Leukotriene D<sub>4</sub>‐induced, epithelial cell‐derived transforming growth factor β1 in human bronchial smooth muscle cell proliferation

Bossé, Ynuk; Thompson, C. S.; McMahon, Stéphanie; Dubois, Claire M.; Staňková, Jana; Rola‐Pleszczynski, Marek

doi:10.1111/j.1365-2222.2007.02873.x

Cited by 45 publications

(28 citation statements)

References 59 publications

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“…Nevertheless, it is also reported that LTD 4 alone can not increase the growth of bronchial fibroblasts and smooth muscle cells, but potentiates the proliferation induced by epidermal growth factor (EGF) (30,31). This indicates that the effect of LTD 4 on cell proliferation relates to cell types and the interaction with other growth factors (32). Taking together, we consider that the angiogenic effect of LTD 4 is incomplete; it facilitates migration, while growth factors / cytokines (like VEGF and EGF) or complex interactions may regulate proliferation of endothelial cells.…”

Section: Discussionmentioning

confidence: 97%

Leukotriene D4 Stimulates the Migration but Not Proliferation of Endothelial Cells Mediated by the Cysteinyl Leukotriene CysLT1 Receptor via the Extracellular Signal-Regulated Kinase Pathway

et al. 2009

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Abstract. The actions of cysteinyl leukotrienes (CysLTs) are mediated by activating CysLT receptors, CysLT 1 , and CysLT 2 . The CysLT 1 receptor mediates vascular responses to CysLTs; however, its effect on the proliferation and migration of endothelial cells is not clarified. To determine this effect, we observed proliferation and migration in EA.hy926 cells, a human endothelial cell line, and the involvement of activation of mitogen-activated protein kinases (MAPKs). We found that LTD 4 did not affect the proliferation, but significantly stimulated the migration of endothelial cells. LTD 4 also induced the phosphorylation of extracellular signalregulated kinase (ERK) 1 / 2, but not those of p38 or JNK. The LTD 4 -induced migration and ERK1/ 2 phosphorylation were blocked by the CysLT 1 -receptor antagonist montelukast and the dual antagonist Bay u9773, but not by the CysLT 2 -receptor antagonist Bay cysLT2; the migration was also inhibited by the ERK1/ 2 inhibitor U0126. Our findings indicate that LTD 4 stimulates the CysLT 1 receptor-mediated migration of endothelial cells; this may be regulated by the ERK1/ 2 pathway.

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Section: Discussionmentioning

confidence: 97%

Leukotriene D4 Stimulates the Migration but Not Proliferation of Endothelial Cells Mediated by the Cysteinyl Leukotriene CysLT1 Receptor via the Extracellular Signal-Regulated Kinase Pathway

et al. 2009

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“…Mf in the M2 spectrum confer fibrosis and remodeling (22,41), and another effect of Cys-LTs is induction of TGFb, furin, and VEGF, leading to tissue remodeling in chronic asthma (44)(45)(46). It is tempting to speculate that the M-CSF-derived Mfs studied here, with high capacity for LTC 4 biosynthesis, may resemble pulmonary M2 cells active in allergic lung inflammation (22).…”

Section: Discussionmentioning

confidence: 98%

GM‐CSF– and M‐CSF–primed macrophages present similar resolving but distinct inflammatory lipid mediator signatures

