Induction of cyclooxygenase‐2 protein by lipoteichoic acid from <i>Staphylococcus aureus</i> in human pulmonary epithelial cells: involvement of a nuclear factor‐κB‐dependent pathway

Lin, Chien Huang; Kuan, I-Hui; Lee, Horng-Mo; Lee, Wen-Sen; Sheu, Joen‐Rong; Ho, Yuan‐Soon; Wang, Chun Hua; Kuo, Han‐Pin

doi:10.1038/sj.bjp.0704290

Cited by 55 publications

(34 citation statements)

References 41 publications

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“…We also provide data supporting a role for NF-B regulation of COX-2 expression in airway smooth muscle cells that has not been previously reported using this cytokine stimulus. In human lung alveolar epithelial cells and epithelial cell lines, COX-2 expression was found to be mediated by NF-B-dependent signaling pathways (5,18). However, in other studies of airway smooth muscle, lung epithelial cells, and vascular smooth muscle, a role for NF-B in COX-2 expression was not found (6,16,24).…”

Section: Discussionmentioning

confidence: 80%

p38 MAPK and NF-κB mediate COX-2 expression in human airway myocytes

Singer¹,

Baker²,

McCaffrey³

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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We have previously demonstrated that p38 and extracellular signal-regulated protein kinase (ERK) mitogen-activated protein kinases (MAPK) are components of proinflammatory induced cytokine expression in human airway myocytes. The experiments described here further these studies by examining p38 MAPK and NF-κB regulation of cyclooxygenase-2 (COX-2) expression in response to a complex inflammatory stimulus consisting of 10 ng/ml interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), and interferon (IFN)-γ. COX-2 expression was induced with this stimulus in a time-dependent manner, with maximal expression seen 12-20 h after treatment. Semiquantitative RT-PCR and immunoblotting experiments demonstrate decreased COX-2 expression following treatment with the p38 MAPK inhibitor SB-203580 (25 μM) or the proteosome inhibitor MG-132 (1 μM). SB-203580 did not affect cytokine-stimulated IκBα degradation, NF-κB nuclear binding activity, or NF-κB-dependent signaling from the COX-2 promoter, indicating that p38 MAPK and NF-κB may affect COX-2 expression via separate signaling pathways. SB-203580, but not MG-132, also increased the initial rate of COX-2 mRNA decay, indicating p38 MAPK, but not NF-κB, participates in the regulation of COX-2 mRNA stability. These findings suggest that although p38 MAPK and NF-κB signaling regulate steady-state levels of COX-2 expression, p38 MAPK additionally affects stability of COX-2 mRNA in cytokine-stimulated human airway myocytes.

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Section: Discussionmentioning

confidence: 80%

p38 MAPK and NF-κB mediate COX-2 expression in human airway myocytes

Singer¹,

Baker²,

McCaffrey³

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Candida albicans was found to upregulate cyclooxygenase (COX)-2 through activation of PKC in epithelial cells [47]. Moreover, pathogen-related expression of COX-2 in Helicobacter pylori-or Staphylococcus aureus-infected epithelial cells was shown to be mediated by PKC activation [48,49]. The current authors recently demonstrated that COX-2 expression and subsequent PGE 2 -synthesis induced by Legionella neumophila infection of the alveolar epithelial cell line A549 was reliant on PKCa and NF-kB activation in lung epithelial cells [28].…”

Section: Pkc Regulates M Catarrhalis-induced Il-8 Release H Slevogtmentioning

confidence: 99%

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

Slevogt

Maqami²,

Vardarowa³

et al. 2008

European Respiratory Journal

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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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“…Prostaglandins are synthesized by two isoforms of cyclooxygenases (COX, also named PTGS for "prostaglandinendoperoxide synthases"): COX-1 is a constitutive isoform that maintains cellular homeostasis, whereas COX-2 is an inducible isoform regulated by many proinflammatory stimuli (31). COX-1/2 transform arachidonic acid into prostaglandin H 2 , a precursor of many prostaglandins such as prostaglandin E 2 (PGE 2 ), prostacyclin, and thromboxanes.…”

Section: Ease Analysismentioning

confidence: 99%