Pathogenesis and Treatment of Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Sethi, Sanjay

doi:10.1055/s-2005-869538

Cited by 21 publications

(10 citation statements)

References 58 publications

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“…Whether the presence of these organisms represents innocent colonization or low-grade infection causing tissue damage is a matter of debate. There are some data that change in strain type of Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae , and Pseudomonas aeruginosa may cause exacerbations of COPD, 64 and numerous bacteria and viruses have been isolated from sputum during COPD exacerbations, 65–67 supporting their role in at least disease activity.…”

Section: Influences Of Cigarette Smokingmentioning

confidence: 99%

Pathogenesis of Inflammation and Repair in Advanced COPD

Cornwell

Kim

Song

et al. 2010

Semin Respir Crit Care Med

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Chronic obstructive pulmonary disease is characterized by an abnormal persistent inflammatory response to noxious environmental stimuli, most commonly cigarette smoke. Although cigarette smoking elicits airway inflammation in all of those who smoke, persistent inflammation and clinically significant COPD occurs in only a minority of smokers. The pathogenesis of COPD involves the recruitment and regulation of neutrophils, macrophages, and lymphocytes to the lung, as well as the induction of oxidative stress, all of which result in lung parenchymal destruction and airway remodeling. Recent research has generated a greater understanding of the mechanisms responsible for COPD development, including new concepts in T cell biology and the increasing recognition that the processes governing lung cell apoptosis are upregulated. We are also starting to understand the reasons for continued inflammation even after smoking cessation, which accelerates the rate of lung function decline in COPD. Herein we review our current knowledge of the inflammatory pathways involved in COPD pathogenesis, as well as newer concepts that have begun to unfold in recent years.

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Section: Influences Of Cigarette Smokingmentioning

confidence: 99%

Pathogenesis of Inflammation and Repair in Advanced COPD

Cornwell

Kim

Song

et al. 2010

Semin Respir Crit Care Med

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“…Disease progression is characterised by frequent acute exacerbations caused by bacterial or viral infection [1][2][3]. Although many studies support the causative role of Haemophilus influenzae and Streptococcus pneumoniae in the pathogenesis of COPD [2,4], Moraxella catarrhalis was widely ignored for decades because this pathogen was considered to be an irrelevant saprophyte of the upper respiratory tract [5].…”

mentioning

confidence: 99%

Moraxella catarrhalis induces ERK- and NF- B-dependent COX-2 and prostaglandin E2 in lung epithelium

N′Guessan

Temmesfeld-Wollbrück²,

Zahlten³

et al. 2007

European Respiratory Journal

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Moraxella catarrhalis is a major cause of infectious exacerbations of chronic obstructive lung disease. Cyclooxygenase (COX)-derived prostaglandins, such as prostaglandin E 2 (PGE 2 ), are considered to be important regulators of lung function. The present authors tested the hypothesis that M. catarrhalis induces COX-2-dependent PGE 2 production in pulmonary epithelial cells.In the present study, the authors demonstrate that M. catarrhalis specifically induces COX-2 expression and subsequent PGE 2 release in pulmonary epithelial cells. Furthermore, the prostanoid receptor subtypes EP2 and EP4 were also upregulated in these cells.The M. catarrhalis-specific ubiquitous cell surface protein A1 was important for the induction of COX-2 and PGE 2 . Moreover, M. catarrhalis-induced COX-2 and PGE 2 expression was dependent on extracellular signal-regulated kinase 1/2-driven activation of nuclear factor-kB, but not on the activation of p38 mitogen-activated protein kinase.In conclusion, the present data suggest that ubiquitous cell surface protein A1 of Moraxella catarrhalis, extracellular signal-regulated kinase 1/2 and nuclear factor-kB control cyclooxygenase-2 expression and subsequent prostaglandin E 2 release by lung epithelial cells. Moraxella catarrhalis-induced prostaglandin E 2 expression might counteract lung inflammation promoting colonisation of the respiratory tract in chronic obstructive pulmonary disease patients.

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“…Among them, important mediators involved in the recruitment and activation of leucocytes are interleukin 8 (IL-8) and granulocyte-macrophage colony stimulating factor (GM-CSF), suggesting that these mediators may play an important role in the pathogenesis of the disease (2,4). Bronchial epithelial cells contribute significantly to the orchestration of the immune response through release of a variety of inflammatory chemokines such as IL-8 and GM-CSF (4,37), thereby inducing COPD-characteristic alteration such as chronic bronchial inflammation and air flow limitation (7,36). Transcriptional regulation of inflammatory genes is achieved by a variety of complex signal transduction pathways involving the mitogen-activated protein (MAP) kinases, extracellular signalregulated kinase (ERK), c-Jun kinase (JNK), and p38 MAP kinase and the transcription factor NF-B, which is particularly strongly activated in epithelial cells of COPD (4,7,8).…”

mentioning

confidence: 99%

Moraxella catarrhalisinduces inflammatory response of bronchial epithelial cells via MAPK and NF-κB activation and histone deacetylase activity reduction

Slevogt

Schmeck²,

Jonatat³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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(COPD) and may also contribute to the pathogenesis of COPD. Little is known about M. catarrhalis-bronchial epithelium interaction. We investigated activation of M. catarrhalis infected bronchial epithelial cells and characterized the signal transduction pathways. Moreover, we tested the hypothesis that the M. catarrhalis-induced cytokine expression is regulated by acetylation of histone residues and controlled by histone deacetylase activity (HDAC). We demonstrated that M. catarrhalis induced a strong time-and dose-dependent inflammatory response in the bronchial epithelial cell line (BEAS-2B), characterized by the release of IL-8 and GM-CSF. For this cytokine liberation activation of the ERK and p38 mitogen-activated protein (MAP) kinases and transcription factor NF-B was required. Furthermore, M. catarrhalis-infected bronchial epithelial cells showed an enhanced acetylation of histone H3 and H4 globally and at the promoter of the il8 gene. Preventing histone deacetylation by the histone deacetylase inhibitor trichostatin A augmented the M. catarrhalis-induced IL-8 response. After exposure to M. catarrhalis, we found a decrease in global histone deacetylase expression and activity. Our findings suggest that M. catarrhalisinduced activation of il8 gene transcription was caused by interference with epigenetic mechanisms regulating il8 gene accessibility. Our findings provide insight into important molecular and cellular mechanisms of M. catarrhalis-induced activation of human bronchial epithelium. chronic obstructive pulmonary disease; bronchial epithelium; immune response; mitogen-activated protein kinase; nuclear factor-B

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Pathogenesis and Treatment of Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Cited by 21 publications

References 58 publications

Pathogenesis of Inflammation and Repair in Advanced COPD

Pathogenesis of Inflammation and Repair in Advanced COPD

Moraxella catarrhalis induces ERK- and NF- B-dependent COX-2 and prostaglandin E2 in lung epithelium

Moraxella catarrhalisinduces inflammatory response of bronchial epithelial cells via MAPK and NF-κB activation and histone deacetylase activity reduction

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