吸烟对人体呼吸道菌群的影响

目的 探讨吸烟对人体呼吸道需氧菌群的影响.方法 采用细菌鉴定及药敏分析系统鉴定健康吸烟者与非吸烟者,患下呼吸道感染与非吸烟者咽后壁分泌物菌群的变化.结果 患下呼吸道感染者较健康者细菌检出率明显增高(P＜0.05),患下呼吸道感染吸烟者细菌检出率较非吸烟者细菌检出率明显增加(P＜0.05),健康吸烟者细菌检出率较非吸烟者明显增加(P＜0.05).结论 吸烟可导致人体口咽部细菌增高致病菌增加以及细菌量的变化,导致呼吸道微生态失调.     

被动吸烟对大鼠口咽部微生态的影响

目的探讨被动吸烟对呼吸道微生态的影响的机制,为预防吸烟对机体健康的损害提供理论依据。方法采用模拟被动吸烟的方法,对健康Wistar大鼠进行大气污染,研究大鼠口咽部菌群污染前后的变化。结果被动吸烟前后大鼠口咽部的微生态菌群明显发生改变（P〈0.5）。吸烟前与吸烟后相比致病菌如金黄色葡萄球菌、肺炎克雷伯菌等检出率明显增高（P〈0.5）,厌氧菌密度减少,随着被动吸烟时间的延长,细菌的密度呈上下波动,且厌氧菌菌群密度变化更为明显（P〈0.5）。结论被动吸烟对大鼠口咽部有破坏作用,导致菌群发生改变,致病菌增多,是呼吸道疾病发病率升高的重要因素之一。     

吸烟对人体呼吸道厌氧菌的影响

目的探究吸烟对人体内的呼吸道微生态的影响。方法采用细菌鉴定及药敏分析系统鉴定健康吸烟者与非吸烟者,患下呼吸道感染吸烟与非吸烟者咽后壁分泌物的细菌密度、细菌数量及种类的改变。结果在健康吸烟者与患有下呼吸道感染患者的呼吸道中,厌氧菌明显升高,其中以韦荣菌和消化链球菌为主。结论吸烟可使人体的呼吸道微生态中细菌密度,细菌数量及种类的改变,易患呼吸系统疾病。     

吸烟对下呼吸道诱导痰中 IFN-γ、IL-4、IL-5表达的影响

目的探究吸烟对下呼吸道诱导痰中干扰素-γ(IFN-γ)、白细胞介素-4(IL-4)和白细胞介素-5(IL-5)表达的影响。方法采用酶联免疫吸附法检测2016年3月-2017年3月沈阳医学院附属第二医院收治的下呼吸道感染患者88例(其中吸烟者44例作为观察组,非吸烟者44例作为对照组)、健康体检者76例(其中吸烟者34例作为观察组,非吸烟者42例作为对照组)诱导痰中IFN-γ、IL-4和IL-5的表达,并对结果进行数据分析。结果 (1)健康体检者中吸烟者与非吸烟者相比,吸烟者IL-4、IL-5水平显著上升,IFN-γ水平显著下降(P0.05);(2)下呼吸道感染患者中吸烟者与非吸烟者相比,吸烟者IL-4、IL-5水平显著上升,INF-γ水平显著下降(P0.05)。结论吸烟与下呼吸道诱导痰中IL-4、IL-5和IFN-γ的水平有关,吸烟可使下呼吸道诱导痰中IL-4、IL-5水平升高而IFN-γ的水平下降。     

