Fine particulate matter (PM2.5) has a damaging effect on the male reproductive system. Baicalin has excellent anti-inflammatory and antioxidant pharmacological functions. The main purpose of this study was to investigate whether baicalin had a protective effect against PM2.5-induced damage to the reproductive system of mice, and to further investigate the mechanism of the protective effect of baicalin. In our experiment, baicalin was administered by gavage 1 h before PM2.5 exposure, followed by exposure to PM2.5 with an oral-nasal exposure system at 750 μg/m3 for 4 h/day, and this experiment was continued for 45 days until the model was established. The results indicated that PM2.5 exposure decreased testicular weight and organ coefficient, sperm count, and serum testosterone level, and down-regulated the mRNA and protein expressions of StAR, CYP11A1, and CYP17A1, which related to testosterone synthesis. After baicalin treatment, our experimental results showed that the 50 and 100 mg/kg baicalin groups showed a gradual increase in sperm counts, testosterone levels, and a significant restoration of genes and protein related to testosterone synthesis and the DKK1-Wnt/β-catenin signaling pathway. In conclusion, baicalin might play a protective role in promoting testicular tissue repair, and this may be associated with the regulation of the DKK1 - Wnt/β-catenin signaling pathway.

Abstract Background Microecological equilibrium is essential for human health. Previous research has demonstrated that Streptococcus strain A, the main bacterial group in the respiratory tract, can suppress harmful microbes and protect the body. In this study, Streptococcus strain D19T was isolated from the oral and pharyngeal cavities of healthy children. Its antibacterial mechanism against Acinetobacter baumannii was examined, as well as its potential to prevent inflammatory damage to cells. We evaluated the effect of the fermentation conditions of D19T on inhibition of Acinetobacter baumannii growth; Isolation and purification of antibacterial active components of strain D19T and molecular mechanism of inhibition of Acinetobacter baumannii; Molecular mechanism of D19T bacteriostatic protein reversing cellular inflammatory injury induced by Acinetobacter baumannii. Results The supernatant of fermentation broth of Streptococcus D19T was the active component against Acinetobacter baumannii, but the bacteria had no antibacterial activity. The supernatant of D19T fermentation broth was precipitated by (NH4)2SO4 solution, and the protein was the active antibacterial component. After gel filtration chromatography and anion gel filtration chromatography, the molecular weight of antibacterial protein was 53kD. D19T antibacterial protein can improve cell membrane permeability, limit extracellular soluble protein release, inhibit Acinetobacter baumannii biofilm formation, and prevent Acinetobacter baumannii adhesion. Acinetobacter baumannii induces inflammatory damage to respiratory cells via ferroptosis, and the D19T antibacterial protein can counteract this damage, protecting the respiratory tract. Conclusion Streptococcus strain D19T, as a potential probiotic, inhibits the growth of Acinetobacter baumannii and the inflammatory damage of respiratory cells, playing a protective role in human respiratory health.

BackgroundMicroecological equilibrium is essential for human health. Previous research has demonstrated that Streptococcus strain A, the main bacterial group in the respiratory tract, can suppress harmful microbes and protect the body. In this study, Streptococcus strain D19T was isolated from the oral and pharyngeal cavities of healthy children. Its antibacterial mechanism against Acinetobacter baumannii was examined, as well as its potential to prevent inflammatory damage to cells. We evaluated the effect of the fermentation conditions of D19T on inhibition of Acinetobacter baumannii growth; Isolation and purification of antibacterial active components of strain D19T and molecular mechanism of inhibition of Acinetobacter baumannii; Molecular mechanism of D19T antibacterial protein reversing cellular inflammatory injury induced by Acinetobacter baumannii.ResultsThe supernatant of fermentation broth of Streptococcus D19T was the active component against Acinetobacter baumannii, but the bacteria had no antibacterial activity. The supernatant of D19T fermentation broth was precipitated by (NH4)2SO4 solution, and the protein was the active antibacterial component. After gel filtration chromatography and anion gel filtration chromatography, the molecular weight of antibacterial protein was 53kD. D19T antibacterial protein can improve cell membrane permeability, limit extracellular soluble protein release, inhibit Acinetobacter baumannii biofilm formation, and prevent Acinetobacter baumannii adhesion. Acinetobacter baumannii induces inflammatory damage to respiratory cells via ferroptosis, and the D19T antibacterial protein can counteract this damage, protecting the respiratory tract.ConclusionStreptococcus strain D19T, as a potential probiotic, inhibits the growth of Acinetobacter baumannii and the inflammatory damage of respiratory cells, playing a protective role in human respiratory health.

