Microbiological components in mainstream and sidestream cigarette smoke

Larsson, Lennart; Pehrson, Christina; Dechen, Tenzin; Crane-Godreau, Mardi A.

doi:10.1186/1617-9625-10-13

Cited by 33 publications

(21 citation statements)

References 22 publications

(38 reference statements)

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“…In the present study, we showed that LPS, a potent inflammatory agent contained in tobacco and tobacco smoke (14,15) enhanced LSCC induced by NTCU, a halogenated nitrosoalkylurea, and these effects were paralleled by significant induction of inflammatory cytokines, activation of pro-inflammatory and pro-oncogenic NF-κB and STAT3 signaling pathways and overexpression of p53 and phospho Akt. In mice treated with NTCU alone, only the incidence of bronchial hyperplasia, a reactive and reversible change, was significantly increased, whereas LPS-treated mice did not show any abnormal lesions.…”

Section: Discussionmentioning

confidence: 52%

“…LPS, the major component of the cell wall of Gram-negative bacteria and a potent inflammatory agent, exists in substantial amounts in mainstream and sidestream cigarette smoke (14,15) and has been shown to induce inflammatory response mimicking COPD in mice (16). Our studies showed that the incidence of LSCC was significantly higher in mice treated with a combination of NTCU and LPS, as compared to the group treated with NTCU alone, and dietary administration of DIM significantly reduced the incidence of LSCC in NTCU plus LPS-treated mice.…”

Section: Introductionmentioning

confidence: 99%

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Dietary Diindolylmethane Suppresses Inflammation-Driven Lung Squamous Cell Carcinoma in Mice

Song

Qian

Teferi

et al. 2015

Cancer Prevention Research

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Inflammatory conditions of the lung such as chronic obstructive pulmonary disease (COPD) are known to increase lung cancer risk, particularly lung squamous cell carcinoma (LSCC). In the present study, we developed a mouse model of inflammation-driven LSCC that was induced by N-nitroso-trischloroethylurea (NTCU) and enhanced by lipopolysaccharide (LPS), a potent proinflammatory agent contained in tobacco and tobacco smoke, and determined the chemopreventive effects of BioResponse diindolylmethane (DIM) in the same model. Compared to mice treated with NTCU alone, mice treated with the combination of NTCU and LPS had a 9-fold increase in the number of bronchioles with LSCC. Also, compared to mice treated with LPS alone, mice treated with NTCU plus LPS showed significantly increased expression of the inflammatory cytokines IL-1α, IL-6, and TNFα (all three increased about 7-fold). Parallel to the increased cytokine gene expression, the NTCU plus LPS-treated group exhibited significantly enhanced activation of NF-κB, STAT3, ERK, p-38, and Akt, expression of p53, COX-2, and Mcl-1, and NF-κB- and STAT3-DNA binding in the lung. Dietary administration of DIM (10 µmol/g diet or 2460 ppm) to mice treated with NTCU plus LPS reduced the incidence of LSCC by 2-fold, suppressed activation/expression of proinflammatory and procarcinogenic proteins and NF-κB- and STAT3-DNA binding, but not the expression of cytokines and p53. This study highlights the potential significance of our mouse model to identify promising drugs or dietary agents for the chemoprevention of human LSCC and that DIM is a very good candidate for clinical lung cancer chemoprevention trials.

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Section: Discussionmentioning

confidence: 52%

Section: Introductionmentioning

confidence: 99%

Dietary Diindolylmethane Suppresses Inflammation-Driven Lung Squamous Cell Carcinoma in Mice

Song

Qian

Teferi

et al. 2015

Cancer Prevention Research

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“…However, this contention can be challenged on two fronts. Firstly, the levels of circulating bacterial endotoxin were comparable in HIV-infected smokers and nonsmokers [54], and secondly, as mentioned earlier, endotoxin is present in both tobacco and tobacco smoke [46,47].…”

