Cigarette Smoke Inhalation Research Articles

Review on carcinogens materials in chemical laboratories

The review recalls the types of carcinogenic chemicals that are used in laboratories, as well as the types of cigarettes and nicotine for smokers, which are considered essential substances for cancer. Smokers are more likely to develop lung cancer, although lung cancer can also affect people who have never smoked. The risk of lung cancer increases with the length of time you smoke and the number of cigarettes you smoke. If you quit smoking, even after smoking for many years, you can significantly reduce your chances of developing lung cancer. Inhalation of carcinogenic lab materials or smoking causes lung cancer by damaging the cells lining the lungs. When you inhale cigarette smoke that is full of cancer-causing substances (carcinogens), changes in lung tissue begin almost immediately. At first, your body may be able to repair this damage. But with each repeated exposure, the normal cells that line your lungs are increasingly damaged. Over time, the damage causes cells to function abnormally and cancer may eventually develops. Many laboratories carry specific risks, including the risk of exposure to carcinogens, and preventing accidents in the laboratory requires high care and constant vigilance. Examples of risk factors include high voltages, pressures, high and low temperatures, corrosive and toxic chemicals, chemical fumes, radiation, fire and explosions, as well as biological hazards including infectious organisms and their toxins.

Transcriptome Analysis of Rat Lungs Exposed to Moxa Smoke after Acute Toxicity Testing.

The increasing use of moxibustion has led to a debate concerning the safety of this treatment in human patients. Inhalation of cigarette smoke induces lung inflammation and granulomas, the proliferation of alveolar epithelial cells, and other toxic effects; therefore, it is important to assess the influence of inhaled moxa smoke on the lungs. In the present study, a novel poisoning cabinet was designed and used to assess the acute toxicity of moxa smoke in rats. We evaluated pathological changes in rat lung tissue and analyzed differentially expressed genes (DEGs) using RNA-seq and transcriptomic analyses. Our results show that the maximum tolerable dose of moxa smoke was 290.036 g/m³ and LC50 was 537.65 g/m³. Compared with that of the control group, the degree of inflammatory cell infiltration in the lung tissues of group A rats (all dead group) was increased, while that in group E rats (all live group) remained unchanged. GO and KEGG enrichment analyses showed that the DEGs implicated in cell components, binding, and cancer were significantly enriched in the experimental groups compared with the profile of the control group. The expressions of MAFF, HSPA1B, HSPA1A, AOC1, and MX2 determined using quantitative real-time PCR were similar to those determined using RNA-seq, confirming the reliability of RNA-seq data. Overall, our results provide a basis for future evaluations of moxibustion safety and the development of moxibustion-based technology.

Pulmonary Functions between Active and Passive Smoking in 18-22 Years Old Male Physical Education Students – A Descriptive Study

To assess and describe the vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and the ratio of FEV1/FVC measurements in smoking male physical education students, ranged between 18 - 22 years. Also compare the FEV1 and ratio of FEV1/FVC between active and passive smoker. A cross-sectional study was applied on male physical education students (n=30) who undergo training for 2 months and between the age range of 18-22 years old. The lung VC, FVC, FEV1, and ratio of FEV1/FVC were measured and compared between active and passive smokers. Thirty male physical education students participated in this study with the average age of 19,53 ? 0,86 years old. All participants underwent training for 2 months in Surabaya. The average BMI was 23,16 ? 4,624. The active to passive smoker ratio was 7:3, with 21 active smokers and 7 passive smokers. The results of all pulmonary function tests in passive smokers were better than in active smokers. The average of VC in passive smokers was 3,45? 0,498, slightly higher than VC in active smokers which was 3,35 ? 1,032. The FVC average in passive smoker was 3,56 ? 0,489, also higher than active smoker with 3,43 ? 0,671. The higher FEV1 mean was in passive smoker with 1,84 ? 0,856, compared to active smoker with 1,53 ? 0,595. Similar results also could be seen in FEV1/FVC ratio. The FEV1/FVC ratio average in passive smokers was 2,39 ? 5,094, higher than those in active smokers with 0,60 ? 0,205. In this study, the total participants with normal results were higher in passive smoker which was 3 (33,333%) participants, and only 1 (4,761%) in active smoker. For moderate COPD, active smoker was higher with 3 (14,286%) participants, while passive smoker with moderate COPD was 2 (22,222%) participants. The amount of severe COPD was high in active smokers with 13 (61,905%) participants, and only 1 (11,111%) in passive smokers. Meanwhile the active smoker with very severe COPD was 4 (19,047%) participants, and in the passive smoker was 3 (33,333%) very severe COPD. Active and passive smokers have an equally greater risk of lung tissue damage. Most of the free radical (OH-) in cigarette will arrive at the alveolus that can damage the lungs while smoking cigarettes in active smoker or inhale cigarette smoke in passive smoker.