Background As probiotics protect host cells, they are used to treat bacterial infections. It has been indicated that probiotics may prevent or reduce the attachment of pathogens to host cells. In this study, Streptococcus strain D19 T was isolated from the oropharynx of a healthy child, and its adhesion performance and Staphylococcus aureus adhesion inhibition effect were analysed using human bronchial epithelial (16-HBE) cells, as an in vitro cell model. We evaluated the probiotic properties of the D19 T strain based on its acid–base, bile salt, and lysozyme tolerance; antibacterial activity; cytotoxicity; antibiotic sensitivity; in vitro adhesion to 16-HBE cells; and competitive, exclusion, and displacement effects against S. aureus . Results Streptococcus strain D19 T showed tolerance to a PH range of 2–5 and 0.5–1% bile. However, it was more tolerant to 0.5% bile than to 1% bile. The strain also demonstrated an ability to adapt to maladaptive oropharyngeal conditions (i.e., tolerating 200 µg/mL lysozyme). It was resistant to 0.8 mM H 2 O 2 . The results also demonstrated that D19 T exhibited inhibitory activities against various common pathogenic bacteria. Furthermore, D19 T was not toxic to 16-HBE cells at different multiplicities of infection and was sensitive to most antibiotics tested. The adhesion rate of D19 T cells to 16-HBE cells was 47% ± 1.2%, which was significantly higher than that of S. aureus to 16-HBE cells. The competition, exclusion, and displacement assay results showed that D19 T has good inhibitory effect against S. aureus adhesion. Conclusions The present study revealed that Streptococcus strain D19 T has the potential to be developed as a respiratory microbiota preparations.

The public health harms caused by fine particulate matter (PM2.5) have become a global focus, with PM2.5 exposure recognized as a critical risk factor for global morbidity and mortality. Chronic inflammation is the common pathophysiological feature of respiratory diseases induced by PM2.5 and is the most critical cause of all these diseases. However, presently there is a lack of effective preventive and therapeutic approaches for inflammatory lung injuries caused by PM2.5 exposure. Baicalin is a herb-derived effective flavonoid compound with multiple health benefits. This study established a murine lung inflammatory injury model via inhalation of PM2.5 aerosols. The data showed that after baicalin intervention, lung injury pathological score of baicalin (4.16 ± 0.54, 3.33 ± 0.76, 4.00 ± 0.45) and claricid (3.00 ± 0.78) treatments were markedly lower than PM2.5-treated mice (6.17 ± 0.31), and pathological damage was alleviated. Compared to the PM2.5 group, the spleen and lung indexes in the baicalin and claricid groups were significantly reduced. The inflammatory cytokines of TNF-α, IL-18, and IL-1β in serum, alveolar lavage fluid, and lung tissue were significantly decreased in the baicalin and claricid groups. The expressions of inflammatory pathway-related genes and proteins HMGB1, NLRP3, ASC, and caspase-1 were up-regulated in the PM2.5 group. The expressions of these genes and proteins were significantly decreased following baicalin treatment. The lung function indicators showed that the MV (65.94 ± 8.19 mL), sRaw (1.79 ± 0.08 cm H2O.s), and FRC (0.52 ± 0.01 mL) in the PM2.5 group were higher than in the control and baicalin groups, and respiratory function was improved by baicalin. PM2.5 exposure markedly altered the bacterial composition at the genus level. The dominant flora relative abundances of uncultured_bacterium_f_Muribaculaceae, Streptococcus, and Lactobacillus, were decreased from the control group (9.20%, 8.53%, 6.21%) to PM2.5 group (6.26%, 5.49%, 4.77%), respectively. Following baicalin intervention, the relative abundances were 9.72%, 6.65%, and 3.57%, respectively. Therefore, baicalin could potentially prevent and improve mice lung inflammatory injury induced by PM2.5 exposure. Baicalin might provide a protective role by balancing oropharyngeal microbiota and affecting the expression of the HMGB1/Caspase1 pathway.

