scholarly journals Cigarette Smoke Exposure Inhibits Bacterial Killing via TFEB-Mediated Autophagy Impairment and Resulting Phagocytosis Defect

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Garrett Pehote ◽  
Manish Bodas ◽  
Kathryn Brucia ◽  
Neeraj Vij
Keyword(s):  
Cigarette Smoke ◽  
Therapeutic Potential ◽  
Underlying Mechanism ◽  
Cigarette Smoke Extract ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Bacterial Clearance ◽  
Bacterial Killing ◽  
Bactericidal Activities ◽  
Autophagy Inhibition

Introduction. Cigarette smoke (CS) exposure is the leading risk factor for COPD-emphysema pathogenesis. A common characteristic of COPD is impaired phagocytosis that causes frequent exacerbations in patients leading to increased morbidity. However, the underlying mechanism is unclear. Hence, we investigated if CS exposure causes autophagy impairment as a mechanism for diminished bacterial clearance via phagocytosis by utilizing murine macrophages (RAW264.7 cells) and Pseudomonas aeruginosa (PA01-GFP) as an experimental model. Methods. Briefly, RAW cells were treated with cigarette smoke extract (CSE), chloroquine (autophagy inhibitor), TFEB-shRNA, CFTR(inh)-172, and/or fisetin prior to bacterial infection for functional analysis. Results. Bacterial clearance of PA01-GFP was significantly impaired while its survival was promoted by CSE (p<0.01), autophagy inhibition (p<0.05; p<0.01), TFEB knockdown (p<0.01; p<0.001), and inhibition of CFTR function (p<0.001; p<0.01) in comparison to the control group(s) that was significantly recovered by autophagy-inducing antioxidant drug, fisetin, treatment (p<0.05; p<0.01; and p<0.001). Moreover, investigations into other pharmacological properties of fisetin show that it has significant mucolytic and bactericidal activities (p<0.01; p<0.001), which warrants further investigation. Conclusions. Our data suggests that CS-mediated autophagy impairment as a critical mechanism involved in the resulting phagocytic defect, as well as the therapeutic potential of autophagy-inducing drugs in restoring is CS-impaired phagocytosis.

scholarly journals Cigarette smoke extract enhances oxytocin-induced rhythmic contractions of rat and human preterm myometrium

Reproduction ◽  
2006 ◽  
Vol 132 (2) ◽  
pp. 343-353 ◽  
Author(s):  
Tsuyoshi Nakamoto ◽  
Katsuhiko Yasuda ◽  
Masahiro Yasuhara ◽  
Tatsuya Nakajima ◽  
Tomomi Mizokami ◽  
...  
Keyword(s):  
Preterm Delivery ◽  
Cigarette Smoke ◽  
Contractile Activity ◽  
Underlying Mechanism ◽  
Cigarette Smoke Extract ◽  
Control Group ◽  
Smoking During Pregnancy ◽  
Expression Levels ◽  
Uterine Contractions ◽  
Uterine Contractile

Although smoking during pregnancy is a major risk factor for preterm delivery, the underlying mechanism by which smoking stimulates uterine contractions is still poorly understood. In the present study, we tried to clarify the effects of smoking on myometrial contractility induced by oxytocin (OT) using cigarette smoke extract (CSE). Myometrial strips, which were taken from the rat on day 16 of pregnancy, and from human preterm and term delivery groups, were incubated overnight with several doses of CSE at 37 ° C under non-hormonal conditions. The uterine contractile sensitivity and activity (force and frequency) upon exposure to OT were investigated. Furthermore, the expression levels of oxytocin receptor (OTR) mRNA in the myometrial strips were investigated by real-time PCR. Contractile sensitivity to OT in the rat CSE (10−7pieces/ml) group was found to be significantly higher than in the control group (P< 0.05). Contractile activity did not differ between the CSE and control groups. The expression levels of rat OTR mRNA in the CSE (10−7pieces/ml) group were significantly higher than in the control group (P< 0.01). Similarly, in preterm myometrial strips, the expression levels of human OTR mRNA in the CSE (10−7pieces/ml) group were significantly higher than in the control group (P< 0.05). These findings suggest that CSE directly increases the contractile sensitivity of preterm myometrium in response to OT by upregulating the expression of OTR mRNA and thereby increases the risk of preterm delivery in women, who smoke during pregnancy.

