Toll-like receptor-4 mediates cigarette smoke-induced cytokine production by human macrophages

Karimi, Khalil; Sarir, Hadi; Mortaz, Esmaeil; Smit, Joost J.; Hosseini, Hossein Mirseyed; Kimpe, Sjef J. De; Nijkamp, Frans P.; Folkerts, Gert

doi:10.1186/1465-9921-7-66

Cited by 134 publications

(115 citation statements)

References 46 publications

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“…64 It has been recently shown that neutralization of TLR4 with anti-human TLR4 antibody significantly blocked CSE-mediated proinflammatory mediator release by human macrophages. 48 Furthermore, NF-B activation induced by CSE was also attenuated in human macrophages pretreated with anti-human TLR4 antibody. 48 Moreover, subacute (5 weeks) and chronic (26 weeks) CS exposure resulted in increased pulmonary expression of TLR4 in WT mice, and targeted disruption of TLR4 protected against acute and chronic CS-induced lung inflammatory response.…”

Section: Discussionmentioning

confidence: 90%

“…48 Furthermore, NF-B activation induced by CSE was also attenuated in human macrophages pretreated with anti-human TLR4 antibody. 48 Moreover, subacute (5 weeks) and chronic (26 weeks) CS exposure resulted in increased pulmonary expression of TLR4 in WT mice, and targeted disruption of TLR4 protected against acute and chronic CS-induced lung inflammatory response. 47,65 Therefore, the TLR4-NF-B signal pathway plays an important role in CS-mediated lung inflammatory response.…”

Section: Discussionmentioning

confidence: 90%

“…47,48 We therefore determined whether genetic ablation of p47 phox and gp91 phox alters the levels of TLR4 mRNA and protein in the lung in response to CS exposure. We used a sensitive real-time RT-PCR approach to quantify the changes in TLR4 mRNA levels in the lung.…”

Section: Increased Levels Of Tlr4 Mrna and Protein In Lungs Of P47 Phmentioning

confidence: 99%

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Genetic Ablation of NADPH Oxidase Enhances Susceptibility to Cigarette Smoke-Induced Lung Inflammation and Emphysema in Mice

Yao

Edirisinghe

Yang

et al. 2008

The American Journal of Pathology

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Cigarette smoke (CS) induces recruitment of inflammatory cells in the lungs leading to the generation of reactive oxygen species (ROS), which are involved in lung inflammation and injury. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is a multimeric system that is responsible for ROS production in mammalian cells. We hypothesized that NADPH oxidase-derived ROS play an important role in lung inflammation and injury and that targeted ablation of components of NADPH oxidase (p47 phox and gp91 phox ) would protect lungs against the detrimental effects of CS. To test this hypothesis, we exposed p47 phox؊/؊ and gp91 phox؊/؊ mice to CS and examined inflammatory response and injury in the lung. Surprisingly, although CS-induced ROS production was decreased in the lungs of p47 phox؊/؊ and gp91 phox؊/؊ mice compared with wild-type mice, the inflammatory response was significantly increased and was accompanied by development of distal airspace enlargement and alveolar destruction. This pathological abnormality was associated with enhanced activation of the TLR4-nuclear factor-B pathway in response to CS exposure in p47 phox؊/؊ and gp91 phox؊/؊ mice. This phenomenon was confirmed by in vitro studies in which treatment of peritoneal macrophages with a nuclear factor-B inhibitor reversed the CS-induced release of proinflammatory mediators. Thus, these data suggest that genetic ablation of components of NADPH oxidase enhances susceptibility to the proinflammatory effects of CS leading to airspace enlargement and alveolar damage.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 90%

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Genetic Ablation of NADPH Oxidase Enhances Susceptibility to Cigarette Smoke-Induced Lung Inflammation and Emphysema in Mice

Yao

Edirisinghe

Yang

et al. 2008

The American Journal of Pathology

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“…19) Furthermore, it was also reported that smokers have increased levels of several inflammatory biomarkers. 20,21) It is thus quite probable that smoking induces inflammation, an atherogenic lipid profile, and a propensity to thrombosis, thereby promoting the development of coronary atherothrombosis.…”

Section: Discussionmentioning

confidence: 99%

<b>The Etiology of ‘Smoker’s Paradox’ in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>

Katayama¹,

Iwasaki²,

Sakoda³

et al. 2008

Int. Heart J.