目的 了解哮喘患儿呼吸道菌群多样性及其组成特征,同时研究所分离的3株优势菌对流感嗜血杆菌的抑制作用,探究哮喘与呼吸道菌群之间的关系.方法 采集沈阳市儿童医院呼吸内科2019年3月至2019年12月收治的21例4～12岁急性发作期哮喘患儿咽拭标本,并同时采集23例同龄健康儿童的咽拭标本作为对照,对呼吸道菌群进行分离培养、纯化和16SrRNA鉴定.采用牛津杯法检测健康儿童口咽部分离的3株优势菌对流感嗜血杆菌的拮抗作用.结果 哮喘和健康儿童呼吸道培养出的需氧菌(t=2.143,P=0.038)和厌氧菌(t=3.270,P=0.002)的密度差异有统计学意义.哮喘患儿咽部需氧菌以肺炎链球菌和流感嗜血杆菌为主,厌氧菌以韦荣球菌为主.健康儿童咽部需氧菌以缓症链球菌和口腔链球菌为主,厌氧菌以干酪乳杆菌为主.健康儿童口咽部的3株优势菌对哮喘儿童口咽部流感嗜血杆菌的生长具有显著抑制作用.结论 与健康儿童相比,哮喘患儿口咽部菌群发生紊乱,且哮喘患儿口咽部需氧菌、厌氧菌密度显著增加.健康儿童口咽部的某些优势菌可能对哮喘致病菌的定植有一定的拮抗作用.

目的 从健康儿童口咽部筛选出多株具有抑菌作用的链球菌D-19,探究链球菌D-19表面疏水性及自动聚集能力的影响因素.方法 利用菌体对碳氢化合物的黏附测定多株链球菌D-19的表面疏水率,紫外分光光度法测定D-19的自动聚集能力,并采用不同环境条件和蛋白酶处理菌体表面来确定菌体表面疏水率及自动聚集能力的影响因素.结果 链球菌D-19经不同因素处理后与未处理相比,其表面疏水性及自动聚集能力均有显著的差异.结论 影响链球菌D-19表面疏水性的因素有培养时间、温度、pH、酶和浓度等,影响其自动聚集能力的因素有培养时间、温度和酶等.研究结果可以为进一步研究链球菌D-19的黏附能力提供依据.

目的 通过高通量测序分析哮喘模型小鼠呼吸道菌群的变化情况.方法 将12只SPF级BALB/c雄性小鼠随机分为对照组和模型组,每组6只.采用卵清蛋白致敏方法建立哮喘小鼠模型后,进行支气管组织切片病理学观察,ELISA法检测血清IgE水平,测定肺指数,采集咽拭子后提取DNA行高通量测序分析.结果 与对照组比较,模型组小鼠血清IgE水平明显升高(P＜0.05),肺指数明显上升(P＜0.05),可见支气管上皮粘膜有水肿,少量淋巴细胞浸润,平滑肌增生.模型组小鼠呼吸道菌群与对照组比较,菌种丰度升高,厚壁菌门较对照组减少(P＜0.05),放线菌门和变形菌门增多(P＜0.05),菌群结构有明显差异.结论 哮喘小鼠存在呼吸道微生态菌群失衡.