PENGARUH PEROKOK AKTIF DIATAS 5 TAHUN TERHADAP KADAR HEMOGLOBIN DI KECAMATAN PANYILEUKAN KOTA BANDUNG

Indonesian people cigarette consumption is high enough, one out of three Indonesian people smoke. Smoking is the act of sucking smoke from burning tobacco. The prevalence of smoke in Indonesian has increased from year to year. The habit of smoking and inhaling cigarette smoke from burning cigarettes will have a negative impact on the health of many people, ranging from active smokers to passive smokers. One of them will have an impact on the effect of hemoglobin levels in the blood. The purpose of this study was to see the effect of active smokers over 5 years on hemoglobin levels. The type of research used is analytic observational research with a cross sectional approach. The sample in this study were male residents in the Panyileukan sub-district, Bandung City, which consisted of 30 respondents who were active smokers over 5 years which were taken by purposive sampling.The results showed that in 30 samples of active smokers, 21 samples (70%) had normal hemoglobin levels, 3 samples (20%) had low hemoglobin levels, and 6 samples (10%) had high (abnormal) hemoglobin levels.The conclusion of this study was that 30 blood samples of active smokers over 5 years had normal hemoglobin levels, although in some samples there were low and high hemoglobin levels.

Morphofunctional study on the effects of passive smoking in kidneys of rats.

ABSTRACTObjective To analyze whether passive inhalation of cigarette smoke causes morphological, structural, and functional changes in kidneys of rats.Methods Wistar rats, aged eight weeks, weighing on average 260g, were divided into Control Group and Smoking Group. Each group was subdivided into four groups of ten animals for morphofunctional analysis, in a period of seven and 28 days. The Smoking Group was exposed to smoke of 40 cigarettes per day, at certain times and in automated equipment for cigarette burning, called smoking machine (SM-MC-01). After the exposure period, urine and blood samples were collected for the functional analyses, and the kidneys were dissected and submitted to histological procedures for morphoquantitative analyses.Results After exposure of animals of the Smoking Group, the following were observed: lower weight gain; lower water and feed intake; decreased renal weight, diameter, and volume; reduction in cortical thickness and glomerular volume density; decrease in glomerular and capsular diameter; increase in mesangial density; decreased urine volume; increased levels of glucose, serum creatinine and microalbuminuria; decreased urinary creatinine levels and creatinine clearance rate.Conclusion Passive smoking negatively influences renal morphology and glomerular filtration rate, with effects similar to those described in the literature regarding active smoking.

Effect of EGCG on bronchial epithelial cell premalignant lesions induced by cigarette smoke and on its CYP1A1 expression.