宫颈癌癌前病变及宫颈癌患者阴道微生态失调相关因素

目的探讨宫颈癌癌前病变及宫颈癌患者阴道微生态失调相关因素。方法选择2016年7月至2018年12月我院收治的200例宫颈癌和癌前病变患者为研究对象,其中宫颈癌患者100例(宫颈癌组),癌前病变患者100例(癌前组),另选50例健康女性为对照组。观察各组对象阴道微生态指标(菌群密集度、菌群多样性、pH和H_2O_2)水平、HPV感染情况及乳杆菌分布情况。分析患者阴道微生态变化与HPV感染的关系。结果癌前组和宫颈癌组阴道菌群密集度Ⅰ-Ⅳ级的患者分别占33.00%和42.00%,显著高于对照组的10.00%(χ~2=15.762 9,P=0.000 1);菌群多样性Ⅰ-Ⅳ级的患者分别占35.00%和41.00%,同样高于对照组的6.00%(χ~2=19.783 1,P0.000 1)。癌前组和宫颈癌组阴道pH4.5的患者分别占53.00%和56.00%,高于对照组的12.00%(χ~2=29.267 3,P0.000 1);H_2O_2阴性患者占比分别为63.00%和70.00%,显著高于对照组的18.00%(χ~2=39.343 7,P0.000 1);此外,癌前组和宫颈癌组患者HPV检测阳性率分别为62.00%和73.00%,显著高于对照组的6.00%(χ~2=63.624 2,P0.000 1)。癌前组和宫颈癌组患者阴道乳杆菌定植密度中位数分别为115(97～279)个/HP和107(81～201)个/HP,显著低于对照组的279(157～365)个/HP(χ~2=8.742 1,P0.000 1)。在HPV感染患者中,乳杆菌阳性率及乳杆菌定植密度中位数均低于对照组。Spearman相关分析显示HPV感染与患者阴道微生态正常程度呈负相关,阴道微生态失调与癌前病变分级呈正相关。结论宫颈癌前病变和宫颈癌的发生与患者阴道微生态失调、HPV感染、乳杆菌减少密切相关;同时癌前病变的发展与阴道微生态失调具有相关性。     

吸烟对下呼吸道感染患者诱导痰中 IL-4和IL-17的影响

目的探究吸烟对下呼吸道感染患者诱导痰中白介素4(IL-4)和白介素17(IL-17)的影响。方法采用酶联免疫吸附法分别对吸烟与非吸烟下呼吸道感染患者(共88例)以及76例健康体检者诱导痰中IL-4和IL-17水平进行检测,并对结果进行分析。结果下呼吸道感染患者中吸烟者与非吸烟者IL-4和IL-17水平比较差异均有统计学意义(P0.05)。健康体检者中吸烟者与非吸烟者IL-4、IL-17比较差异也具有统计学意义(P0.05)。结论吸烟与下呼吸道诱导痰中IL-4、IL-17的表达水平具有相关性,吸烟可使下呼吸道诱导痰中IL-4、IL-17水平升高。     

妊娠中晚期阴道微生态失调及乳酸菌胶囊干预对不良妊娠结局的作用

目的观察妊娠中晚期妇女阴道微生态状况,探讨应用乳杆菌活菌胶囊纠正阴道微生态失调对不良妊娠结局的预防价值。方法选择孕13~36周单胎妊娠期妇女560例,取其阴道分泌物,经革兰染色后油镜下观察,进行阴道微生态(阴道菌群的密集度、多样性、优势菌、炎症反应等)状况评价,检测阴道分泌物成分、阴道病原菌类型。对阴道微生态失调孕妇,根据是否接受乳杆菌活菌胶囊治疗分为治疗组和对照组,治疗组给予乳杆菌活菌胶囊,对照组不采用药物干预。追踪随访所有孕妇的妊娠情况,比较阴道微生态正常组、微生态失调治疗组及微生态失调对照组的不良妊娠结局。结果 560例研究对象中,阴道微生态正常335例(59.82%),微生态失调225例(40.18%)。225例微生态失调孕妇中,细菌性阴道病(bacterial vaginosis,BV)32例(14.22%),阴道假丝酵母菌病(vulvovaginal candidiasis,VVC)56例(24.89%),滴虫性阴道炎(triehomonal vaginitis,TV)11例(4.89%),BV和VVC混合感染4例(1.78%),BV和TV混合感染3例(1.33%),菌群增殖过度75例(33.33%),菌群抑制44例(19.56%)。微生态失调组pH值4.5、过氧化氢、白细胞酯酶、唾液酸苷酶、脯氨酸氨基肽酶、乙酰氨基葡萄糖苷酶阳性比例均明显高于微生态正常组(χ2=55.59~340.06,Ps0.05)。微生态失调孕妇中,治疗组135例,对照组90例,对照组胎膜早破、早产、产褥感染、新生儿感染及低出生体重儿发生率均明显高于微生态正常组(χ2=12.63~32.42,Ps0.05)和微生态失调治疗组(χ2=5.16~12.28,Ps0.05),微生态正常组与微生态失调治疗组之间差异无统计学意义(P0.05)。结论妊娠中晚期容易导致阴道微生态失调,造成不良妊娠结局,乳杆菌活菌胶囊纠正阴道微生态失调对于改善不良妊娠结局有较好的预防作用。     