Section: Cumulative Effects Of Hiv Infection and Smoking On Immunitymentioning

confidence: 60%

“…These include various hydrocarbons, gases, highly reactive free radicals and heavy metals [45]. Tobacco also contains various pro-inflammatory microbial products, including bacterial endotoxin, which remain biologically active in cigarette smoke, albeit at a lower level [46,47]. Prolonged exposure to the cytotoxic and pro-inflammatory agents in cigarette smoke results in chronic inflammation, oxidative stress and immunosuppression, increasing susceptibility to respiratory infection, particularly with the bacterial pathogens, Streptococcus pneumoniae and Mycobacterium tuberculosis [45].…”

Section: Smoking and Immunitymentioning

confidence: 99%

Impact of HIV infection and smoking on lung immunity and related disorders

2015

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HIV-infected persons not only have higher rates of smoking than the general population, but are also unusually vulnerable to the associated adverse health effects, both infective and noninfective in origin. Indeed, in the setting of well-organised care and availability of highly active antiretroviral therapy, HIV-infected smokers lose more life-years to smoking than to HIV infection per se, presenting a major challenge to healthcare providers. Not surprisingly, the respiratory system is particularly susceptible to the damaging interactive chronic inflammatory and immunosuppressive effects of HIV and smoking, intensifying the risk of the development of opportunistic infections, as well as lung cancer and obstructive lung disorders. The impact of smoking on the immunopathogenesis and frequencies of these respiratory conditions in the setting of HIV infection, as well as on the efficacy of antiretroviral therapy, represent the primary focus of this review. @ERSpublications Smoking exacerbates the immunosuppressive/pro-inflammatory effects of HIV, increasing the risk of pulmonary disease

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“…This is an orphan receptor involved in the homing of effector, pro-inflammatory Th1 and Th17 cells to the colon [64]. Although altered expression in the lungs of smokers has not yet been described, it is noteworthy that increased expression of GPR15 has been detected on circulating neutrophils and monocytes fom RA patients, as well as on CD14 + /CD68 + dual-positive synovial macrophages [65]  chronic inhalation of highly pro-inflammatory bacterial endotoxin, which is present in cured tobacco and remains biologically active, albeit at a lower level, in cigarette smoke [66,67]. Leakage from the lungs may explain the increased levels of endotoxin present in the blood of "healthy" smokers [68], and possibly the joints of RA patients who smoke [5,6].…”

Section: Pro-inflammatory Effects Of Smokingmentioning

confidence: 99%

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Anderson

Meyer

Ally

et al. 2016

NICTOB

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Smoking is now well recognised not only as a risk factor for rheumatoid arthritis (RA), but also as a determinant of disease activity, severity, response to therapy, and possibly mortality. Recent studies have provided significant insights into the molecular and cellular mechanisms which underpin the pathogenesis of smokingrelated RA. These involve release of the enzymes, peptidylarginine deiminases (PADs) 2 and 4 from smoke-activated, resident and infiltrating pulmonary phagocytes. PADs, in turn, mediate the conversion of various endogenous proteins to putative citrullinated autoantigens. In genetically susceptible individuals, these autoantigens trigger the production of anti-citrullinated peptide/protein pathogenic autoantibodies (ACPA), an event which precedes the development of RA. This review is focused primarily on smoking-mediated harmful chronic inflammatory responses, both local and systemic, which promote the formation of ACPA, as well as the possible involvement of other types of outdoor and indoor pollution in the pathogenesis of RA. This is preceded by a brief overview of the evidence implicating smoking as a risk factor for development of ACPA-positive RA.Keywords: Anti-citrullinated peptide/protein antibodies; airway microbiota; atmospheric pollution; heavy metals; peptidylarginine deiminases; smoking cessation strategies. ImplicationsChronic inflammatory mechanisms operative in the lungs of smokers lead to the production of anti-citrullinated protein antibodies which, in turn, drive the development of rheumatoid arthritis. These mechanistic insights not only reinforce the association between smoking and risk for rheumatoid arthritis, but also the necessity to increase the level of awareness in those at highest risk.

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Microbiological components in mainstream and sidestream cigarette smoke

Cited by 33 publications

References 22 publications

Dietary Diindolylmethane Suppresses Inflammation-Driven Lung Squamous Cell Carcinoma in Mice

Dietary Diindolylmethane Suppresses Inflammation-Driven Lung Squamous Cell Carcinoma in Mice

Impact of HIV infection and smoking on lung immunity and related disorders

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

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