Epigallocatechin-3-gallate (EGCG) has been demonstrated to exhibit anticancer effects; however, the mechanisms behind these are not yet clear. The objective of the present study was to assess the effect of EGCG on smoking-induced, precancerous, bronchial epithelial cell lesions and determine a potential protective mechanism. Human bronchial epithelial (HBE) cells were treated with cigarette smoke extract (CSE). Benzopyrene-DNA adducts were detected by immunofluorescence cytochemistry. Changes to microRNA (miRNA) expression levels were detected via microarray. The effects of EGCG on smoke-induced benzopyrene-DNA adduct formation and the subsequent change in miRNA expression were analyzed. Subsequently, the protective effect of EGCG on smoke inhalation-induced precancerous lesions was investigated. The expression levels of miRNA target genes were also analyzed. After CSE treatment, benzopyrene-DNA adducts appeared in HBE cells, along with a resultant change in miRNA expression. EGCG inhibited the effects of CSE exposure; benzopyrene-DNA adduct formation was reduced and miRNA expression changes were suppressed. In vivo, EGCG significantly reduced benzopyrene-DNA adduct formation and the subsequent development of precancerous lesions in rat lungs induced by cigarette smoke inhalation. Moreover, EGCG downregulated CYP1A1 overexpression, a target gene of multiple smoking-induced miRNAs, in rat lungs. EGCG may reduce the risk of lung cancer by downregulating the expression of the key gene CYP1A1, preventing the formation of smoking-induced benzopyrene-DNA adducts and alleviating smoking-induced bronchial epithelial dysplasia and heterogeneity.

AROMATHERAPY MAY NOT BE SO RELAXING AFTER ALL: A CASE OF ACUTE EOSINOPHILIC PNEUMONIA

TOPIC: Diffuse Lung Disease TYPE: Global Case Reports INTRODUCTION: Acute eosinophilic pneumonia (AEP) is a rare entity of eosinophilic lung diseases, with around 200 cases reported worldwide (1). The cause is unknown, but it has mostly been linked to cigarette smoking inhalation. We present a unique case of AEP associated with a history of deep inhalation of fragrance oil. CASE PRESENTATION: Our patient is a 19-year-old medically free female who presented to the emergency department (ED) complaining of acute cough, fever, and dyspnea which started one day after deeply inhaling fragrance oil while trying to open the bottle with her mouth. She was febrile, in respiratory distress with an Oxygen saturation of 51%. The patient was managed as a case of possible COVID infection. She was intubated and admitted to the ICU. She received Dexamethasone for 3 days. Afterward, she was extubated and discharged home on room air the next day. Four days later, she presented to the ED with a similar picture. Chest x-ray (figure 1) showed bilateral patchy opacities. Computed tomography of the chest (CT) showed bilateral areas of consolidation and ground-glass opacities (figure 2). She was started empirically on antibiotics and a single dose of Hydrocortisone intravenously prior to CT scan as premedication protocol for Intravenous Contrast. Clinical, biochemical, and radiological improvement were noticed the next day. On the fourth day of admission, she became febrile and required more oxygen with an increase in neutrophils. At this point, she was started on Methylprednisone for a suspected diagnosis of acute eosinophilic pneumonia. The patient's condition improved with steroids. Bronchoalveolar lavage fluid analysis showed a WBC count of 614 cells /cumm with eosinophils of 84%. The patient was discharged home on prednisone 50mg which was tapered off within six weeks. On a follow-up clinic visit, the patient had complete resolution of her symptoms and her chest X-ray showed no lung infiltrates (figure 1 and 2). DISCUSSION: Acute eosinophilic pneumonia (AEP) is a rare disease with few reported cases worldwide. It usually presents similarly to pneumonia and acute respiratory distress syndrome. The cause of AEP is unknown but it has been suggested to be the result of an acute hypersensitivity reaction to an unknown allergen in a previously healthy individual (2) such as smoking. Our patient is the first case of AEP to occur after deep and sudden inhalation of fragrance oi which was made up of essence, scent stabilizer, deionized water, and ethyl alcohol. Our patient fulfills all the clinical criteria for AEP diagnosis.The mainstay of treatment in AEP is corticosteroids and patients usually have a rapid response as clinical recovery happens after 3 days of steroids (3). Prognosis in AEP is excellent with rapid initiation of steroids (1). CONCLUSIONS: We reported a unique case of AEP that occurred post fragrance oil inhalation and was resolved rapidly and completely with steroids. REFERENCE #1: Pizzuto, M., Seychell, M., Caruana Montaldo, B., & Mizzi, A. (2019). Idiopathic acute eosinophilic pneumonia. BMJ Case Reports, 12(9), e231095. REFERENCE #2: Badesch, D. B., King, T. E., & Schwarz, M. I. (1989). Acute Eosinophilic Pneumonia: A Hypersensitivity Phenomenon? American Review of Respiratory Disease, 139(1), 249–252. REFERENCE #3: Rhee, C. K., Min, K. H., Yim, N. Y., Lee, J. E., Lee, N. R., Chung, M. P., & Jeon, K. (2013). Clinical characteristics and corticosteroid treatment of acute eosinophilic pneumonia. The European respiratory journal, 41(2), 402–409. DISCLOSURES: No relevant relationships by Riyad Al-Lehebi, source=Web Response no disclosure on file for Mais AlSardi; No relevant relationships by Shaya Alshaya, source=Web Response

