Cigarette Smoke Suppresses Type I Interferon-Mediated Antiviral Immunity in Lung Fibroblast and Epithelial Cells

The objective of this study was to investigate the impact of cigarette smoke on innate antiviral defense mechanisms; specifically, we examined the effects of cigarette smoke on the induction of type I interferon (IFN). We observed a dose-dependent decrease in the ability of human lung fibroblast and epithelial cells to elicit an antiviral response against a viral double-strand RNA (dsRNA) mimic, polyI:C, in the presence of cigarette smoke-conditioned medium (SCM). Mechanistically, SCM decreases the expression of IFN-stimulated gene 15 (ISG15) and IFN regulatory factor-7 (IRF-7) transcripts and suppresses the nuclear translocation of key transcription factors, nuclear factor-κB (NF-κB) and IRF-3, after polyI:C stimulation. Furthermore, we provide evidence that the intercellular defense strategy against viral infection is also impaired. We observed a decrease in the ability of fibroblasts to elicit an antiviral state in response to IFN-β stimulation. This was associated with decreased nuclear translocation of phosphorylated Stat1 in response to IFN-β treatment. The effects elicited by SCM are reversible and are almost entirely abrogated in the presence of an antioxidant, such as glutathione. Our findings suggest that cigarette smoke affects the immediate-early, inductive, and amplification phases of the type I IFN response

Efek Proteksi Mengkudu (Morinda Citrifolia L.)terhadap Jumlah Spermatid Testis Mencit (Mus Musculus) Yang Dipapar Asap Rokok

Free radicals of the cigarette smoke can decrease the male fertility. In present study, Morinda citrifolia L. extract was evaluated for its protective effect on the number of spermatids which induced by cigarette smoke in Swiss webster mice. Four groups of mice were arranged as follows: KK (control group), KP0 (cigarette smoke), KP1(low dose extract + cigarette smoke), KP2 (high dose extract + cigarette smoke). After 14-day treatment, all mice were sacrificed. The LSD test showed significant differences between each pair of groups. Morinda citrifolia L. extract showed protective effect to the number of spermatids which induced by cigerette smoke

The Anti-inflammatory Effects of Hydrogen-Rich Water Acts in a Volume-Dependent Manner on Rats’ Lungs Exposed to Cigarette Smoke

Cigarette smoke can activate various ROS-sensitive signaling pathways in the lungs, triggering airway inflammation and leading to mucus hypersecretion. Meanwhile, hydrogen has shown anti-inflammatory activity in various injury models. This study aims to determine the anti-inflammatory effect of hydrogen-rich water on lungs exposed to cigarette smoke in rats. Male wistar rats were divided into four groups randomly (n=5), namely CI group (given aquades + exposed to free air), CII group (given aquades + exposed to cigarette smoke), HI group (given HRW 5 mL once a day + exposed to cigarette smoke), and HII group (given HRW 5 mL twice a day + exposed to cigarette smoke). HRW/aquades was administered orally 30 minutes before cigarette smoke exposure. Exposure to cigarette smoke lasts about 15-25 minutes with 5 cigarettes/day for 28 days. Subsequently, we examine the levels of lung NF-kB p65 using the ELISA method and perform pulmonary histopathological examination. The results showed that the administration of HRW reduced the levels of NF-κB p65 induced by cigarette smoke exposure, which is significant in the HII group (p<0.01). From the histopathological examination, administration of HRW significantly reduced the degree of lung inflammation caused by cigarette smoke exposure in the HI and HII group (p<0.05)

Cigarette Smoke Detection And Cleaner Based On Internet Of Things (IoT) Using Arduino Microcontroller And MQ-2 Sensor

The detector and neutralize cigarette smoke in the STMIK Hang Tuah Pekanbaru there is no. To simplify detector and neutralize cigarette smoke in the campus area made a system detector and neutralize cigarette smoke Arduino Uno microcontroller based using an notification iot. The whole tool is divided into several parts, consisting of sensor mq-2, module ESP8266-01S, module LCD, mikrokontroller arduino uno, buzzer, and DC FAN. This tool works when module ESP8266-01S looking for the nearest internet network and sensor mq-2 detect cigarette smoke, from module ESP8266-01S and sensor mq-2  then to Arduino Uno  microcontroller to process, from Arduino Uno  microcontroller then Turn on buzzer as a warning alarm and  Turn on DC FAN as a fan to neutralize cigarette smoke  which then transfers data through module ESP8266-01S to the website and give notification  the room detected cigarette smoke to the smartphone  head of equipment and officers. The results showed that the smoke content was more than 300 detected as cigarette smoke, because it has been to test the system to several prototypes and 2hen there is no cigarette smoke was value is less than 300