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SUMMARYDespite increased risk for coronary artery disease and acute myocardial infarction (AMI), prior studies have found that smokers with AMI have lower mortality rates than nonsmokers, a phenomenon often termed 'smoker's paradox'. The present study was designed to examine the etiology of 'smoker's paradox', especially with respect to the association with inflammation.The subjects included 528 consecutive AMI patients who were admitted within 24 hours of onset and underwent successful coronary intervention. Of the 528 subjects, 232 (44%) were smokers.The cardiac mortality rates over a 6 month period was significantly lower in the smoking group than the nonsmoking group (3% versus 9%, P = 0.01). There were significantly more male patients in the smoking group, and the smoking group was significantly younger than the nonsmoking group (P < 0.0001). The value of high sensitivity C-reactive protein (hs-CRP) on admission and 24 hours after onset, and serum amyloid A protein (SAA) were significantly higher, and acute phase BNP was significantly lower (hs-CRP on admission 1.36 ± 1.03 mg/dL versus 0.75 ± 0.82 mg/dL, P = 0.02, hs-CRP at 24 hours 3.86 ± 4.32 mg/dL versus 2.90 ± 3.46 mg/dL, P = 0.008, SAA; 288 ± 392 µg/dL versus 176 ± 206 µg/dL, P < 0.05, BNP; 248 ± 342 pg/mL versus 444 ± 496 pg/mL, P = 0.0002) in the smoking group than in the nonsmoking group. The early ST-segment resolution rate was higher in the smoking group compared with the nonsmoking group (80% versus 66%, P = 0.003).The reason why smokers with AMI have lower mortality rates than nonsmokers, the so-called 'smoker's paradox', is believed to be because smoking induces inflammation and smokers may have less damage to microvascular function after primary percutaneous coronary intervention. (Int Heart J 2008; 49: 13-24) Key words: Myocardial infarction, Smoking, Inflammation EVEN though many epidemiologic studies have shown that cigarette smoking is associated with higher rates of myocardial infarction and death from coronary From the

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“…Cigarette smoking is an important etiologic factor linked to the development of many diseases such as pulmonary, cardio and cerebrovascular diseases, cancers, asthma, chronic obstructive pulmonary disease (COPD) and several others JINQIANG HU, TAO WEI, SIWEN SUN, AIJING ZHAO and CHUNPING XU (Karimi et al 2006). Cigarette smoke is a complex mixture of over 4700 identified constituents that include numerous reactive substances such as a large quantity of reactive aldehydes, free radical species and diverse metals (Hecht 2006).…”

Section: Introductionmentioning

confidence: 99%

Effects of cigarette smoke condensate on the production and characterization of exopolysaccharides by Bifidobacterium

Wei

Sun

et al. 2015

An. Acad. Bras. Ciênc.

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The aim of the study was to investigate the effect of cigarette smoke on the production and characterization of exopolysaccharides (EPSs) produced by Bifidobacterium. Cigarettes of Shanhua brand (nicotine: 1.1 mg, tar: 11 mg) were utilized to prepare a cigarette smoke condensate (CSC). The standard strain of Bifidobacterium animalis was cultured in MRS media under anaerobic addition of CSC. The results showed that CSC significantly decreased the growth of B. animalis as well as EPSs and acetic acid production. Furthermore, two EPSs fractions (Fr-I and Fr-II) were isolated and purified for chemical and molecular determination. By comparison with control, CSC was found to be of great impact on EPSs carbohydrate composition. The molecular weight mass of Fr-I changed from 3.33×10 5 g/mol (without CSC) to 2.99×10 5 (with CSC). In conclusion, in vitro studies revealed that CSC was directly able to affect the production of metabolites for B. animalis, which could be an essential factor in certain pathological disorders.

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Toll-like receptor-4 mediates cigarette smoke-induced cytokine production by human macrophages

Cited by 134 publications

References 46 publications

Genetic Ablation of NADPH Oxidase Enhances Susceptibility to Cigarette Smoke-Induced Lung Inflammation and Emphysema in Mice

Genetic Ablation of NADPH Oxidase Enhances Susceptibility to Cigarette Smoke-Induced Lung Inflammation and Emphysema in Mice

<b>The Etiology of ‘Smoker’s Paradox’ in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>

Effects of cigarette smoke condensate on the production and characterization of exopolysaccharides by Bifidobacterium

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Toll-like receptor-4 mediates cigarette smoke-induced cytokine production by human macrophages

Cited by 134 publications

References 46 publications

Genetic Ablation of NADPH Oxidase Enhances Susceptibility to Cigarette Smoke-Induced Lung Inflammation and Emphysema in Mice

Genetic Ablation of NADPH Oxidase Enhances Susceptibility to Cigarette Smoke-Induced Lung Inflammation and Emphysema in Mice

<b>The Etiology of &lsquo;Smoker&rsquo;s Paradox&rsquo; in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>

Effects of cigarette smoke condensate on the production and characterization of exopolysaccharides by Bifidobacterium

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<b>The Etiology of ‘Smoker’s Paradox’ in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>