Effects of Prostaglandin E<sub>2</sub>and cAMP Elevating Drugs on GM-CSF Release by Cultured Human Airway Smooth Muscle Cells

Lazzeri, Nicola; Belvisi, Maria G.; Patel, Hema J; Yacoub, Magdi H.; Chung, Kwun Bum; Mitchell, Jane A.

doi:10.1165/ajrcmb.24.1.4027

Cited by 75 publications

(58 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, other expected mediators, such as IL-6, IL-8, MIP-1a and VEGF, failed to be induced, indicating either cell-specific expression in the bronchial compartment that is not present in this model or differences in the mediator regulation in human lung tissue per se. Furthermore, it has been shown that COX-2/PGE 2 may contribute to the inflammatory control by inducing IL-10, or inhibiting GM-CSF, TNF-a, IL-12 or PDGF expression in vitro [15][16][17][18]34]. In line with these studies COX-2 inhibition led to a significant induction of PDGF [18], but only slight increases for TNF-a [16,34] and GM-CSF [15].…”

Section: Induction Of Cox-2 Metabolites By S Pneumoniaementioning

confidence: 57%

“…One of the most prominent PGs is PGE 2 , which has been shown to contribute to the inflammatory response of various cell types [15][16][17][18]. PGE 2 seems to signal through four distinct G protein-coupled E prostanoid receptors, EP 1 -EP 4 [9].…”

Section: Abstract: Alveolar Epithelial Cells Cytokines Inflammationmentioning

confidence: 99%

“…COX-2 regulation of S. pneumoniae-induced cytokine release in human lung tissue PGE 2 induction has previously been demonstrated to significantly contribute to chemo-/cytokine regulation [15][16][17][18]. Therefore, we analysed five infected human lung tissue samples for chemo-/cytokine release in the presence or absence of COX-2 inhibitor NS-398.…”

Section: Induction Of Cox-2 Metabolites By S Pneumoniaementioning

confidence: 99%

See 2 more Smart Citations

Streptococcus pneumoniae-induced regulation of cyclooxygenase-2 in human lung tissue

et al. 2012

View full text Add to dashboard Cite

The majority of cases of community-acquired pneumonia are caused by Streptococcus pneumoniae and most studies on pneumococcal host interaction are based on cell culture or animal experiments. Thus, little is known about infections in human lung tissue.Cyclooxygenase-2 and its metabolites play an important regulatory role in lung inflammation. Therefore, we established a pneumococcal infection model on human lung tissue demonstrating mitogen-activated protein kinase (MAPK)-dependent induction of cyclooxygenase-2 and its related metabolites.In addition to alveolar macrophages and the vascular endothelium, cyclooxygenase-2 was upregulated in alveolar type II but not type I epithelial cells, which was confirmed in lungs of patients suffering from acute pneumonia. Moreover, we demonstrated the expression profile of all four E prostanoid receptors at the mRNA level and showed functionality of the E prostanoid 4 receptor by cyclic adenosine monophosphate production. Additionally, in comparison to previous studies, cyclooxygenase-2/prostaglandin E 2 related pro-and anti-inflammatory mediator regulation was partly confirmed in human lung tissue after pneumococcal infection.Overall, cell type-specific and MAPK-dependent cyclooxygenase-2 expression and prostaglandin E 2 formation in human lung tissue may play an important role in the early phase of pneumococcal infections.

show abstract

Section: Induction Of Cox-2 Metabolites By S Pneumoniaementioning

confidence: 57%

Section: Abstract: Alveolar Epithelial Cells Cytokines Inflammationmentioning

confidence: 99%

Section: Induction Of Cox-2 Metabolites By S Pneumoniaementioning

confidence: 99%

See 1 more Smart Citation

Streptococcus pneumoniae-induced regulation of cyclooxygenase-2 in human lung tissue

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Histamine caused a similar increase in IL-1b-induced GM-CSF release by nonasthmatic and asthmatic ASM cells, although the change was not significant in the latter. The increase was surprising as previous studies have demonstrated that ASM cell GM-CSF release is inhibited by agents that increase intracellular cAMP [12,34]. As histamine directly increases intracellular cAMP through H2 receptors [21], it was expected to inhibit further GM-CSF release.…”

Section: Discussionmentioning

confidence: 95%

Histamine and tryptase modulate asthmatic airway smooth muscle GM-CSF and RANTES release