Comparison of Oxidative Effects of Electronic Cigarette and Tobacco Smoke Exposure Performed Experimentally

2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Electronic Cigarette ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Exposure Group ◽  
Oxidative Effects

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

scholarly journals Prenatal cigarette smoke exposure slightly alters neurobehavioral development in neonatal rats: Implications for developmental origins of health and disease (DoHAD)

2020 ◽  
Vol 107 (1) ◽  
pp. 55-66
Author(s):  
B. Mammel ◽  
T. Kvárik ◽  
Zs. Szabó ◽  
J. Gyarmati ◽  
T. Ertl ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Motor Coordination ◽  
Smoke Exposure ◽  
Whole Body ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Developmental Origins ◽  
Smoking During Pregnancy ◽  
Neurobehavioral Development ◽  
Health And Disease

AbstractNumerous studies indicate that smoking during pregnancy exerts harmful effects on fetal brain development. The aim of this study was to determine the influence of maternal smoking during pregnancy on the early physical and neurobehavioral development of newborn rats. Wistar rats were subjected to whole-body smoke exposure for 2 × 40 min daily from the day of mating until day of delivery. For this treatment, a manual closed-chamber smoking system and 4 research cigarettes per occasion were used. After delivery the offspring were tested daily for somatic growth, maturation of facial characteristics and neurobehavioral development until three weeks of age. Motor coordination tests were performed at 3 and 4 weeks of age. We found that prenatal cigarette smoke exposure did not alter weight gain or motor coordination. Critical physical reflexes indicative of neurobehavioral development (eyelid reflex, ear unfolding) appeared significantly later in pups prenatally exposed to smoke as compared to the control group. Prenatal smoke exposure also resulted in a delayed appearance of reflexes indicating neural maturity, including hind limb grasping and forelimb placing reflexes. In conclusion, clinically relevant prenatal exposure to cigarette smoke results in slightly altered neurobehavioral development in rat pups. These findings suggest that chronic exposure of pregnant mothers to cigarette smoke (including passive smoking) results in persisting alterations in the developing brain, which may have long-lasting consequences supporting the concept of developmental origins of health and disease (DoHAD).

scholarly journals Pengaruh pemberian ubi jalar ungu (Ipomoea batatas L.Poir) terhadap kadar superoksida dismutase (SOD) tikus wistar jantan (Rattus Norvegicus) yang dipapar asap rokok

2020 ◽  
Vol 8 (1) ◽  
pp. 45
Author(s):  
Alfreda Sabrina Widyanti ◽  
Martha Ardiaria ◽  
Nurmasari Widyastuti
Keyword(s):  
Superoxide Dismutase ◽  
Sweet Potato ◽  
Cigarette Smoke ◽  
Ipomoea Batatas ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Standard Diet ◽  
Control Group Design ◽  
Significant Difference

Background: Cigarette smoke exposure is one of the source of free radicals that causes oxidative stress and decreases superoxide dismutase (SOD) level. Purple fleshed sweet potato is a type of food that contains antioxidants to neutralize oxidative stress.Objectives: To study the effect of purple fleshed sweet potato on superoxide dismutase (sod) level on rats exposed to cigarette smoke.Methods: This was a true experimental study with a post-test randomized control group design. The rats were randomized into 4 groups (6 rats in each group). The negative control group (K-) was treated with standard diet; the positive control group (K+) was treated with cigarette smoke exposure and standard diet; the treatment 1 (P1) group was treated with standard diet and purple fleshed sweet potato with the dose of 8 g / 200 g bw/day, and the treatment 2 (P2) group was treated with cigarette smoke exposure and purple fleshed sweet potato with the dose of 8 g /200 g bw/day.Results: There was a significant difference of SOD levels in each group (p=0.00) except between group K- and P1. Giving purple fleshed sweet potatoes increased SOD levels as much as 85.81±4.59 (P1). The K+ group had the lowest SOD level 22.34±3.98. The SOD level for K- group and P2 group was 82.27±4.59 and 67.73±6.68 respectively.Conclusion: The highest SOD level is on the treatment 1 group which is administered with purple fleshed sweet potato.

scholarly journals Cigarette Smoke Extract Stimulates MMP-2 Production in Nasal Fibroblasts via ROS/PI3K, Akt, and NF-κB Signaling Pathways

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 739
Author(s):  
Joo-Hoo Park ◽  
Jae-Min Shin ◽  
Hyun-Woo Yang ◽  
Tae Hoon Kim ◽  
Seung Hoon Lee ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Chronic Rhinosinusitis ◽  
Cigarette Smoke ◽  
Molecular Mechanisms ◽  
Gelatin Zymography ◽  
Cigarette Smoke Extract ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Luciferase Assay ◽  
Cigarette Smoke Exposure ◽  
Ros Production