目的 基于广义相加模型定量分析某地级市大气污染物PM2.5与居民呼吸系统疾病及恶性肿瘤死亡风险的相关性.方法 收集2016～2018年该地级市逐日PM2.5浓度数据、气象数据、居民呼吸系统疾病及恶性肿瘤死亡数据,进行描述性统计分析;采用基于Quasi-Poisson回归的广义相加模型(GAM),分析PM2.5与该市居民呼吸系统疾病和恶性肿瘤死亡风险间的相关关系.结果 2016～2018年该地级市大气PM2.5日均值为49μg/m3,共有631 d超出《环境空气质量标准》GB3095-2012污染物浓度一级限值标准,占三年总天数的57.6％;广义相加模型滞后效应(Lag0～Lag7)显示,PM2.5浓度升高10μg/m3,呼吸系统疾病死亡率在滞后5 d的影响最大(ER=0.699％(95％CI:0.121％～1.277％)),恶性肿瘤死亡率在滞后3 d时的影响最大(ER=0.443％(95％CI:0.013％～0.873％));寒季(11月 ～4月)期间,PM2.5浓度升高10μg/m3,呼吸系统疾病死亡率在滞后6 d的影响最大(ER=0.952％(95％CI:0.269％～1.635％)),恶性肿瘤死亡率在滞后1 d时的影响最大(ER=0.819％(95％CI:0.177％～1.461％)).结论 该地级市PM2.5浓度升高会引起呼吸系统疾病和恶性肿瘤死亡率增加,特别是在寒季,PM2.5暴露对呼吸系统疾病的负性效应更显著.

In the microbiome, probiotics modulate oral diseases. In this study, Streptococcus strain C17(T) was isolated from the oropharynx of a 5-year-old healthy child, and its potential probiotic properties were analysed using human bronchial epithelial cells (16-HBE) used as an in vitro oropharyngeal mucosal model. The results demonstrated that the C17(T) strain showed tolerance to moderate pH ranges of 4-5 and 0 center dot 5-1% bile. However, it was more tolerant to 0 center dot 5% bile than 1% bile. It also demonstrated an ability to accommodate maladaptive oropharyngeal conditions (i.e. tolerating lysozyme at 200 mu g ml(-1)). It was also resistant to hydrogen peroxide at 0 center dot 8 mM. In addition, we found out that the strain possesses inhibitory activities against various common pathogenic bacteria. Furthermore, C17(T) was not cytotoxic to 16-HBE cells at different multiplicities of infection. Scanning electron microscopy disclosed that C17(T) adhesion to 16-HBE cells. Competition, exclusion and displacement assays showed that it had good anti-adhesive effect against S. aureus. The present study revealed that Streptococcus strain C17(T) is a potentially efficacious oropharyngeal probiotic.

益生菌作为一种活的微生物形式的膳食补充剂,适当使用可以为人类健康带来益处.在过去的几十年中,关于益生菌领域的研究取得了很大的进步,并且在益生菌对于人体健康所发挥的功能方面取得了重大进展.目前,益生菌在预防和治疗疾病方面具有广阔的前景.本文就益生菌的生理功能及其抑癌、抑菌机制进行综述.

目的 对分离自健康儿童口咽部1株对金黄色葡萄球菌、大肠埃希菌等致病菌具有拮抗作用的链球菌C-17株做体内安全性评估,为今后呼吸道微生态制剂的研发与应用提供基础.方法 通过急性毒性及亚急性毒性试验,给予小鼠口服不同剂量的链球菌C-17株菌液,观察动物是否出现死亡、中毒现象以及体质量、采食量、血常规指标、生化指标等的变化,然后对结果进行统计学分析.结果 实验组小鼠均未出现死亡、中毒的现象,其体质量、采食量和脏器指数同对照组相比差异无统计学意义(均P＞0.05).同时,在亚急性毒性试验中,各剂量组小鼠的血常规及生化指标与对照组相比差异无统计学意义(均P＞0.05),各脏器也未出现任何病理学变化.结论 口服链球菌C-17株对小鼠并无毒性作用,具有良好的体内安全性,但作为呼吸道微生态制剂还需做呼吸毒性试验.