Mouse Protocadherin-1 gene expression is regulated by cigarette smoke exposure in vivo

Protocadherin-1 (PCDH1) is a novel susceptibility gene for airway hyperresponsiveness, first identified in families exposed to cigarette smoke and is expressed in bronchial epithelial cells. Here, we asked how mouse Pcdh1 expression is regulated in lung structural cells in vivo under physiological conditions, and in both short-term cigarette smoke exposure models characterized by airway inflammation and hyperresponsiveness and chronic cigarette smoke exposure models. Pcdh1 gene-structure was investigated by Rapid Amplification of cDNA Ends. Pcdh1 mRNA and protein expression was investigated by qRT-PCR, western blotting using isoform-specific antibodies. We observed 87% conservation of the Pcdh1 nucleotide sequence, and 96% conservation of the Pcdh1 protein sequence between men and mice. We identified a novel Pcdh1 isoform encoding only the intracellular signalling motifs. Cigarette smoke exposure for 4 consecutive days markedly reduced Pcdh1 mRNA expression in lung tissue (3 to 4-fold), while neutrophilia and airway hyperresponsiveness was induced. Moreover, Pcdh1 mRNA expression in lung tissue was reduced already 6 hours after an acute cigarette-smoke exposure in mice. Chronic exposure to cigarette smoke induced loss of Pcdh1 protein in lung tissue after 2 months, while Pcdh1 protein levels were no longer reduced after 9 months of cigarette smoke exposure. We conclude that Pcdh1 is highly homologous to human PCDH1, encodes two transmembrane proteins and one intracellular protein, and is regulated by cigarette smoke exposure in vivo

Exposure of a 23F serotype strain of <i>Streptococcus pneumoniae</i> to cigarette smoke condensate is associated with selective upregulation of genes encoding the two-component regulatory system 11 (TCS11)

Alterations in whole genome expression profiles following exposure of the pneumococcus (strain 172, serotype 23F) to cigarette smoke condensate (160 μg/mL) for 15 and 60 min have been determined using the TIGR4 DNA microarray chip. Exposure to CSC resulted in the significant (P &#60; 0.014–0.0006) upregulation of the genes encoding the two-component regulatory system 11 (TCS11), consisting of the sensor kinase, hk11, and its cognate response regulator, rr11, in the setting of increased biofilm formation. These effects of cigarette smoke on the pneumococcus may contribute to colonization of the airways by this microbial pathogen

Effect of Calina Papaya Leaves Extract on Respiratory Tract in Cigarette Smoke Exposed Rats

Cigarette smoke is a source of free radicals that cause health problems throughout the world. Indonesia is a country that has many sources of natural antioxidants in counteracting free radicals, one of which is Calina papaya leaves. The study aimed to determine the potential of Calina papaya leaves antioxidants in improving the respiratory organs of Wistar rats after being exposed to cigarette smoke. The study using 25 male Wistar rats consisted of Control (not exposed to cigarette smoke and given distilled water), KN (cigarette smoke and given distilled water), P1 (cigarette smoke and Calina Papaya Leaves Ethanolic extracts (CPLE) 100 mg/kg BW), P2 (cigarette smoke and CPLE 200 mg/kg BW), and P3 (cigarette smoke and given CPLE 300 mg/kg BW). Exposure to cigarette smoke and administration of extracts was carried out for 21 days. On day 22, the rats were euthanized and dissected to remove the lungs and trachea. Organs were prepared using the paraffin method and hematoxylin-eosin staining. Parameters consisted of histopathological observations of the lungs and trachea. All data parameters were analyzed using a one-way ANOVA test and Duncan's advanced test (p<0.05). The results showed that there was an improvement in histopathology of the lungs and trachea at a dose of 200 mg/Kg BW compared to other doses (p<0.05). The study showed that the Calina papaya leaves ethanolic extracts have the potential as a source of antioxidants in improving the respiratory organs of Wistar rats after being exposed to cigarette smoke

Vitamin A depletion induced by cigarette smoke is associated with an increase in lung cancer-related markers in rats