MiRNAomics analysis reveals the promoting effects of cigarette smoke extract-treated Beas-2B-derived exosomes on macrophage polarization

Inhalation of cigarette smoke induces airway and parenchyma inflammation that predisposes smokers to multiple lung diseases such as COPD. Macrophage polarization, an important specifying feature of inflammation, is involved in the progression of pulmonary inflammation. Exosomes and their loaded miRNAs provide a medium for cross-talk between alveolar macrophages and lung epithelial cells to maintain lung homeostasis. In this study, we treated Beas-2B with CSE to speculate the effects of Beas-2B-derived exosomes on macrophage polarization and performed exosomal miRNAomics analysis to explore the mechanism. We found that CSE-treated Beas-2B-derived exosomes could not only increase the percentages of CD86+, CD80+ CD163+, and CD206+ cells but also induce the secretion of TNF-α, IL-6, iNOS, IL-10, Arg-1, and TGF-β, indicating both M1 and M2 polarization of RAW264.7 macrophages were promoting. We performed miRNAomics analysis to identify 27 differentially expressed exosomal miRNAs such as miR-29a-3p and miR-1307-5p. Next, we obtained 14942 target genes of these miRNAs such as SCN1A and PLEKHA1 through the prediction of TargetScan and miRanda. We utilized KEGG enrichment analysis for these targets to identify potential pathways such as the PI3K-Akt signaling pathway and the MAPK signaling pathway on the regulation of macrophage polarization. We further found that miR-21-3p or miR-27b-3p may play critical roles in the promotion of CSE-Exo on macrophage polarization by miRNA interference. Collectively, this study provided novel information for diagnostic and therapeutic tactics of cigarette smoke-related lung diseases.