Cigarette smoke exposure has been shown to be associated with chronic rhinosinusitis and tissue remodeling. The present study aimed to investigate the effects of cigarette smoke extract (CSE) on matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP) production in nasal fibroblasts and to determine the underlying molecular mechanisms. Primary nasal fibroblasts from six patients were isolated and cultured. After the exposure of fibroblasts to CSE, the expression levels of MMP-2, MMP-9, TIMP-1, and TIMP-2 were measured by real-time PCR, ELISA, and immunofluorescence staining. The enzymatic activities of MMP-2 and MMP-9 were measured by gelatin zymography. Reactive oxygen species (ROS) production was analyzed using dichloro-dihydro-fluorescein diacetate and Amplex Red assays. PI3K/Akt phosphorylation and NF-κB activation were determined by Western blotting and luciferase assay. CSE significantly increased MMP-2 expression and inhibited TIMP-2 expression but did not affect MMP-9 and TIMP-1 expression. Furthermore, CSE significantly induced ROS production. However, treatment with ROS scavengers, specific PI3K/Akt inhibitors, NF-κB inhibitor, and glucocorticosteroids significantly decreased MMP-2 expression and increased TIMP-2 expression. Our results suggest that steroids inhibit CSE-regulated MMP-2 and TIMP-2 production and activation through the ROS/ PI3K, Akt, and NF-κB signaling pathways in nasal fibroblasts. CSE may contribute to the pathogenesis of chronic rhinosinusitis by regulating MMP-2 and TIMP-2 expression.

scholarly journals Erythromycin Suppresses the Cigarette Smoke Extract-Exposed Dendritic Cell-Mediated Polarization of CD4+ T Cells into Th17 Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Jifeng Liu ◽  
Xiaoning Zhong ◽  
Zhiyi He ◽  
Jianquan Zhang ◽  
Jing Bai ◽  
...  
Keyword(s):  
T Cells ◽  
Cigarette Smoke ◽  
Th17 Cells ◽  
Mixed Lymphocyte Reaction ◽  
Mononuclear Cells ◽  
Cigarette Smoke Extract ◽  
Exposed Group ◽  
Control Group ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Cigarette smoke is a major effector of chronic obstructive pulmonary disease (COPD), and Th17 cells and dendritic cells (DCs) involve in the pathogenesis of COPD. Previous studies have demonstrated the anti-inflammatory effects of macrolides. However, the effects of macrolides on the cigarette smoke extract- (CSE-) induced immune response are unclear. Accordingly, in this study, we evaluated the effects of erythromycin (EM) on CSE-exposed DCs polarizing naïve CD4+ T cells into Th17 cells. DCs were generated from bone marrow-derived mononuclear cells isolated from male BALB/c mice and divided into five groups: control DC group, CSE-exposed DC group, CD40-antibody-blocked CSE-exposed DC group, and EM-treated CSE-exposed DC group. The function of polarizing CD4+ T cells into Th17 cells induced by all four groups of DCs was assayed based on the mixed lymphocyte reaction (MLR) of naïve CD4+ T cells. CD40 expression in DCs in the CSE-exposed group increased significantly compared with that in the control group (P<0.05). The Th17 cells in the CSE-exposed DC/MLR group increased significantly compared with those in the control DC/MLR group (P<0.05). Moreover, Th17 cells in the CD40-blocked CSE-exposed DC/MLR group and EM-treated CSE-exposed DC/MLR group were reduced compared with those in the CSE-exposed DC/MLR group (P<0.05). Thus, these findings suggested that EM suppressed the CSE-exposed DC-mediated polarization of CD4+ T cells into Th17 cells and that this effect may be mediated through inhibition of the CD40/CD40L pathway.

Differential induction of apoptosis by cigarette smoke extract in primary human lung fibroblast strains: implications for emphysema

2006 ◽  
Vol 291 (1) ◽  
pp. L19-L29 ◽  
Author(s):  
Carolyn J. Baglole ◽  
Seth M. Bushinsky ◽  
Tatiana M. Garcia ◽  
Aruna Kode ◽  
Irfan Rahman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Mitochondrial Membrane ◽  
Human Lung ◽  
Cigarette Smoke Extract ◽  
Lung Fibroblast ◽  
Cigarette Smoke Exposure ◽  
Human Lung Fibroblast

Cigarette smoke is the principal cause of emphysema. Recent attention has focused on the loss of alveolar fibroblasts in the development of emphysema. Fibroblasts may become damaged by oxidative stress and undergo apoptosis as a result of cigarette smoke exposure. Not all smokers develop lung diseases associated with tobacco smoke, a fact that may reflect individual variation among human fibroblast strains. We hypothesize that fibroblasts from different human beings vary in their ability to undergo apoptosis after cigarette smoke exposure. This could account for emphysematous changes that occur in the lungs of some but not all smokers. Primary human lung fibroblast strains were exposed to cigarette smoke extract (CSE) and assessed for viability, morphological changes, and mitochondrial transmembrane potential as indicators of apoptosis. We also examined the generation of intracellular reactive oxygen species (ROS), 4-hydroxy-2-nonenal, and changes in glutathione (GSH) and glutathione disulfide (GSSG) levels. Each human lung fibroblast strain exhibited a differential sensitivity to CSE as judged by changes in mitochondrial membrane potential, viability, ROS generation, and glutathione production. Interestingly, the thiol antioxidants N-acetyl-l-cysteine and GSH eliminated CSE-induced changes in fibroblast morphology such as membrane blebbing, nuclear condensation, and cell size and prevented alterations in mitochondrial membrane potential and the generation of ROS. These findings support the concept that oxidative stress and apoptosis are responsible for fibroblast death associated with exposure to tobacco smoke. Variations in the sensitivity of fibroblasts to cigarette smoke may account for the fact that only some smokers develop emphysema.