Lipid metabolism is an important biochemical process in the body. Recent studies have found that environmental endocrine disruptors play an important role in the regulation of lipid metabolism. Bisphenol A (BPA), a common environmental endocrine disruptor, has adverse effects on lipid metabolism, but the mechanism is still unclear. This study aimed to investigate the effects of gestational BPA exposure on hepatic lipid metabolism and its possible mechanism in male offspring. The pregnant Sprague-Dawley rats were exposed to BPA (0, 0.05, 0.5, 5 mg/kg/day) from day 5 to day 19 of gestation to investigate the levels of triglyceride (TG) and total cholesterol (TC), and the expression of liver lipid metabolism-related genes in male offspring rats. The results showed that compared with the control group, the TG and TC levels in serum and liver in BPA-exposed groups was increased. And the expressions of liver fatty acid oxidation related genes, such as peroxisome proliferators-activated receptor α (PPARα) and carnitine palmitoyl transferase 1α (CPT1α), were down-regulated. However, the expressions of fatty acid synthesis related genes, such as sterol regulatory element binding proteins 1 (SREBP-1), acetyl-CoA carboxylase 1 (ACC1), fatty acid synthase (FAS) and stearoyl-CoA desaturase 1 (SCD-1), were up-regulated. The increased protein levels of mTOR and p-CRTC2 suggested that CREB-regulated transcription coactivator 2 (CRTC2) might be an important mediator in the mTOR/SREBP-1 pathway. In conclusion, these results demonstrated that mTOR/CRTC2/SREBP-1 could be affected by gestational BPA exposure, which may involve in the lipid metabolic disorders in later life.

目的 观察潜在益生菌链球菌C17、D19株与香菇多糖联合应用对PM2.5暴露肺癌荷瘤小鼠呼吸道菌群多样性的影响.方法 尾静脉注射A549细胞悬液构建荷瘤SCID小鼠模型,气管滴注40 μL 20 mg/mL的PM2.5溶液,每周1次,持续4周.实验组(LS组)给予链球菌C17、D19株混合菌液喷雾给药,每周2次,同时腹腔注射3 mg/kg香菇多糖.对照组(PM组)仅喷雾生理盐水.比较组(LE组)喷雾生理盐水同时给予香菇多糖.全部小鼠均持续处理4周.利用高通量测序对咽拭子样本中的菌群进行16SrDNA序列检测,进行OTU统计、物种组成分析、指示物种分析、Alpha多样性分析、Beta多样性分析.结果 PM组小鼠OTU数量大于LE组、LS组.各组主要优势菌为厚壁菌门、变形菌门、放线菌门、蓝细菌门、拟杆菌门.与 PM 组比较,LE 组(t=3.206 4,P=0.007 1)、LS 组(t=3.406 1,P=0.009 8)放线菌门丰度增加显著,LE组蓝细菌门丰度减少显著(t=2.7316,P=0.034 0).属水平上,LS组与LE组各优势菌属总丰度显著高于PM组.与PM组比较,LS组小鼠呼吸道嗜气杆菌属(t=7.168 6,P=0.000 8)和普雷沃菌属(t=2.270 2,P=0.023 0)丰度显著增加,LE组嗜气杆菌属(t=2.523 8,P=0.042 9)、加德纳菌属(t=2.472 0,P=0.044 5)、奇异菌属(t=4.812 3,P=0.003 0)、弧菌属(t=2.459 7,P=0.0210)、普雷沃菌属(t=2.607 6,P=0.031 9)丰度差异显著.种水平上,与PM组比较,LS 组小鼠呼吸道酸性链球菌(t=2.445 6,P=0.045 0)、Rodentibacter_heylii(t=7.168 6,P=0.000 8)增加显著,LE 组普雷沃菌(t=2.275 1,P=0.046 2)、Rodentibacter_heylii(t=2.523 8,P=0.034 0)增加显著.Alpha多样性分析显示,LE组与PM组间、LS组与PM组间菌群Chao 指数(t=2.386 7,P=0.038 8;t=5.878 0,P=0.000 6),Ace 指数(t=2.826 7,P=0.019 2;t=6.131 6,P=0.000 9)差异有统计学意义.Beta多样性分析显示,LS组与PM组间(t=2.999 4,P=0.005 6)、LE组与PM组间(t=4.893 8,P＜0.000 1)OTU水平比较差异有统计学意义.结论 潜在益生菌C17、D19株与香菇多糖联合应用可调节PM2.5暴露肺癌小鼠呼吸道的菌群多样性.