The role of airway remodeling in the pathogenesis and treatment of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is currently considered the third leading cause of death in the world. COPD represents an important public health challenge and a socio-economical problem that is preventable and treatable. The main cause of COPD is chronic inhalation of cigarette smoke, and other harmful constituents of air pollution, which cause epithelial injury, chronic inflammation and airway remodeling. Airway remodeling is most prominent in small airways. It is due to infiltration of the airways by inflammatory cells, such as neutrophils, eosinophils, macrophages, and immune cells, including CD8+ T-cells, Th1, Th17 lymphocytes, and innate lymphoid cells group 3. Fibroblasts, myofibroblasts, and airway smooth muscle (ASM) cells also contribute to airway remodeling by depositing extracellular matrix (ECM) proteins, which increase the thickness of the airway wall. Activated inflammatory cells, and structural cells secrete cytokines, chemokines, growth factors, and enzymes which propagate airway remodeling. Airway remodeling is an active process which leads to thickness of the reticular basement membrane, subepithelial fibrosis, peribronchiolar fibrosis, and ASM cells hyperplasia and hypertrophy. It is also accompanied by submucosal glands and goblet cells hypertrophy and mucus hypersecretion, and angiogenesis. Epithelial mesenchymal transmission (EMT) plays a key role in airway remodeling. In patients with COPD and smokers, cellular reprograming in epithelial cells leads to EMT, whereby epithelial cells assume a mesencymal phenotype. Additionally, COPD is associated with increased parasympathetic cholinergic activity, which leads to ASM cells hypercontractility, increased mucus secretion, and vasodilatation. Treatment of COPD is intricate because of the heterogeneous nature of the disease, which requires specific treatment of the pathophysiological pathways, such as airway inflammation, ASM cell hypercontractility, and parasympathetic cholinergic hyperreactivity. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2020 strategy report recommends personalized approach for the treatment of COPD. However, some patients with COPD are unresponsive to the standards of care. They may require a triple combination of LABA/LAMA/ICS. Single-inhaler triple therapy (SITT), such as fluticasone fuorate/vilanterol/umeclidinium has been shown to significantly improve symptoms and asthma control, reduce moderate and severe exacerbations, and to improve lung function.

Metformin: Experimental and Clinical Evidence for a Potential Role in Emphysema Treatment.

Rationale: Cigarette smoke (CS) inhalation triggers oxidative stress and inflammation, leading to accelerated lung aging, apoptosis, and emphysema, as well as systemic pathologies. Metformin is beneficial for protecting against aging-related diseases. Objectives: We sought to investigate whether metformin may ameliorate CS-induced pathologies of emphysematous chronic obstructive pulmonary disease (COPD). Methods: Mice were exposed chronically to CS and fed metformin-enriched chow for the second half of exposure. Lung, kidney, and muscle pathologies, lung proteostasis, endoplasmic reticulum (ER) stress, mitochondrial function, and mediators of metformin effects invivo and/or invitro were studied. We evaluated the association of metformin use with indices of emphysema progression over 5 years of follow-up among the COPDGene (Genetic Epidemiology of COPD) study participants. The association of metformin use with the percentage of emphysema and adjusted lung density was estimated by using a linear mixed model. Measurements and Main Results: Metformin protected against CS-induced pulmonary inflammation and airspace enlargement; small airway remodeling, glomerular shrinkage, oxidative stress, apoptosis, telomere damage, aging, dysmetabolism invivo and invitro; and ER stress. The AMPK (AMP-activated protein kinase) pathway was central to metformin's protective action. Within COPDGene, participants receiving metformin compared with those not receiving it had a slower progression of emphysema (-0.92%; 95% confidence interval [CI], -1.7% to -0.14%; P = 0.02) and a slower adjusted lung density decrease (2.2 g/L; 95% CI, 0.43 to 4.0 g/L; P = 0.01). Conclusions: Metformin protected against CS-induced lung, renal, and muscle injury; mitochondrial dysfunction; and unfolded protein responses and ER stress in mice. In humans, metformin use was associated with lesser emphysema progression over time. Our results provide a rationale for clinical trials testing the efficacy of metformin in limiting emphysema progression and its systemic consequences.

Customer’s Acceptance Level towards Smoke-Free Policy at Restaurants in Terengganu

Smoke-free policy at restaurants has gained great support among Malaysians since its implementation. However, the evidence of acceptance level among people eating at the restaurants is limited. This study aims to investigate customers’ acceptance level towards smoke-free policy at restaurants in Kuala Terengganu, Malaysia. Quantitative, cross-sectional study was conducted using convenience sampling technique. Survey questionnaires using five-point Likert scale were distributed and 384 usable questionnaires were analyzed. Descriptive analysis showed a majority of the respondents perceived that they have their rights to enjoy the food without worry about inhaling cigarette smoke (M=4.58, SD=.685). It can be concluded that the implementation of smoke-free policy in restaurants received high level of acceptance among customers. Therefore, customers supported the smoke-free policy in reducing exposure to secondhand smokes and prohibit smoking behavior at restaurants in Malaysia.