阴道菌群结构分析在 宫腔粘连患者中的临床意义

目的对宫腔粘连患者菌群结构进行评价,探讨阴道微生态在宫腔粘连中的临床意义。方法选取2014年8月至2016年8月在我院计划生育病区诊断为宫腔粘连的患者100例为试验组,同期门诊100例健康体检者为对照组。对其阴道分泌物进行湿片镜检及微生态学检测,比较两组研究对象的阴道微生态情况。结果宫腔粘连组与对照组在阴道分泌物的多样性、密集度、优势菌、pH、清洁度和病原体检出率等方面比较差异有统计学意义(Ps0.05)。宫腔粘连组阴道微生态失调检出率(48%)高于对照组(31%),差异有统计学意义(P0.05)。结论宫腔粘连患者阴道微生态失调发生率明显增高,阴道微生态失调可能与宫腔粘连的发生有关。     

HPV感染患者阴道微生态、Th17/Treg细胞及相关细胞因子表达分析CSCD

目的 分析人乳头瘤病毒（HPV）感染患者阴道微生态、辅助性T细胞17(Th17)/调节性T细胞（Treg）及相关细胞因子表达情况,为该类患者的治疗提供参考。方法 选取2020年5月至2022年6月厦门大学附属妇女儿童医院收治的HPV感染患者108例作为研究组,另选取我院同期健康体检者108例作为对照组。两组受试者均进行HPV筛查、阴道菌群检测以及阴道微生态检测,采用流式细胞仪检测Th17/Treg细胞;采用酶联免疫吸附法（ELISA）检测白细胞介素-6(IL-6)、 IL-10和IL-17水平;采用Spearman法分析HPV感染患者阴道菌群和Th17/Treg细胞及相关细胞因子的相关性。结果 HPV共检出9种亚型,主要以HPV 16和HPV 18为主。研究组患者阴道乳杆菌阳性率显著低于对照组,衣原体、解脲支原体、滴虫和细菌性阴道病阳性率均显著高于对照组（均P<0.05）。研究组患者阴道pH>4.5、阴道菌群密集度Ⅱ～Ⅳ级、阴道菌群多样性Ⅱ～Ⅳ级和微生态失调率均显著高于对照组（均P<0.05）。研究组患者Th17/Treg、IL-6、IL-10和IL-17水平显著高于对照组（均P<0.05）。Spearman相关性分析显示,阴道中乳杆菌与Th17/Treg、IL-6、IL-10和IL-17水平均呈负相关;衣原体、解脲支原体、滴虫和细菌性阴道病与Th17/Treg、IL-6、IL-10和IL-17水平均呈正相关（均P<0.05）。结论 HPV感染患者存在阴道微生态失调,而且Th17/Treg细胞、IL-6、IL-10和IL-17水平均异常升高。     

