Accumulation of Dendritic Cells and Increased CCL20 Levels in the Airways of Patients with Chronic Obstructive Pulmonary Disease

Demedts, Ingel K.; Bracke, Ken R.; Pottelberge, Geert Van; Testelmans, Dries; Verleden, Geert M.; Vermassen, Frank; Joos, Guy; Brusselle, Guy

doi:10.1164/rccm.200608-1113oc

Cited by 211 publications

(205 citation statements)

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“…Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by persistent airway inflammation associated with irreversible airflow limitation, excessive mucus production, and progressive decline in lung function (Barnes, 2003). The chronically inflamed airways of COPD patients contain several inflammatory cells including neutrophils, macrophages, B and T lymphocytes, and DCs (Barnes, 2003;Demedts et al, 2007;Turato et al, 2002). The relative contributions of these various inflammatory cells to airway injury and remodeling are not entirely clear.…”

Section: Discussionmentioning

confidence: 99%

“…Lung DCs are distributed in sub and intra-epithelial regions of the airways, where neutrophilic influx occurs in COPD (Demedts et al, 2007). To determine whether cigarette smoke induces neutrophilic chemokine production from DCs, human monocyte-derived DCs were incubated with CSE, in the presence or absence of either 100ng/ml LPS, or 1µg/ ml recombinant human CD40L as maturational agents.…”

Section: Cigarette Smoke Extract Stimulates Cxcl8 Release From Immatumentioning

confidence: 99%

“…The chronically inflamed airways of COPD patients contain several inflammatory cells that persist even in the absence of overt infection (Barnes, 2003). Among the cells know to infiltrate and persist in the lungs of COPD patients are neutrophils, macrophages, B and T lymphocytes, and dendritic cells (DCs) (Barnes, 2003;Demedts et al, 2007). The specific triggers that lead to recruitment and retention of these inflammatory cells are not entirely clear.…”

Section: Introductionmentioning

confidence: 99%

“…A recent study described significant increase in DC numbers in the small airways of patients with COPD, and found a positive correlation between DC infiltration and disease severity, suggesting a direct pathogenic role for these cells in the COPD lung (Demedts et al, 2007). Potential mechanisms by which DCs may participate in the chronic airway inflammation in COPD are not well understood.…”

Section: Introductionmentioning

confidence: 99%

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Nicotine and oxidative cigarette smoke constituents induce immune-modulatory and pro-inflammatory dendritic cell responses

Vassallo

Kroening

Parambil

et al. 2008

Molecular Immunology

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Chronic airway inflammation is a cardinal feature of chronic obstructive pulmonary disease (COPD), a destructive cigarette smoke-induced lung disease. Although it is apparent that dendritic cells (DCs) are an important constituent of the chronic inflammatory cell influx found in airways of COPD patients, the functional roles of DCs in the pathogenesis of smoking-induced emphysema are unknown. We postulated that DCs activated by cigarette smoke constituents directly participate in the chronic inflammation that characterizes COPD airways. Concordant with this hypothesis, we observed that incubation of DCs with cigarette smoke extract (CSE), and chronic exposure of mice to cigarette smoke, both augmented the generation of neutrophilic chemokines by immature and lipopolysaccharide (LPS) or CD40L-matured DCs. The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the antioxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation. Cigarette smoke extract and nicotine also augment the production of secreted prostaglandin E 2 and intracellular cyclooxygenase-2 (COX-2) in maturing DCs. Whereas NAC suppressed production of CXCL8 by CSEconditioned DCs, it augmented production of PGE 2 and cellular COX-2 levels in maturing DCs. These studies indicate that the stimulation of DCs by cigarette smoke-induced oxidative stress and nicotine promote the generation of pro-inflammatory responses that promote chronic inflammation in smokers. Certain pharmacologic strategies such as anti-oxidant therapy may be only partially effective in mitigating cigarette smoke-induced pro-inflammatory DC-mediated responses in smokers.

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Section: Discussionmentioning

confidence: 99%

Section: Cigarette Smoke Extract Stimulates Cxcl8 Release From Immatumentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Nicotine and oxidative cigarette smoke constituents induce immune-modulatory and pro-inflammatory dendritic cell responses

Vassallo

Kroening

Parambil

et al. 2008

Molecular Immunology

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“…While some reports demonstrate an increase in mature dendritic cell numbers in the lungs associated with COPD, others show that DC numbers are decreased and have a diminished T cell stimulatory capacity (24)(25)(26)(27)(28). Such discrepencies likely reflect differences in terms of markers used to detect DC subsets as well as analysis of DC subsets from either whole lung tissue, bronchoalveolar lavage or immunohistochemistry on specific tissue sections such as the small airways.…”

Section: Dendritic Cellsmentioning

confidence: 99%

Chronic Obstructive Pulmonary Disease: Evidence for an Autoimmune Component

Stefańska

Walsh

2009

Cell Mol Immunol

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Chronic obstructive pulmonary disease (COPD) is characterized by an irreversible limitation on pulmonary airflow associated with chronic inflammation and mucous hypersecretion (chronic bronchitis) and/or the pathological destruction of alveolar airspaces leading to emphysema. COPD, predominantly as a result of tobacco smoke exposure, represents the fourth leading cause of mortality worldwide and its prevalence is increasing. Despite this, much of the basic mechanisms which contribute to disease progression remain to be elucidated and current therapeutic approaches are, for the most part, based upon alleviating patient symptoms (bronchodilators) as opposed to treating the underlying pathological mechanisms triggered in response to cigarette smoke exposure. The classic disease paradigm suggests that an imbalance of pulmonary matrix proteases versus anti-proteases underlies the tissue destruction and inflammation associated with COPD. However, there is a growing appreciation of the complex and multifaceted nature of the pathological mechanisms associated with disease progression. Recently, there has been mounting evidence indicating that COPD patients exhibit many of the characteristics of a classical autoimmune response. We will discuss current evidence in support of this paradigm and outline how future therapeutic approaches may be tailored to address this. Cellular & Molecular Immunology. 2009;6(2):81-86.

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Novel Anti‐Inflammatory Treatments for Asthma and COPD

Kirkham

Caramori

Chung

et al. 2012

Advances in Combination Therapy for Asthma and COPD

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Accumulation of Dendritic Cells and Increased CCL20 Levels in the Airways of Patients with Chronic Obstructive Pulmonary Disease

Abstract: This is the first description of airway infiltration by DC in COPD. Moreover, interaction between CCL20 and CCR6 provides a possible mechanism for accumulation of DC in the lungs in COPD.

Cited by 211 publications

References 50 publications

Nicotine and oxidative cigarette smoke constituents induce immune-modulatory and pro-inflammatory dendritic cell responses

Nicotine and oxidative cigarette smoke constituents induce immune-modulatory and pro-inflammatory dendritic cell responses

Chronic Obstructive Pulmonary Disease: Evidence for an Autoimmune Component

Novel Anti‐Inflammatory Treatments for Asthma and COPD

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