen and phosphorus variations in river waters at different spatial and temporal scales in the Huixian karst wetland basin, and will help managers to protect and restore river water environments in karst basin from a catchment-scale perspective.

When considering the factors affecting the spatial and temporal variation of nitrogen and phosphorus in karst watersheds, the unique karst hydrogeology as an internal influencing factor cannot be ignored, as well as natural factors such as meteorological hydrology and external factors such as human activities. A watershed-scale field investigation was completed to statistically analyze spatial and temporal dynamics of nitrogen and phosphorus through the regular monitoring and collection of surface water and shallow groundwater in the agricultural-dominated Mudong River watershed in the Huixian Karst Wetland over one year (May 2020 to April 2021). Our research found that non-point source pollution of nitrogen (84.5% of 239 samples TN > 1.0 mg/L) was more serious than phosphorus (7.5% of 239 samples TP > 0.2 mg/L) in the study area, and shallow groundwater nitrogen pollution (98.3% of 118 samples TN > 1.0 mg/L) was more serious than surface water (68.6% of 121 samples TN > 1.0 mg/L). In the three regions with different hydrodynamic features, the TN concentration was higher and dominated by NO3−-N in the river in the northern recharge area, while the concentrations of TN and TP were the highest in shallow groundwater wells in the central wetland core area and increased along the surface water flow direction in the western discharge area. This research will help improve the knowledge about the influence of karst hydrodynamic features on the spatial patterns of nitrogen and phosphorus in water, paying attention to the quality protection and security of water in karst areas with a fragile water ecological environment.

Background: Acute lung injury (ALI) is a clinical syndrome characterized by hyperosmotic pulmonary edema and increased alveolar fluid. Phospholipase C epsilon-1 (PLCE1), identified as a member of phospholipase family, and the relationship between PLCE1 and lung injury is not clear. Objective: To assess the possible role of Phospholipase C Epsilon 1 (PLCE1) in Acute lung injury (ALI) progression and related mechanisms. Materials and methods: The effects of LPS and PLCE1 on cell viability and apoptosis were examined by MTT and flow cytometry. Also, the level of PLCE1 was controlled by transfection of its plasmid and shRNA. The inflammatory response in response to PLCE1 overexpression or ablation was analyzed by quantitative PCR and ELISA assay. And the involvement of PKC and NF-κB signal pathway were detected by Immunoblot. Results: In this study, we developed a LPS-induced ALI cell model. We found PLCE1 was upregulated in LPS-induced pneumonia cells and affected cell viability. Also, knockdown of PLCE1 reduced LPS-induced apoptosis of pneumonia cells. In addition, depletion of PLCE1 suppressed LPS-induced secretion of proinflammatory cytokines in pneumonia cells. Mechanically, we found depletion of PLCE1 inhibited PKC and NF-κB signal pathway, and therefore alleviated LPS-induced ALI. Conclusion: We therefore thought PLCE1 could serve as a promising drug for ALI.