Flavonoids which are extracted from citrus peel and pulp have been reported to have multiple beneficial effects on human health. Isosinensetin (ISO) is a type of flavonoid compound, which has several protective effects including anticancer, antioxidant, antiviral, anti-inflammatory and bacteriostatic. However, the molecular mechanism of its antioxidant and anti-inflammatory effects remain unclear. The present study aimed to investigate the intervention effect and possible mechanism of ISO on human bronchial epithelial cells injured by fine particular matter ≤2.5 µm in diameter (PM2.5). In the present study, the cell viability was detected by Cell Counting Kit-8 method. The levels of pro-inflammatory cytokines were analyzed by ELISA. The level of reactive oxygen species (ROS) was detected by fluorescence probe. The expression levels of proliferating cell nuclear antigen (PCNA), nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor кΒ (NF-кB) proteins were detected by western blotting. The results revealed that ISO evidently increased the viability of 16-HBE cells and sharply decreased the levels of pro-inflammatory factors in cell culture supernatant. ISO significantly inhibited ROS release caused by PM2.5. Moreover, the expression levels of PCNA, Nrf2 and NF-кB proteins were downregulated after ISO incubation. These results indicated that ISO alleviated 16-HBE-cell injury by PM2.5 through the ROS-Nrf2/NF-кB signaling pathway.

Background： We performed this study to explore the inflammation and oxidative stress responses of rat trachea and lung caused by PM 2.5 and mixed toxic gas. Materials and methods： Eighty-four Wistar rats were randomly assigned to receive exposure to PM2.5 and toxic gases containing carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2) or saline. Microflora in rat respiratory tract were investigated through testing secretion taken from posterior pharyngeal wall on Day 1, 7 and 30. Trachea and lung tissues were processed for scanning electron microscopic (SEM) and transmission electron microscopic (TEM) examinations. Cytokines in rat bronchoalveolar lavage fluid (BALF), serum and lung tissues were analyzed via enzyme-linked immunosorbent assay and real-time quantitative PCR. Results： Eight aerobes and seven anaerobes were firstly detected after exposure ( p <0.01, respectively). Most of them are the pathogenic bacteria or opportunistic pathogen. SEM and TEM observations suggested that both normal structure of trachea and lung tissue were injured after exposure to PM 2.5 with mixed toxic gas and the injure degree was concentration- and time-dependent. Interleukin 4 (IL-4), interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) expression in the BALF and lung tissue markedly increased on Day 1 and 7 ( p <0.01, respectively). Interferon γ (IFN-γ) did not show significant change after exposure. On Day 30, all the detected cytokines decreased and even disappeared. All detected cytokines in the serum had no significant difference before and after exposure ( p >0.05, respectively). Conclusion： PM 2.5 with mixed toxic gas can lead to dysbacteriosis in respiratory tract and destroy the normal structure of trachea and lung tissue. The injure degree was concentration- and time-dependent. Local inflammatory response instead of systemic reaction may be predominant in the response of rat respiratory tract to PM 2.5 with mixed toxic gas.