Purple corn extract (PCE) alleviates cigarette smoke (CS)-induced DNA damage in rodent blood cells by activation of AMPK/Foxo3a/MnSOD pathway

ABSTRACT Purple corn extract (PCE) is a nutraceutical, an activator of AMPK, and it has antioxidants and anticancer properties. Therefore, PCE could be a candidate for alleviating cigarette smoke (CS)-induced oxidative DNA damage. This study examined whether PCE can have a protective effect on blood cells in an animal model of cigarette smoke (CS)-induced DNA damage. PCE was orally administered to CS-inhaled Spraque-Dawley (SD) rats, followed by the target cells being examined for markers of DNA damage. The study also sought to elucidate the mechanism of PCE action in the PCE treated animals. SD rat inhalation of CS was for once a day for 30 min, repeated for 7 days. PCE was administered orally before CS inhalation. Pretreatment of the animals with oral PCE kept the numbers of white blood cells (WBC) as well as neutrophils (NE), lymphocytes (LY), monocytes (Mo), eosinophils (EO), abd jasophils (BA) from increasing as those were increased in the CS-inhaling SD rats. The amount of phosphorylated γ-H2AX, a DNA damage marker, was assayed in the circulating blood cells collected from the animals and western blot analysis with anti-Foxo3a, p-Foxo3a, p-AMPK, MnSOD antibodies were performed on those cells. PCE protected the circulating blood cells from CS inhalation-induced DNA damage by 44% as assayed by increases in γ-H2AX. PCE also increased the nuclear localization of Foxo3a by 52% over control cells. Mechanistically, PCE appears to efficiently protect various blood cell types from CS-induced DNA damage through removal of ROS via activation of the AMPK/Foxo3a/MnSOD pathway.

Acute Effects of Heated Tobacco Product (IQOS) Aerosol Inhalation on Lung Tissue Damage and Inflammatory Changes in the Lungs.

Emerging heated tobacco products (HTPs) were designed to reduce exposure to toxicants from cigarette smoke (CS) by avoiding burning tobacco and instead heating tobacco. We studied the effects of short-term inhalation of aerosols emitted from HTP called IQOS, on lung damage and immune-cell recruitment to the lungs in mice. Numerous markers of lung damage and inflammation including albumin and lung immune-cell infiltrates, proinflammatory cytokines, and chemokines were quantified in lungs and bronchoalveolar (BAL) fluid from IQOS, CS, or air-exposed (negative control) mice. Importantly, as a surrogate marker of lung epithelial-cell damage, we detected significantly increased levels of albumin in the BAL fluid of both HTP- and CS-exposed mice compared with negative controls. Total numbers of leukocytes infiltrating the lungs were equivalent following both IQOS aerosols and CS inhalation and significantly increased compared with air-exposed controls. We also observed significantly increased numbers of CD4+IL-17A+ T cells, a marker of a T-cell immune response, in both groups compared with air controls; however, numbers were the highest following CS exposure. Finally, the numbers of CD4+RORγt+ T cells, an inflammatory T-cell subtype expressing the transcription factor that is essential for promoting differentiation into proinflammatory Th17 cells, were significantly augmented in both groups compared with air-exposed controls. Levels of several cytokines in BAL were significantly elevated, reflecting a proinflammatory milieu. Our study demonstrates that short-term inhalation of aerosols from IQOS generates damage and proinflammatory changes in the lung that are substantially similar to that elicited by CS exposure. Exposure of mice to IQOS, one of the candidate modified-risk tobacco products, induces inflammatory immune-cell accumulation in the lungs and augments the levels of proinflammatory cytokines and chemokines in the BAL fluid. Such an exacerbated pulmonary proinflammatory microenvironment is associated with lung epithelial-cell damage in IQOS-exposed mice, suggesting a potential association with the impairment of lung function.

