Elevated expression of TARC (CCL17) and MDC (CCL22) in models of cigarette smoke-induced pulmonary inflammation

Ritter, Mirko; Göggel, Rolf; Chaudhary, Nveed; Wiedenmann, Alexander; Jung, Birgit; Weith, Andreas; Seither, Peter

doi:10.1016/j.bbrc.2005.06.084

Cited by 54 publications

(41 citation statements)

References 27 publications

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“…In spite of these elevated chemoattractants, the authors observed no increase in Th2 cell migration to smoke-exposed rat lungs. 161 These findings may also help explain earlier data of Goel et al in which reformed smokers showed significantly greater airways obstruction than current smokers. 120 It may be that after cessation of smoking, the suppression of T cell function is relieved, permitting restoration of either or both of the Th1 inflammatory and Th2 sensitization inflammatory responses.…”

Section: Toxicological Consequences Of Metallo-particle Inhalation Spsupporting

confidence: 80%

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

2011

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Biochemically and pathologically, there is strong evidence for both atopic and nonatopic airway sensitization, hyperresponsiveness, and inflammation as a consequence of exposure to tobacco mainstream or sidestream smoke particulate. There is growing evidence for the relation between exposure to mainstream and sidestream smoke and diseases resulting from reactive oxidant challenge and inflammation directly as a consequence of the combined activity of neutrophils, macrophages, dendritic cells, eosinophils, basophils, as a humoral immunological consequence of sensitization, and that the metal components of the particulate play a role in adjuvant effects. As an end consequence, carcinogenicity is a known outcome of chronic inflammation.Smokeless tobacco has been evaluated by the IARC as a group 1 carcinogen. Of the many harmful constituents in smokeless tobacco, oral tissue metallothionein gradients suggest that metals contribute to the toxicity from smokeless tobacco use and possibly sensitization.This work reviews and examines work on probable contributions of toxic metals from tobacco and smoke to pathology observed as a consequence of smoking and the use of smokeless tobacco. Metals and metalloids in tobaccoThough exposure to substances from tobacco use is obviously a complex exposure, the carcinogens in tobacco smoke have been classified for health risk determinations into five major chemical classes. 1 Some of these have been carefully studied, contributing to a strong weight of evidence for associated health risks. 2 Toxic metals and metalloids constitute one of the more understudied major carcinogenic chemical classes in smokeless tobacco products and tobacco smoke. Eight of the top forty substances in the Fowles and Dybing table of cancer risk indices are metals or metalloid compounds. 1 In their table of non-cancer risk indices for individual chemical constituents of mainstream cigarette smoke based on a single cigarette per day, three of the top eight listed for respiratory effect health risk, cadmium, hexavalent chromium, and nickel, were metals. Another metalloid, silicon in the form of silicates, poses serious health risks by inhalation, but limited data is available, likely due to analytical difficulties.Metals and metalloids in smoke from biomass combustion including tobacco are generally considered to be present in ionic form, but may also occur in a gaseous elemental form, as is the case for mercury. 3 Whether a tobacco product is consumed by smoking or in a smokeless form, the exposure to toxic metals is directly related to the concentration in the tobacco leaf, assuming no metal containing additives are included during manufacture. [4][5][6] The soil (including any amendments to the soil such as sludge, fertilizers, or irrigation with

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Section: Toxicological Consequences Of Metallo-particle Inhalation Spsupporting

confidence: 80%

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

2011

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“…Our data suggest that cigarette smoking also increases bronchial mucosal expression of TSLP at least at the level of mRNA. Similarly, pulmonary expression of TARC/CCL17 and MDC/CCL22, two chemokines strongly induced in dendritic cells by TSLP, was selectively elevated in an animal model of chronic cigarette smoke exposure (33), consistent with the hypothesis that smoke inhalation is a stimulus to TSLP production. Endogenous cytokines, particularly TNF-␣ and IL-1␤ and particularly acting in synergy with Th2-type cytokines such as IL-4 and IL-13 can induce TSLP in bronchial (22,32) and skin (34) epithelium.…”

Section: Discussionsupporting

confidence: 64%

Expression and Cellular Provenance of Thymic Stromal Lymphopoietin and Chemokines in Patients with Severe Asthma and Chronic Obstructive Pulmonary Disease

Ying

O’Connor

Ratoff

et al. 2008

The Journal of Immunology

334

149

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Asthma and chronic obstructive pulmonary disease (COPD) are associated with Th2 and Th1 differentiated T cells. The cytokine thymic stromal lymphopoietin (TSLP) promotes differentiation of Th2 T cells and secretion of chemokines which preferentially attract them. We hypothesized that there is distinct airways expression of TSLP and chemokines which preferentially attract Th1- and Th2-type T cells, and influx of T cells bearing their receptors in asthma and COPD. In situ hybridization, immunohistochemistry, and ELISA were used to examine the expression and cellular provenance of TSLP, Th2-attracting (TARC/CCL17, MDC/CCL22, I-309/CCL1), and Th1-attracting (IP-10/CXCL10, I-TAC/CXCL11) chemokines in the bronchial mucosa and bronchoalveolar lavage fluid of subjects with moderate/severe asthma, COPD, and controls. Cells expressing mRNA encoding TSLP, TARC/CCL17, MDC/CCL22, and IP-10/CXCL10, but not I-TAC/CXCL11 and I-309/CCL1, were significantly increased in severe asthma and COPD as compared with non-smoker controls (p < 0.02). This pattern was reflected in bronchoalveolar lavage fluid protein concentrations. Expression of the same chemokines was also increased in ex- and current smokers. The cellular sources of TSLP and chemokines were strikingly similar in severe asthma and COPD. The numbers of total bronchial mucosal T cells expressing the chemokine receptors CCR4, CCR8, and CXCR3 did not significantly differ in asthma, COPD, and controls. Both asthma and COPD are associated with elevated bronchial mucosal expression of TSLP and the same Th1- and Th2-attracting chemokines. Increased expression of these chemokines is not, however, associated with selective accumulation of T cells bearing their receptors.

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“…TSLP in epithelial cells, as well as TARC in DCs, is up-regulated with exposure to airborne pollutants, including diesel exhaust (40) and cigarette smoke extract (32). Exposure to cigarette smoke was also shown to up-regulate the expression of TARC mRNA in whole murine lungs (41). We showed here that infection with influenza upregulates the secretion of TSLP in co-cultures using NECs from smokers, but not nonsmokers, suggesting that in smokers, the activation of the TSLP pathway may occur in concert with the suppression of Th1 chemokines such as IP-10.…”

Section: Discussionmentioning

confidence: 95%

Epithelial Cells from Smokers Modify Dendritic Cell Responses in the Context of Influenza Infection

Horvath

Brighton²,

Zhang³

et al. 2011

Am J Respir Cell Mol Biol

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Elevated expression of TARC (CCL17) and MDC (CCL22) in models of cigarette smoke-induced pulmonary inflammation

Cited by 54 publications

References 27 publications

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

Toxic elements in tobacco and in cigarette smoke: inflammation and sensitization

Expression and Cellular Provenance of Thymic Stromal Lymphopoietin and Chemokines in Patients with Severe Asthma and Chronic Obstructive Pulmonary Disease

Epithelial Cells from Smokers Modify Dendritic Cell Responses in the Context of Influenza Infection

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