The investigation of the physiochemical factors and bacterial communities indicates a low-toxic infectious risk of the Qiujiang River in Shanghai, China.

The overall water quality of urban rivers is closely related to the community structure and the physiochemical factors in them. In this study, the bacterial communities and physiochemical factors of the Qiujiang River, an important urban river in Shanghai, were explored. Water samples were collected from nine sites of the Qiujiang River on November 16, 2020. The water quality and bacterial diversity were studied through physicochemical detection, microbial culture and identification, luminescence bacteria method, and 16S rRNA Illumina MiSeq high-throughput sequencing technology. The water pollution of the Qiujiang River was quite serious with three water quality evaluation indexes, including Cd2+, Pb2+, and NH4+-N, exceeding the Class V standard set by the Environmental Quality Standards for Surface Water (China, GB3838-2002), while the luminescent bacteria test indicated low toxicity of nine sampling sites. Through 16S rRNA sequencing, a total of 45 phyla, 124 classes, and 963 genera were identified, in which Proteobacteria, Gammaproteobacteria, and Limnohabitans were the most abundant phylum, class, and genus, respectively. The Spearman correlation heatmap and redundancy analysis showed that the bacterial communities in the Qiujiang River were correlated with pH; the concentrations of K+, and NH4+-N, and the Limnohabitans were significantly correlated with the concentrations of K+, and NH4+-N in the Zhongyuan Road bridge segment. In addition, opportunistic pathogens Enterobacter cloacae complex and Klebsiella pneumoniae in the samples collected in the Zhongyuan Road bridge segment and Huangpu River segment, respectively, were successfully cultured. The Qiujiang River was a heavily polluted urban river. The bacterial community structure and diversity were greatly affected by the physiochemical factors of the Qiujiang River, and it displayed low toxicity while a relatively high infectious risk of intestinal and lung infectious diseases.

Role of lung and gut microbiota on lung cancer pathogenesis.

BACKGROUND: Lung cancer is the leading cause of cancer-related deaths worldwide (Ferlay et al., Int J Cancer 136:E359-386, 2015). In addition, lung cancer is associated with the highest mortality among all cancer types (Wu et al., Exp Ther Med 16:3004-3010, 2018). Previous studies report that microbiota play an important role in lung cancer. Notably, changes in lung and gut microbiota, are associated with progression of lung cancer. Several studies report that lung and gut microbiome promote lung cancer initiation and development by modulating metabolic pathways, inhibiting the function of immune cells, and producing pro-inflammatory factors. In addition, some factors such as microbiota dysbiosis, affect production of bacteriotoxins, genotoxicity and virulence effect, therefore, they play a key role in cancer progression. These findings imply that lung and gut microbiome are potential markers and targets for lung cancer. However, the role of microbiota in development and progression of lung cancer has not been fully explored. PURPOSE: The aim of this study was to systemically review recent research findings on relationship of lung and gut microbiota with lung cancer. In addition, we explored gut-lung axis and potential mechanisms of lung and gut microbiota in modulating lung cancer progression. CONCLUSION: Pulmonary and intestinal flora influence the occurrence, development, treatment and prognosis of lung cancer, and will provide novel strategies for prevention, diagnosis, and treatment of lung cancer.

The distinct microbial community in Aurelia coerulea polyps versus medusae and its dynamics after exposure to 60Co-γ radiation.

Radiation (e.g., nuclear leakage) is a common harmful factor in the ocean that potentially affects the microbial community in nearby benthic hosts such as jellyfish polyps, which is essential for the maintenance of jellyfish populations and high-quality medusae. After comparison with the microbial community of medusae, the effect of 60Co-γ on the microbial community in Aurelia coerulea polyps was dynamically tested using 16S rRNA gene sequencing. Our results suggested that Proteobacteria (76.19 ± 3.24%), Tenericutes (12.93 ± 3.20%) and Firmicutes (8.33 ± 1.06%) are most abundant in medusae, while Proteobacteria (29.49 ± 2.29%), Firmicutes (46.25 ± 5.59%), and Bacteroidetes (20.16 ± 2.65%) are the top three phyla in polyps. After 60Co-γ radiation, the proportion of Proteobacteria increased from 29.49 ± 2.29% to 59.40 ± 3.09% over 5 days, while that of Firmicutes decreased from 46.25 ± 5.59% to 13.58 ± 3.74%. At the class level, Gammaproteobacteria continually increased during the 5 days after radiation exposure, whereas Bacilli declined, followed by partial recovery, and Alphaproteobacteria and Flavobacteriia remained almost unchanged. Intriguingly, Staphylococcus from Firmicutes and three other genera, Rhodobacter, Vibrio, and Methylophaga, from Proteobacteria greatly overlapped according to their KEGG functions. It is concluded that the microbial community in A. coerulea polyps is distinct from that in the medusae and is greatly affected by 60Co-γ exposure, with a growth (0-3 d) period and a redistribution (3-5 d) period. The dynamic change in the microbial community is probably an important self-defense process in response to external interference that is regulated by the host's physiological characteristics and the intense interspecific competition among symbiotic microbes with similar functions and functional redundancies.

Pravastatin protects hyperbaric hyperoxia-induced lung injury via inhibiting inflammation in mice.