Review: Gambaran Nikotin pada Perokok Pasif di Kabupaten Tulungagung

Passive smokers do not have a smoking habit but inhale cigarette smoke exhaled by those around them who smoke. Exposure to cigarette smoke, one of which nicotine, can trigger harmful substances to the body. This study aimed to analyze the presence or absence of nicotine in passive smokers in Tulungagung Regency. The method used is descriptive qualitative with a sample of 30 urine of passive smokers. The results of the examination showed negative nicotine (93%) with the criteria of the female sex (77%), 11-20 years old (20%), 11-20 years of exposure (37%), and the level of elementary school education (37%). Respondents who were positive for nicotine were 2 people (7%) with characteristics of male sex (7%), aged 31-40 years (7%), long exposure for 31-40 years (7%), and level education of elementary school and junior high school (3.3%). This study concludes that nicotine negative respondents (93%). Nicotine is hazardous for the health of passive smokers. The longer exposure to cigarette smoke, the higher the nicotine content in the body so that the body's nicotine content can be detected. People are advised to use masks and avoid exposure to cigarette smoke too often to prevent the entry of harmful substances into the body

Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System.

Close to 14% of adults in the United States were reported to smoke cigarettes in 2018. The effects of cigarette smoke (CS) on lungs and cardiovascular diseases have been widely studied, however, the impact of CS in other tissues and organs such as blood and bone marrow remain incompletely defined. Finding the appropriate system to study the effects of CS in rodents can be prohibitively expensive and require the purchase of commercially available systems. Thus, we set out to build an affordable, reliable, and versatile system to study the pathologic effects of CS in mice. This whole-body inhalation exposure system (WBIS) set-up mimics the breathing and puffing of cigarettes by alternating exposure to CS and clean air. Here we show that this do-it-yourself (DIY) system induces airway inflammation and lung emphysema in mice after 4-months of cigarette smoke exposure. The effects of whole-body inhalation (WBI) of CS on hematopoietic stem and progenitor cells (HSPCs) in the bone marrow using this apparatus are also shown.

Cigarette Smoke Exposure Promotes Virulence of Pseudomonas aeruginosa and Induces Resistance to Neutrophil Killing.

It is widely known that cigarette smoke damages host defenses and increases susceptibility to bacterial infections. Pseudomonas aeruginosa, a Gram-negative bacterium that commonly colonizes the airways of smokers and patients with chronic lung disease, can cause pneumonia and sepsis and can trigger exacerbations of lung diseases. Pseudomonas aeruginosa colonizing airways is consistently exposed to inhaled cigarette smoke. Here, we investigated whether cigarette smoke alters the ability of this clinically significant microbe to bypass host defenses and cause invasive disease. We found that cigarette smoke extract (CSE) exposure enhances resistance to human neutrophil killing, but this increase in pathogenicity was not due to resistance to neutrophil extracellular traps. Instead, Pseudomonas aeruginosa exposed to CSE (CSE-PSA) had increased resistance to oxidative stress, which correlated with increased expression of tpx, a gene essential for defense against oxidative stress. In addition, exposure to CSE induced enhanced biofilm formation and resistance to the antibiotic levofloxacin. Finally, CSE-PSA had increased virulence in a model of pneumonia, with 0% of mice infected with CSE-PSA alive at day 6, while 28% of controls survived. Altogether, these data show that cigarette smoke alters the phenotype of P. aeruginosa, increasing virulence and making it less susceptible to killing by neutrophils and more capable of causing invasive disease. These findings provide further explanation of the refractory nature of respiratory illnesses in smokers and highlight cigarette smoking as a potential driver of virulence in this important airway pathogen.