目的建立长期暴露高浓度PM 2.5 的ICR小鼠动物模型,探索长期暴露于PM 2.5 对呼吸道微生物组成的影响。方法以沈阳市黄河北大街为采样点,收集空气中细颗粒物,用浓度为200μg/mL的PM 2.5 建立染尘染毒ICR小鼠模型,染尘周期为6个月,用无菌棉拭子进行咽拭取材后,使用靶向16S rRNA基因的V3-V4区域进行高通量测序来研究它们的微生物群。结果染尘组小鼠呼吸道菌群OTU总数大于对照组,物种分类分析后主要优势菌门为拟杆菌门、厚壁菌门和变形菌门。2组差异物种分析得出拟杆菌门和螺旋体菌门丰度染尘组大于对照组,变形菌门丰度染尘组小于对照组。此外α多样性分析Chao1指数和Ace指数差异具有统计学意义（均P＜0.05）。结论染尘组与对照组小鼠呼吸道菌群具有明显差异性,证实长期高浓度PM 2.5 暴露导致呼吸道菌群失调。

对分离于健康儿童口咽部的2株对金黄色葡萄球菌等常见致病菌具有广谱拮抗作用的甲型链球菌菌株1-4和4-2的安全性进行评价,为其作为呼吸道益生菌产品的研发和制备提供安全性依据.通过给予SPF级小鼠口服含有菌株1-4和4-2不同剂量的菌液的急性毒性实验以及耐药性的测定,观察动物是否出现死亡,急性毒性体征,细菌移位生长等情况.未发现动物死亡情况,实验组的体重变化采食量以及脏器指数均与对照组无显著差异,未有细菌移位生长的现象发生.菌株1-4和4-2均对9种常见抗生素的检测结果为敏感,其中菌株4-2对红霉素具有抗性.菌株1-4和4-2的安全性评价初步显示对小鼠无毒副作用,具有良好的安全性,可以作为呼吸道微生态制剂等产品的备用菌株.

目的 探究沈阳市大气主要污染物对居民慢性下呼吸道疾病死亡的影响.方法 收集2013～2017年沈阳居民慢性下呼吸道疾病死亡资料,2005～2017年沈阳市SO2、NO2、PM10、PM2.5资料,对沈阳大气主要污染物与居民慢性下呼吸道疾病年死亡率进行灰色关联分析.结果 2013～2017年沈阳市SO2的[M(QR)]为54(85)μg/m3,NO2,PM10,PM2.5的[M(QR)]依次为42(22)μg/m3,93(70)μg/m3,50(49)μg/m3;居民慢性下呼吸道疾病日均死亡2人,全年以1月和2月的死亡率相对较高,且与同期大气主要污染物(SO2、NO2、PM10、PM2.5)日均浓度存在正相关(均P<0.05).灰色定量结果显示,SO2致慢性下呼吸道疾病的潜伏期是5年,而NO2与PM10显示出对慢性下呼吸道疾病的潜伏期为<1年和6年.结论 沈阳市SO2、NO2、PM10影响居民慢性下呼吸道疾病的流行.

人体是个巨大的生态系统,各个器官的表面附着大量的微生物,微生物群通过与宿主细胞之间的相互作用来保证机体的正常营养代谢和微生态稳定.长期以来由于呼吸道的生理功能和特性,其微生物菌群的调节作用没有引起足够重视.自"肠-肺轴"的提出,更多学者开始致力于研究呼吸道微生态,并发现一些呼吸道疾病如慢性阻塞性肺疾病、特发性肺纤维化以及支气管哮喘等的发生发展与呼吸道微生态存在一定的关系,这为进一步研究呼吸道疾病,并寻求更好的治疗方式提供新的方向和选择.本文就支气管哮喘与呼吸道微生态之间的作用关系作一综述.