This study aimed to investigate the protective effects of pravastatin on hyperbaric hyperoxia-induced lung injury (HILI). C57BL/6 mice were randomly assigned into three groups: control group, HILI group and pravastatin (Pra) group. Mice in the HILI and Pra groups were subjected to exposure to pure oxygen at 2.5 atm abs for six hours. Mice in the Pra group were intraperitoneally treated with pravastatin at 15 mg/kg. immediately after exposure. At 24 hours, the lungs were collected for HE staining, TUNEL staining and detection of lung edema, myeloperoxidase (MPO) activity and cytokines, and bronchoalveolar lavage fluid (BALF) was harvested for cell-counting. Pravastatin treatment significantly improved the pathology of the lung after HILI (reduction in thickness of alveolar septum, attenuation of lung edema, fracturing of alveolar septa and decrease in infiltrated leukocytes); reduced the number of apoptotic cells; inhibited lung MPO activity; and regulated the balance between pro-inflammatory and anti-inflammatory cytokines. Our findings suggest that pravastatin may exert a protective effect on lung injury after hyperbaric hyperoxia exposure by inhibiting inflammation.

Protective effect of hydrogen sulfide on hyperbaric hyperoxia-induced lung injury in a rat model.

Hyperbaric oxygen therapy is one of the most widely used clinical interventions to counteract insufficient pulmonary oxygen delivery in patients with severe lung injury. However, prolonged exposure to hyperoxia leads to inflammation and acute lung injury. This study aimed to investigate the protective effect of hydrogen sulfide on hyperbaric hyperoxia-induced lung injury. Rats were intraperitoneally treated with sodium hydrosulphide (NaHS) at 28 µmol/kg immediately before hyperoxia exposure and then exposed to pure oxygen at 2.5 atmospheres absolute (atm abs) with continuous ventilation for six hours, Immediately after hyperoxia exposure, rats were sacrificed via anesthesia. The bronchoalveolar lavage fluid (BALF) was harvested for the detection of protein concentration and IL-1 content, and the lungs were collected for HE staining, TUNEL staining and detection of wet/dry weight ratio. Our results showed hyperbaric hyperoixa exposure could significantly damage the lung (HE staining), increase the protein and IL-13 in the BALF, elevate the wet/dry Weight ratio and raise the TUNEL positive cells. However, pre-treatment with hydrogen sulfide improved the lung morphology, reduced the TUNEL positive cells and attenuated the lung inflammation (reduction in IL-13 of BALF and HE staining). Taken together, our findings indicate that hydrogen sulfide pretreatment may exert protective effects on hyperbaric hyperoxia-induced lung injury.

SC5b-9-induced pulmonary microvascular endothelial hyperpermeability participates in ventilator-induced lung injury.

Mechanical ventilation with large tidal volumes can increase lung alveolar permeability and initiate inflammatory responses, termed ventilator-induced lung injury (VILI). VILI is characterized by an influx of inflammatory cells, increased pulmonary permeability, and endothelial and epithelial cell death. But the underlying molecular mechanisms that regulate VILI remain unclear. The purpose of this study was to investigate the mechanisms that regulate pulmonary endothelial barrier in an animal model of VILI. These data suggest that SC5b-9, as the production of the complement activation, causes increase in rat pulmonary microvascular permeability by inducing activation of RhoA and subsequent phosphorylation of myosin light chain and contraction of endothelial cells, resulting in gap formation. In general, the complement-mediated increase in pulmonary microvascular permeability may participate in VILI.

Normoxic induction of cerebral HIF-1alpha by acetazolamide in rats: role of acidosis.

Acetazolamide has been recognized as an effective treatment for acute mountain sickness. The efficacy of acetazolamide is related to metabolic acidosis, which promotes chemoreceptors to respond to hypoxic stimuli at altitude. In this study, adult male Sprague-Dawley rats were treated with acetazolamide (100mg/kg or 50mg/kg, I.P.) for 3 days. Primary cultured cortical neurons and PC12 cell lines were exposed to acidosis-permissive (pH 6.5) or standard (pH 7.2) media for 20h. HIF-1alpha and its target genes were assayed by Western blot, real-time PCR, HIF-1 DNA-binding assay and chloramphenicol acetyltransferase reporter gene assay. HIF-1alpha protein level and HIF-1 DNA-binding activities were increased in cerebral cortices of rats treated with acetazolamide. Moreover, the mRNA levels of erythropoietin, vascular endothelial growth factor, and glucose transporter-1 also increased. The HIF-1alpha protein level and activity of HIF-driven chloramphenicol acetyltransferase reporters of cortical neurons and PC12 cells treated with acidosis media were significantly enhanced. We conclude that the normoxic induction of HIF-1alpha and HIF-1 mediated genes by acetazolamide may mediate the effect of acetazolamide in the reduction of symptoms of acute mountain sickness.

Up-regulated HIF-1alpha is involved in the hypoxic tolerance induced by hyperbaric oxygen preconditioning.

Hyperbaric oxygen preconditioning (HBO-PC) has been shown to be effective in preventing hypoxic injuries in many animal models. The aim of the present study was to examine the hypoxic tolerance induced by HBO-PC and to explore the role of hypoxia-inducible factor-1alpha (HIF-1alpha) in a global hypoxia model. Male mice received HBO-PC before hypoxia exposure and swimming. HBO-PC significantly prolonged the survival time and the tolerance time of swimming under normobaric hypoxia. HBO-PC increased the protein content of HIF-1alpha and erythropoietin (EPO) in the cerebral cortex and hippocampus and prevented the changes of blood brain barrier (BBB) permeability and brain edema caused by hypoxia exposure. The results suggested that HBO-PC induced hypoxic tolerance in mice via up-regulation of HIF-1alpha and its downstream genes.