scholarly journals Effects of Folic Acid Intake during Pregnancy whose Mother was Exposed to Cigarette Smoke towards Brain Neurons Apoptosis Index and Quantity of Mice (Mus musculus) Offspring

2018 ◽  
Vol 54 (1) ◽  
pp. 34
Author(s):  
Nyna Puspa Ningrum ◽  
Hermanto Tri Joewono ◽  
Widjiati Widjiati
Keyword(s):  
Folic Acid ◽  
Cigarette Smoke ◽  
Gestational Age ◽  
Mus Musculus ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Folic Acid Intake ◽  
Brain Neurons ◽  
Apoptosis Index

Folic acid contains 5-methyltetrahydrofolate (5-MTHF), one of antioxidants that can be used to inhibit reaction caused by cigarette smoke exposure. Folic acid is able to inhibit the levels of Reactive Oxygen Species (ROS) so as to reduce the occurrence of neuronal apoptosis. The objectives of this study was to determine the effect of folic acid intake during pregnancy whose mother was exposed to cigarette smoke on brain neurons apoptosis index and quantity of mice (Mus musculus) offspring. This study was an experimental laboratory study with posttest-only control group design. The subjects were 24 female mice divided into 4 groups consisting of one control group and three treatment groups. Sampling used simple random sampling, each group consisting of 6 animals. Control group 1 was not given treatment during pregnancy, group 2 was given with folic acid orally on days 0-17 of gestational age as much as 0.06 mg/day/mice. Group 3 was given with cigarette smoke exposure on days 7-17 of gestational age, amounting to 2 cigarettes/day. Group 4 was given with cigarette smoke exposure on days 7-17 of gestational age, amounting to 2 cigarettes/day and folic acid orally on days 0-17 of gestational age as much as 0.06 mg/day/mice. The result showed significant differences in all variables. In neurons apoptosis index, there were significant differences between groups 1 and 3, groups 2 and 3, groups 3 and 4, significant differences in the quantity of neurons between groups 1 and 3, groups 2 and 3, groups 2 and 4. The study concluded that there were significant difference in neural apoptosis index between all groups, and there were also significant differences in the quantity of neurons between all groups.

scholarly journals Perubahan Kualitas Sperma Mencit (Mus musculus) Yang Terpapar Asap Rokok Elektrik

2019 ◽  
Vol 3 (2) ◽  
pp. 122-128
Author(s):  
Andita Ayu Mandasari ◽  
Siti Nur Asiyah ◽  
Kurnia Lintang
Keyword(s):  
Treatment Group ◽  
Cigarette Smoke ◽  
Mus Musculus ◽  
Group Treatment ◽  
Time Lag ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Male Mice ◽  
Suction Device ◽  
Treatment Groups

Smoking is one of the habits that can affect human health. One type of cigarette that is currently the choice is electric cigarettes. The e-cigarette content includes nicotine, propylene glycol, flavorings and glycerin. The purpose of this study was to determine the effect of exposure to e-cigarette smoke on mice strain balb / c with the parameters of the number of spermatozoa. This study used 15 male mice which were 8-10 weeks old and weighed 25-30 grams of male mice which were divided into 3 treatment groups namely control group, treatment group one and treatment group two. In the control group no exposure to cigarette smoke was carried out while in the treatment group one was exposed to cigarette smoke in mice with a dose of 0 mg nicotine and the second treatment group was exposed to e-cigarette smoke at a dose of 18 mg nicotine. Electric cigarette smoke exposure is carried out for 30 days using a suction device from a syringe. The exposure of cigarette smoke is carried out every day with successive doses of 20 times as much as 3 times with a time lag of 10 minutes (5 minutes the chamber is closed and 5 minutes of the chamber is opened). The results showed that the average number of spermatozoa in the control group was 16.816 million / ml. The average number of spermatozoa in treatment one was 10.432 million / ml and the average number of spermatozoa in treatment two was 5.234 million / ml. This shows that exposure to cigarette smoke can reduce the number of spermatozoa from the control group to the first treatment by 42.56% and the second treatment shows a decrease from the first group by 34.65%.

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