Citation: Xue, Y., Harris, E., Wang, W. Q., & Baybutt, R. C. (2015). Vitamin A depletion induced by cigarette smoke is associated with an increase in lung cancer-related markers in rats. Journal of Biomedical Science, 22, 9. doi:10.1186/s12929-015-0189-0Background: We have previously demonstrated that cigarette smoke is associated with a significant reduction of retinoic acid in rat lungs and the formation of tracheal precancerous lesions. However, the underlying mechanism of cancer risk induced by vitamin A deficiency is unclear. The purpose of this study was to determine whether the cigarette smoke-induced depletion of vitamin A is related to changes in lung cancer risk-related molecular markers. Results: We investigated the roles of the retinoic acid receptors (RARs) as well as other biomarkers for potential cancer risk in the lungs of rats exposed to cigarette smoke. Twenty-four male weanling rats were fed a purified diet and divided equally into four groups. Three experimental groups were exposed to increasing doses of cigarette smoke from 20, 40 or 60 commercial cigarettes/day for 5 days/week. After 6 weeks, the retinoic acid concentrations in the lung tissue as measured via high performance liquid chromatography (HPLC) significantly decreased (P < 0.01) in cigarette smoke exposed groups. Western Blot analysis revealed that cigarette smoke exposure increased lung protein expression of RAR alpha in a threshold manner and decreased RAR beta and RAR gamma expression in a dose-dependent fashion. Protein expressions of cyclin E and proliferating cell nuclear antigen (PCNA) were increased significantly in a dose-dependent manner in cigarette smoke exposed-groups. Additionally, there was a significant increase in protein expression of cJun and cyclin D1 demonstrating a threshold effect similar to that exhibited by RAR alpha, suggesting a potential independent signaling pathway for RAR alpha in lung carcinogenesis. Conclusions: Findings from this study suggest that cigarette smoke-induced lung retinoic acid depletion may involve two independent pathways, RAR alpha- and RAR beta-mediated, responsible for the increased cancer risk associated with cigarette smoke-induced vitamin A deficiency

Epigenetic Effects and Molecular Mechanisms of Tumorigenesis Induced by Cigarette Smoke: An Overview

Cigarette smoking is one of the major causes of carcinogenesis. Direct genotoxicity induced by cigarette smoke leads to initiation of carcinogenesis. Nongenotoxic (epigenetic) effects of cigarette smoke also act as modulators altering cellular functions. These two effects underlie the mechanisms of tumor promotion and progression. While there is no lack of general reviews on the genotoxic and carcinogenic potentials of cigarette smoke in lung carcinogenesis, updated review on the epigenetic effects and molecular mechanisms of cigarette smoke and carcinogenesis, not limited to lung, is lacking. We are presenting a comprehensive review of recent investigations on cigarette smoke, with special attentions to nicotine, NNK, and PAHs. The current understanding on their molecular mechanisms include (1) receptors, (2) cell cycle regulators, (3) signaling pathways, (4) apoptosis mediators, (5) angiogenic factors, and (6) invasive and metastasis mediators. This review highlighted the complexity biological responses to cigarette smoke components and their involvements in tumorigenesis

Pengaruh Pemberian Calcitriol terhadap Kadar Limfosit pada Tikus Putih (Rattus norvegicus) Galur Wistar Jantan yang Dipapar Asap Rokok

The health impact for active and passive smokers is damage to the organs and respiratory tract. The body organs initially experience inflammation which increases the number of white blood cells, one of which is an increase in lymphocytes. One of the efforts to reduce the damage caused free radical by cigarette smoke is by consuming Calcitriol. Objective: To determine the effect of presenting Calcitriol on lymphocyte levels in male Wistar rats (Rattus norvegicus) exposed to cigarette smoke. Methods: This type of research is a pure experimental (true-experiment) using a pre and post-test research design with a control group design to check lymphocyte levels in male Wistar rats (Rattus norvegicus). 24 rats were divided into 6 groups simultaneously. Random, namely the control group 1 (exposed to cigarette smoke and not given Calcitriol), group 2 (exposed to cigarette smoke and not given Calcitriol), placebo control group (exposed to cigarette smoke and given olive oil), treatment 1 (exposed to cigarette smoke and given Calcitriol with a dose of 0.25 µgr / head), treatment 2 (exposed to cigarette smoke and given Calcitriol at a dose of 0.5 µgr / head) and treatment 3 (exposed to cigarette smoke and given Calcitriol at a dose of 1 µgr / head). Results: Paired t-test lymphocyte levels showed evidence that stated (p &lt;0.05) in the K2 group (p = 0.014), the K3 group (p = 0.049), the P1 group (p = 0.012) and the P3 group (0.001) . Meanwhile, group K1 (p = 0.115) and group P2 (p = 0.066) had no statistical difference. Conclusion: Calcitriol administration can reduce lymphocyte levels in male Wistar rats exposed to cigarette smoke