反复呼吸道感染患者的微生态学分析

冬季是呼吸道反复感染的多发季节。我们对反复发生呼吸道感染病人口咽粘膜菌群的定植进行了分析。结果表明,正常组需氧菌群密度为４．１１３５±０．０８８４,厌氧菌群密度为４．４１０１±０．３５８６１;患者需氧菌群密度为４．５２９０±０．００８６,厌氧菌群密度为４．８７１８±０．３４２４。反复呼吸道感染患者需氧菌和厌氧菌的含量均不于正常对照组（Ｐ＜０．０５）。１８例病人分离出两种以上需氧菌,奈瑟氏菌和肺炎链球菌检出率较高,分别为３８．７％和２２．６％;厌氧菌以韦荣氏球菌和消化链球菌为多见,检出率分别为３２．２％和５８．１％。有７例病人分离出白色念珠菌。４例病人分离出绿脓杆菌,明显表现出微生态失调。药敏结果表明,不同菌株对抗生素均有一定的耐药性存在。     

Shunt in the diagnosis of initial lung lesion in smokers

Cigarette smoking is an important risk factor for all respiratory tract diseases. Unfortunately, the symptoms develop slowly, thus patients feel the consequences of the slowly developing inflammation too late. The inflammation first develops in the area of respiratory bronchioles. In this stage, the disease is asymptomatic. The study included a sample of 31 smokers, mean age 36.38 years, with normal spirometry indices, acid-base status and arterial blood gases. The mean smoking index was 11.28 smoking/years. All subjects were healthy, without any subjective health problems or disease indicators. The aim was to define dead lung area (V/Q) as an early indicator of changes in smokers. Study results demonstrated the mean shunt value in smokers of 8.25%, which showed positive correlation with smoking. The shunt size yielded negative correlation with the forced expiratory volume in one second and midexpiratory flow in smokers. In conclusion, determination of lung shunt is a simple method that is sensitive enough in the diagnosis of initial lung lesion due to cigarette smoking.     

Cotinine levels and self-reported smoking status in patients attending a bronchoscopy clinic.

The reliability of self-reported smoking behaviour can vary and may result in bias if errors in misclassification vary with outcome. We examined whether self-report was an accurate measure of current smoking status in patients with malignant or non-malignant respiratory disease. Smoking behaviour was assessed by self-report and by analysis of whole blood for cotinine, a biomarker of exposure to cigarette smoke, in 166 patients attending a bronchoscopy clinic. Cotinine levels ranged from 2.5 to >400 ng ml(-1) blood and were higher in self-reported current smokers (173+/-123 ng ml(-1)) than in never smokers (3.7+/-8.7 ng ml(-1)) or ex-smokers (20.5+/-49.0 ng ml(-1)). Cotinine levels in self-reported current smokers increased with the numbers of cigarettes smoked (p=0.06), and levels in smokers and ex-smokers decreased with the reported length of time since the last cigarette (p=0.001). Using a cotinine level of 20 ng ml(-1) and self-report as the gold standard, the sensitivity and specificity for defining current smoking status were 90.2% and 82.4%, respectively. Out of a total of 125 self-reported current non-smokers, 23 (18.4%) had cotinine levels greater than 20 ng ml(-1). Smoking prevalence was significantly underestimated by self-report (24.7%) when compared with that defined using blood cotinine levels (36.1%: p<0.001). Misclassification of current smoking status was particularly high in ex-smokers, in patients without malignant respiratory disease, in men, and in those below the median age. Such differential misclassification may result in bias in studies examining associations between current smoking habits and disease risk.     

Respiratory effects of non-tobacco cigarettes.

Data from the Tucson epidemiological study of airways obstructive disease on smoking of non-tobacco cigarettes such as marijuana were analysed to determine the effect of such smoking on respiratory symptoms and pulmonary function. Among adults aged under 40, 14% had smoked non-tobacco cigarettes at some time and 9% were current users. The prevalence of respiratory symptoms was increased in smokers of non-tobacco cigarettes. After tobacco smoking had been controlled for men who smoked non-tobacco cigarettes showed significant decreases in expiratory flow rates at low lung volumes and in the ratio of the forced expiratory volume in one second to the vital capacity. This effect on pulmonary function in male non-tobacco cigarette smokers was greater than the effect of tobacco cigarette smoking. These data suggest that non-tobacco cigarette smoking may be an important risk factor in young adults with respiratory symptoms or evidence of airways obstruction.     

