Adhesion of Moraxella catarrhalis to human bronchial epithelium characterized by a novel fluorescence-based assay

Slevogt, Hortense; Tiwari, Krishna N.; Schmeck, Bernd; Hocke, Andreas C.; Opitz, Bastian; Suttorp, Norbert; Seybold, Joachim

doi:10.1007/s00430-005-0003-9

Cited by 12 publications

(14 citation statements)

References 31 publications

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“…In addition, UspA1 targets the human CEACAM1 a member of the carcinoembryonic antigen family and the immunglobulin superfamily [29]. Recently, the present authors demonstrated that adhesion of M. catarrhalis wild-type strain O35E to BEAS-2B cells did not differ compared with the UspA1-deficient mutant [22]. Thus, the present findings suggest that the UspA1-dependent interaction to epithelial cells is essential for COX-2 expression and PGE 2 release.…”

Section: Discussionmentioning

confidence: 49%

“…It is reported herein, that COX-2 expression and PGE 2 release was dependent on UspA1 of M. catarrhalis. UspA1, an important adhesin, mediating the adherence of M. catarrhalis to human respiratory epithelial cells, has been described as being present on the surface of most M. catarrhalis disease isolates examined to date [6,9,22,28]. UspA1 is known to adhere to the epithelial cell-associated laminin and fibronectin [9].…”

Section: Discussionmentioning

confidence: 99%

“…Although M. catarrhalis efficiently infects and activates lung epithelial cells [19][20][21][22], mechanisms of M. catarrhalis-induced activation of COX-2 and PGE 2 release in lung epithelial cells are widely unknown.…”

mentioning

confidence: 99%

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Moraxella catarrhalisinduces ERK- and NF-κB-dependent COX-2 and prostaglandin E₂in lung epithelium

N′Guessan

Temmesfeld-Wollbrück²,

Zahlten³

et al. 2007

Eur Respir J

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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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Section: Discussionmentioning

confidence: 49%

Section: Discussionmentioning

confidence: 99%

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Moraxella catarrhalisinduces ERK- and NF-κB-dependent COX-2 and prostaglandin E₂in lung epithelium

N′Guessan

Temmesfeld-Wollbrück²,

Zahlten³

et al. 2007

Eur Respir J

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“…Antimicrobial supplementation for the M. catarrhalis mutant O35E.1 and O35E.2 involved kanamycin (15 mg?mL -1 ). M. catarrhalis was grown overnight at 37uC on brain-heart infusion (BHI) agar (Dibco Laboratories, BD, Heidelberg, Germany) supplemented with 5% heated sheep blood as previously described [17,25,26]. For infection experiments, single colonies of bacterial overnight cultures were expanded by resuspension in BHI broth and incubation at 37uC for 2-3 h to mid-log phase (absorbance at 405 nm 0.4-0.6).…”

Section: Bacterial Strainsmentioning

confidence: 99%

Differential regulation ofMoraxella catarrhalis-induced interleukin-8 response by protein kinase C isoforms

Slevogt

Maqami²,

Vardarowa³

et al. 2008

Eur Respir J

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Moraxella catarrhalis is a major cause of infectious exacerbations of chronic obstructive lung disease. In pulmonary epithelial cells, M. catarrhalis induces release of the proinflammatory cytokine interleukin (IL)-8, which plays a pivotal role in orchestrating airway inflammation.The present study demonstrated that protein kinase (PK)C was activated by Moraxella infection and positively regulated M. catarrhalis-triggered nuclear factor (NF)-kB activation and subsequent IL-8 release. Activation of the PKC/NF-kB signalling pathway was found to be dependent on expression of the Moraxella-specific ubiquitous surface protein A2. In addition, it was shown that specific isoforms of PKC play differential roles in the fine-tuning of the M. catarrhalis-induced NFkB-dependent gene expression through controlling il8 promoter activity. Inhibition of PKCa and e with chemical inhibitors or using short interfering RNA-mediated gene silencing significantly suppressed, whereas inhibition of PKCh increased, the M. catarrhalis-induced IL-8 transcription and cytokine release.In conclusion, it was shown that Moraxella catarrhalis infection activates protein kinase C and its isoforms a, e and h, which differentially regulate interleukin-8 transcription in human pulmonary epithelial cells.