Chhabra¹,

Yz²,

Alkhouri³

et al. 2007

European Respiratory Journal

View full text Add to dashboard Cite

Degranulating mast cells are increased in the airway smooth muscle (ASM) of asthmatics, where they may influence ASM function. The aim of the present study was to determine whether histamine and tryptase modulate ASM cell granulocyte-macrophage colonystimulating factor (GM-CSF) and RANTES (regulated on activation, normal T-cell expressed and secreted) release and also to examine which receptors are involved in this release.Confluent, quiescent ASM cells from asthmatic and nonasthmatic donors were treated with histamine (1 mM-100 mM) with and without histamine receptor antagonist pre-treatment, or the protease-activated receptor (PAR)-2 agonists tryptase (0.5-5 nM) and SLIGKV (100 and 400 mM). The cells were then stimulated with interleukin (IL)-1b and/or tumour necrosis factor (TNF)-a (10 ng?mL -1 ) or left unstimulated for 24 h. Release of GM-CSF and RANTES was determined by ELISA and prostaglandin (PG)E 2 measured by enzyme immunoassay. Neither histamine nor tryptase induced ASM GM-CSF or RANTES secretion. However, histamine increased IL-1b-induced GM-CSF release and markedly reduced TNF-a-induced RANTES release by both asthmatic and nonasthmatic cells to a similar extent, but did not modulate PGE 2 release. All changes involved activation of the histamine H1 receptor as they were partially or fully blocked by chlorpheniramine, but not ranitidine. Tryptase, via its proteolytic activity, also potentiated GM-CSF, but not RANTES, release from asthmatic and nonasthmatic ASM cells induced by both cytokines. PAR-2 involvement in the tryptase potentiation was unlikely because SLIGKV had no effect.In conclusion, mast cells, through histamine and tryptase, may locally modulate airway smooth muscle-induced inflammation in asthma.

show abstract

“…Nötrofil ve eozinofil infiltrasyonunu inhibe ettiği, aktive T-helper hücreleri, hava yolu epitel hücreleri, bazofil ve makrofajlardan sitokin salınımını baskıladığı bulunmuştur (20,21). Ayrıca, tümör nekroz faktorü-alfa (TNF-α) ve interlökin-1beta (IL-1β) etkisiyle bronş düz kas hücrelerinden granülosit makrofaj koloni stimüle edici faktör salınımını baskılamaktadır (22). Ancak rolipramın hastalarda tolere edilemeyen bulantı ve kusmalara neden olması, yeni FDE-4 inhibitörlerinin geliş-tirilmesine yol açmıştır.…”

Section: Fde-4 Inhibitörlerinin Koah'da Etkinlik Ve Tolerabilitesini unclassified

A new alternative treatment in COPD: phosphodiesterase-4 inhibitors

Sezgı

Şenyiğit²

2011

Tuberk Toraks

View full text Add to dashboard Cite

ÖZET KOAH'da yeni tedavi seçeneği: Fosfodiesteraz-4 inhibitörleri Kronik obstrüktif akciğer hastalığı (KOAH) ilerleyici hava akımı kısıtlanması ile karakterize, zararlı gaz ve tozlara karşı abartılı inflamatuvar yanıtla ortaya çıkan bir hastalıktır. İnflamatuvar hücrelerin aktivasyonunu engelleyen oral fosfodiesteraz-4 (FDE-4) inhibitörleri son yıllarda KOAH tedavisinde yeni bir yaklaşım olarak denenmektedir. Çalışmalar FDE-4 inhibitörlerinin orta-ağır KOAH hastalarının semptomlarını, solunum fonksiyonlarını ve yaşam kalitesini düzelttiğini, akut atak sayısını azalttığını, bronşlardaki inflamasyonu baskıladığını göstermiştir. Ancak bu ilaçlar bulantı, ishal ve baş ağrısı gibi istenmeyen yan etkilere neden olmaktadır. Bu derlemede özellikle "Food and Drug Administration (FDA)" onayı almış, yeni "The Global Initiative for Chronic Obstructive Lung Disease (GOLD)" rehberinde ağır KOAH tedavisine dahil edilmiş selektif bir fosfodiesteraz inhibitörü olan roflumilast tartışılmıştır.

show abstract

Effects of Prostaglandin E₂and cAMP Elevating Drugs on GM-CSF Release by Cultured Human Airway Smooth Muscle Cells

Cited by 75 publications

References 24 publications

Streptococcus pneumoniae-induced regulation of cyclooxygenase-2 in human lung tissue

Streptococcus pneumoniae-induced regulation of cyclooxygenase-2 in human lung tissue

Histamine and tryptase modulate asthmatic airway smooth muscle GM-CSF and RANTES release

A new alternative treatment in COPD: phosphodiesterase-4 inhibitors

Contact Info

Product

Resources

About

Effects of Prostaglandin E2and cAMP Elevating Drugs on GM-CSF Release by Cultured Human Airway Smooth Muscle Cells

Cited by 75 publications

References 24 publications

Streptococcus pneumoniae-induced regulation of cyclooxygenase-2 in human lung tissue

Streptococcus pneumoniae-induced regulation of cyclooxygenase-2 in human lung tissue

Histamine and tryptase modulate asthmatic airway smooth muscle GM-CSF and RANTES release

A new alternative treatment in COPD: phosphodiesterase-4 inhibitors

Contact Info

Product

Resources

About

Effects of Prostaglandin E₂and cAMP Elevating Drugs on GM-CSF Release by Cultured Human Airway Smooth Muscle Cells