Cotinine levels and self-reported smoking status in patients attending a bronchoscopy clinic

The reliability of self-reported smoking behaviour can vary and may result in bias if errors in misclassification vary with outcome. We examined whether self-report was an accurate measure of current smoking status in patients with malignant or non-malignant respiratory disease. Smoking behaviour was assessed by self-report and by analysis of whole blood for cotinine, a biomarker of exposure to cigarette smoke, in 166 patients attending a bronchoscopy clinic. Cotinine levels ranged from 2.5 to &gt;400 ng ml^?1 blood and were higher in self-reported current smokers (173±123 ng ml^?1) than in never smokers (3.7±8.7 ng ml^?1) or ex-smokers (20.5±49.0 ng ml^?1). Cotinine levels in self-reported current smokers increased with the numbers of cigarettes smoked (p=0.06), and levels in smokers and ex-smokers decreased with the reported length of time since the last cigarette (p=0.001). Using a cotinine level of 20 ng ml^?1 and self-report as the gold standard, the sensitivity and specificity for defining current smoking status were 90.2% and 82.4%, respectively. Out of a total of 125 self-reported current non-smokers, 23 (18.4%) had cotinine levels greater than 20 ng ml^?1. Smoking prevalence was significantly underestimated by self-report (24.7%) when compared with that defined using blood cotinine levels (36.1%: p&lt;0.001). Misclassification of current smoking status was particularly high in ex-smokers, in patients without malignant respiratory disease, in men, and in those below the median age. Such differential misclassification may result in bias in studies examining associations between current smoking habits and disease risk.     

Disordered microbial communities in the upper respiratory tract of cigarette smokers

Cigarette smokers have an increased risk of infectious diseases involving the respiratory tract. Some effects of smoking on specific respiratory tract bacteria have been described, but the consequences for global airway microbial community composition have not been determined. Here, we used culture-independent high-density sequencing to analyze the microbiota from the right and left nasopharynx and oropharynx of 29 smoking and 33 nonsmoking healthy asymptomatic adults to assess microbial composition and effects of cigarette smoking. Bacterial communities were profiled using 454 pyrosequencing of 16S sequence tags (803,391 total reads), aligned to 16S rRNA databases, and communities compared using the UniFrac distance metric. A Random Forest machine-learning algorithm was used to predict smoking status and identify taxa that best distinguished between smokers and nonsmokers. Community composition was primarily determined by airway site, with individuals exhibiting minimal side-of-body or temporal variation. Within airway habitats, microbiota from smokers were significantly more diverse than nonsmokers and clustered separately. The distributions of several genera were systematically altered by smoking in both the oro- and nasopharynx, and there was an enrichment of anaerobic lineages associated with periodontal disease in the oropharynx. These results indicate that distinct regions of the human upper respiratory tract contain characteristic microbial communities that exhibit disordered patterns in cigarette smokers, both in individual components and global structure, which may contribute to the prevalence of respiratory tract complications in this population.     

Serum surfactant protein-A, but not surfactant protein-D or KL-6, can predict preclinical lung damage induced by smoking

Serum surfactant protein (SP)-A offers a useful clinical marker for interstitial lung disease (ILD). However, SP-A is occasionally elevated in non-ILD pulmonary patients. The present study was conducted to investigate factors that affect serum SP- A levels in respiratory medicine. Serum SP-A, serum SP-D, serum Klebs von den Lungen (KL)-6 and pulmonary function tests were evaluated in 929 patients (current smokers, n=255; ex-smokers, n=242; never-smokers, n=432) without ILD or pulmonary alveolar proteinosis. Serum SP-A was significantly higher in current smokers than in never- or ex-smokers (p<0.01 and p<0.05, respectively). Serum SP- A was significantly higher in chronic obstructive pulmonary disease (COPD) and pulmonary thromboembolism than in other diseases (p<0.01). Serum SP-A correlated positively with amount of smoking (p<0.01) and negatively with forced expiratory volume in 1 s/forced vital capacity (p<0.05). Serum SP-D and KL-6 were unaffected by smoking. Smoking should be taken into account when evaluating serum SP-A levels, and different baseline levels of serum SP-A should be established for smokers and non-smokers. Serum SP-A may also represent a useful marker for predicting COPD in the preclinical stage.     