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“…The signal intensity was enhanced by application of Alexa 488 anti-FITC antibody (1:1,000, 1 h at 37°C) and analyzed by using a Zeiss Pascal 5 confocal microscope. F-actin was visualized by being marked with Alexa 546-labeled phalloidin (1:200, 30 min) as described previously (23,38,55).…”

Section: Methodsmentioning

confidence: 99%

Legionella pneumophila-induced PKCα-, MAPK-, and NF-κB-dependent COX-2 expression in human lung epithelium

N′Guessan¹,

Etouem²,

Schmeck³

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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Legionella pneumophila causes community-and hospital-acquired pneumonia. Lung airway and alveolar epithelial cells comprise an important barrier against airborne pathogens. Cyclooxygenase (COX) and microsomal PGE2 synthase-1 (mPGES-1)-derived prostaglandins like prostaglandin E2 (PGE2) are considered as important regulators of lung function. Herein we tested the hypothesis that L. pneumophila induced COX-2 and mPGES-1-dependent PGE 2 production in pulmonary epithelial cells. Legionella induced the release of PGE2 in primary human small airway epithelial cells and A549 cells. This was accompanied by an increased expression of COX-2 and mPGES-1 as well as an increased PLA 2 activity in infected cells. Deletion of the type IV secretion system Dot/Icm did not impair Legionella-related COX-2 expression or PGE2 release in A549 cells. L. pneumophila induced the degradation of IB␣ and activated NF-B. Inhibition of IKK blocked L. pneumophila-induced PGE 2 release and COX-2 expression. We noted activation of p38 and p42/44 MAP kinase in Legionella-infected A549 cells. Moreover, membrane translocation and activation of PKC␣ was observed in infected cells. PKC␣ and p38 and p42/44 MAP kinase inhibitors reduced PGE2 release and COX-2 expression. In summary, PKC␣ and p38 and p42/44 MAP kinase controlled COX-2 expression and subsequent PGE2 release by Legionella-infected lung epithelial cells. These pathways may significantly contribute to the host response in Legionnaires' disease. alveolar epithelium; protein kinase C; prostaglandin E2; cyclooxygenase-2; phospholipase A2; microsomal PGE2 synthase-1; mitogenactivated protein kinase LEGIONELLA PNEUMOPHILA is an important causative agent of severe community-acquired pneumonia and the second most commonly detected pathogen in patients with pneumonia that are admitted to intensive care units in industrialized countries (48,61). In addition, since Legionella spp. urine antigen detection is still not routinely used in some settings, worldwide the prevalence of Legionellosis is underestimated (47,48). Approximately 15% of Legionellosis appears in community outbreaks. Although more than 40 Legionella species are known, the majority of human infections is caused by L. pneumophila serogroup 1 (57). L. pneumophila is a gramnegative, facultative intracellular pathogen of amoeba in natural and man-made aquatic environments. Infection of humans occurred after inhalation of contaminated water aerosol droplets.L. pneumophila contain an array of important virulence factors including the DotA/Icm type IV secretion system, which is important for bacteria invasion and replication in the host cell (4). For L. pneumophila pathogenesis, essential results were obtained by analyzing infection of protozoans or immune cells like macrophages (4, 40). However, although Legionella replicate efficiently within lung epithelial cells, and recent studies pointed to the lung epithelium as an important sentinel and effector of innate immunity (6,22,52,53,56), little is known of the consequences of pulmonary epit...

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Adhesion of Moraxella catarrhalis to human bronchial epithelium characterized by a novel fluorescence-based assay

Cited by 12 publications

References 31 publications

Moraxella catarrhalisinduces ERK- and NF-κB-dependent COX-2 and prostaglandin E₂in lung epithelium

Moraxella catarrhalisinduces ERK- and NF-κB-dependent COX-2 and prostaglandin E₂in lung epithelium

Differential regulation ofMoraxella catarrhalis-induced interleukin-8 response by protein kinase C isoforms

Legionella pneumophila-induced PKCα-, MAPK-, and NF-κB-dependent COX-2 expression in human lung epithelium

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Adhesion of Moraxella catarrhalis to human bronchial epithelium characterized by a novel fluorescence-based assay

Cited by 12 publications

References 31 publications

Moraxella catarrhalisinduces ERK- and NF-κB-dependent COX-2 and prostaglandin E2in lung epithelium

Moraxella catarrhalisinduces ERK- and NF-κB-dependent COX-2 and prostaglandin E2in lung epithelium

Differential regulation ofMoraxella catarrhalis-induced interleukin-8 response by protein kinase C isoforms

Legionella pneumophila-induced PKCα-, MAPK-, and NF-κB-dependent COX-2 expression in human lung epithelium

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Moraxella catarrhalisinduces ERK- and NF-κB-dependent COX-2 and prostaglandin E₂in lung epithelium

Moraxella catarrhalisinduces ERK- and NF-κB-dependent COX-2 and prostaglandin E₂in lung epithelium