Visualized movement of cough particles discharged from an adult male at the dummy in the positive pressure booth without a front curtain. The cough particles were substituted by a smoke associated with a voluntary cough after one inhalation of cigarette smoke. An adult male sitting outside the booth coughed at the dummy doctor inside the booth sitting at an angle

Visualized movement of cough particles discharged from an adult male at the dummy in the positive pressure booth without a front curtain. The cough particles were substituted by a smoke associated with a voluntary cough after one inhalation of cigarette smoke. An adult male sitting outside the booth coughed at the dummy doctor inside the booth sitting at an angle

Visualized movement of cough particles discharged from an adult male at the dummy sitting at an angle of 45° to the air stream from the FFU and standing close to the front curtain in the positive pressure booth with a stair-cut front curtain. The cough particles were substituted by a smoke associated with a voluntary cough after one inhalation of

Visualized movement of cough particles discharged from an adult male at the dummy sitting at an angle of 45° to the air stream from the FFU and standing close to the front curtain in the positive pressure booth with a stair-cut front curtain. The cough particles were substituted by a smoke associated with a voluntary cough after one inhalation of

The Impact of Smoking on Pulmonary Metastasis in Colorectal Cancer.

IntroductionRecently, clinical studies have revealed that smoking can contribute to the poor prognosis of colorectal cancer (CRC) and, additionally, can be a risk factor for pulmonary metastasis of CRC. However, there has been no basic research regarding the underlying molecular mechanism. The purpose of this study was to clarify the mechanism by which smoking causes pulmonary metastasis of CRC.MethodsFirst, pulmonary metastasis model mice inhaled cigarette smoke or air (control) for 1 h once a day for 3 weeks. We attempted to clarify the effect of smoking on the incidence of pulmonary metastasis. On the 15th day, CMT-93 cells were injected into the tail vein. At 6 and 8 weeks following injection, the extent of pulmonary metastasis was evaluated using in vivo micro CT. After the last CT examination, the mice were sacrificed, and the lungs were extracted for pathological examination.ResultsThe number of mice with pulmonary metastases in the smoking group was significantly higher than in the control group. Three weeks of smoking induced mild inflammation in the lungs, as evidenced by increases in the levels of IL-6 and TNF-α in bronchoalveolar lavage. Moreover, the adhesion-related molecule ICAM-1 was overexpressed in pulmonary tissue, which allowed drained cancer cells to remain in the lung and contribute to the formation of pulmonary metastasis.ConclusionCollectively, cigarette smoking may contribute to the pathogenesis and development of pulmonary metastasis in CRC through enhancement of adhesion and inflammation.

Síndrome de Moünier-Kuhn: um relato de caso

Introdução: Traqueobroncomegalia ou síndrome de Mounier-Kuhn é uma doença rara, observada principalmente em homens de meia idade antes da 5ª década de vida, caracterizada por atrofia ou ausência das fibras elásticas ou da musculatura lisa da parede da traquéia e dos brônquios principais, determinando dilatação dessas estruturas. Acredita-se que a fraqueza do tecido conjuntivo, associada à inalação de poluentes aéreos e fumaça de cigarro, sejam os principais fatores no desenvolvimento desta síndrome. O diagnóstico pode ser ocasional em indivíduos assintomáticos, contudo cursa frequentemente com infeções respiratórias de repetição e bronquiectasias. Descrição: A.H.A.G., 65 anos, masculino, solteiro, branco. Relatava tosse crônica com aumento da frequência há 10 dias associado a um aumento de expectoração, no momento, esverdeado. Queixava-se também de febre irregular diária não termometrada, dispneia aos mínimos esforços, e sudorese noturna. Paciente menciona diagnóstico de bronquiectasia, porém sem adesão ao acompanhamento ambulatorial de pneumologia no HRT desde 2015. Conclusão: A síndrome de Mounier-Kuhn se caracteriza pelo aumento do diâmetro da traqueia e dos brônquios principais associado a redução do clearence mucociliar, o que leva o indivíduo a desenvolver infecções respiratórias com frequência. O diagnóstico é feito por TC de tórax. O tratamento só é realizado nos sintomáticos, objetivando tratar o fator desencadeante da descompensação.