Relationship between blood velocity and conduit artery diameter and the effects of smoking on vascular responsiveness.

Transient changes in arterial diameter in response to transient ischemia-induced changes in arterial blood velocity have been used as an index of vascular health. The purpose of this study was to determine the relationship between blood velocity and diameter in the brachial artery by different methods of increasing blood velocity. Acute cigarette smoking was used with otherwise healthy young occasional smokers to determine the influence of endothelial-nitric oxide pathways on the arterial diameter-blood velocity relationship. Nine nonsmokers and 12 occasional smokers (<1 pack/wk) were tested. Blood flow to the forearm was manipulated to indirectly investigate the relationship between blood velocity and diameter in the brachial artery. Blood flow to forearm was manipulated through the use of 1) 5-min ischemia; 2) handgrip exercise; 3) indirect local heating; and 4) 5-min ischemia plus indirect local heating. A strong relationship was observed between blood velocity and diameter independent of the method used to increase blood velocity (R(2) = 0.89). The mean slope of the velocity-diameter relationship was not different between nonsmokers and occasional smokers who abstained from smoking at least 2 days. Acute smoking did not alter the slope of the velocity-diameter relationship although the mean intercept was decreased as a result of consistent vasoconstriction (7-10%). The mechanisms by which smoking impairs vascular health are largely unknown. These findings differ from previous smoking studies that used chronic and/or heavier smokers. The velocity-diameter relationship appears independent of the method for increasing velocity. Acute smoking in occasional smokers results in vasoconstriction without altering vascular responsiveness. The velocity-diameter relationship may be a useful measure of the progression of vascular disease.     

Smoking and leanness: evidence for change in Finland.

Many studies have shown smokers to weigh less than non-smokers, which is plausible given the metabolic effects of cigarette smoke. The interrelation between smoking and relative body weight and its change over time were analysed by using data from Finnish population based surveys from 1982 and 1987. Among both men and women the inverse association between smoking and body mass index was clearly weakened between 1982 and 1987. In 1987 among men aged 25-44 smoking was positively related to body mass index. Moreover, the relation between smoking and waist to hip girth ratio was positive in both sexes at all ages. Years of smoking was nevertheless confirmed as a significant inverse predictor of relative weight. A cluster of unfavourable health habits, including high consumption of alcohol and saturated fats, especially emerged among younger smokers. This may have been due to different selection of smokers in Finland, where smoking increasingly seems to be a form of deviant or risk taking behaviour. It is concluded that at a population level the metabolic effects of smoking seem to be increasingly overridden by several other unfavourable health behaviours of smokers.     

Association between cutaneous occlusive vascular disease, cigarette smoking, and skin slough after rhytidectomy

This prospective study attempted to determine if nonreversible occlusive vascular changes in the skin contribute to skin slough after rhytidectomy. The dermal microvasculature from 83 consecutive rhytidectomies was evaluated for intimal proliferation and/or hyalin sclerosis. Occlusive vascular disease increased progressively with age in all patients, but smokers and ex-smokers had significantly greater involvement than nonsmokers at any given age (p = 0.03). Severe occlusive vascular disease and skin slough were associated (p = 0.02), and there was a strong trend toward an association between active smoking and skin slough (p = 0.06). Among smokers, there was a significant relationship between skin slough and failure to abstain from smoking postoperatively (p = 0.006). We conclude that with aging, nonreversible occlusive changes develop in the dermal microvasculature. These changes appear to be accelerated by cigarette smoking. Our data, however, show that these nonreversible occlusive vascular changes by themselves do not completely account for the occurrence of skin slough after rhytidectomy.