et al. 2017

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M1 and M2 activated macrophages (Mfs) have different roles in inflammation. Because pathogens may first encounter resting cells, we investigated lipid mediator profiles prior to full activation. Human monocytes were differentiated with granulocyte Mf colony-stimulating factor (GM-CSF) or Mf colony-stimulating factor (M-CSF), which are known to prime toward M1 or M2 phenotypes, respectively. Lipid mediators released during resting conditions and produced in response to bacterial stimuli (LPS/N-formylmethionyl-leucyl-phenylalanine or peptidoglycan) were quantified by liquid chromatography-mass spectrometry. In resting conditions, both Mf phenotypes released primarily proresolving lipid mediators (prostaglandin E 2 metabolite, lipoxin A 4 , and 18-hydroxyeicosapentaenoic acid). A striking shift toward proinflammatory eicosanoids was observed when the same cells were exposed (30 min) to bacterial stimuli: M-CSF Mfs produced considerably more 5-lipoxygenase products, particularly leukotriene C 4 , potentially linked to M2 functions in asthma. Prostaglandins were formed by both Mf types. In the M-CSF cells, there was also an enhanced release of arachidonic acid and activation of cytosolic phospholipase A 2 . However, GM-CSF cells expressed higher levels of 5-lipoxygenase and 5-lipoxygenase-activating protein, and in ionophore incubations these cells also produced the highest levels of 5-hydroxyeicosatetraenoic acid. In summary, GM-CSF and M-CSF Mfs displayed similar proresolving lipid mediator formation in resting conditions but shifted toward different proinflammatory eicosanoids upon bacterial stimuli. This demonstrates that preference for specific eicosanoid pathways is primed by CSFs before full M1/M2 activation.-Lukic, A., Larssen, P., Fauland, A., Samuelsson, B., Wheelock, C. E., Gabrielsson, S., Radmark, O. GM-CSF-and M-CSF-primed macrophages present similar resolving but distinct inflammatory lipid mediator signatures. FASEB J. 31, 4370-4381 (2017). www.fasebj.orgMacrophages (Mfs) orchestrate the inflammatory process from early onset to the resolution phase (1, 2). A major issue in Mf biology is to characterize functional phenotypes, currently described as a heterogeneous spectrum of activated states, from M1 to M2 (3, 4). Stimulating factors, such as cytokines and pathogens, can induce specific phenotypes: originally IFN-g + LPS activation resulted in a proinflammatory M1 state, whereas IL-4 activation induced the alternatively activated M2 state. Polarized cells express distinct markers, such as transcription factors, cytokines, and surface markers; these are the main tools to define Mf phenotypes. A number of transcripts have been reported to differ between M1 and M2 Mfs, including mRNAs for enzymes involved in eicosanoid metabolism (5).Eicosanoids originate from arachidonic acid (AA), released from membrane phospholipids by phospholipases, typically cytosolic phospholipase A 2 (cPLA 2 ) (6). Free AA is further metabolized via 3 enzymatic pathways: lipoxygenase (LO), cyclooxygenase (COX), and cyto...

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“…It is possible that the increased cysLT production in AECs induces the secretion of TGF-b1. Leukotriene D 4 has been shown to induce TGF-b1 production in human bronchial epithelial cells (43). The production of cysLTs by latently infected AECs is likely to promote fibrosis via effects on mesenchymal cells.…”

Section: Discussionmentioning

confidence: 99%

Latent Herpesvirus Infection Augments Experimental Pulmonary Fibrosis

Vannella¹,

Luckhardt²,

Wilke³

et al. 2010

Am J Respir Crit Care Med

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Rationale: No effective treatment exists for idiopathic pulmonary fibrosis, and its pathogenesis remains unclear. Accumulating evidence implicates herpesviruses as cofactors (either initiating or exacerbating agents) of fibrotic lung disease, but a role for latent herpesvirus infection has not been studied. Objectives: To develop a murine model to determine whether latent herpesvirus infection can augment fibrotic responses and to gain insight into potential mechanisms of enhanced fibrogenesis. Methods: Mice were infected with murine gherpesvirus 14 to 70 days before a fibrotic challenge with fluorescein isothiocyanate or bleomycin so that the virus was latent at the time of fibrotic challenge. Measurements were made after viral infection alone or after the establishment of fibrosis. Measurements and Main Results: gHerpesvirus is latent by 14 days post infection, and infection 14 to 70 days before fibrotic challenge augmented fibrosis. Fibrotic augmentation was not dependent on reactivation of the latent virus to a lytic state. Total cell numbers and fibrocyte numbers were increased in the lungs of latently infected mice administered fibrotic challenge compared with mock-infected mice that received fibrotic challenge. Latent infection up-regulates expression of proinflammatory chemokines, transforming growth factor-b1, and cysteinyl leukotrienes in alveolar epithelial cells. Conclusions: Latent gherpesvirus infection augments subsequent fibrotic responses in mice. Enhanced fibrosis is associated with the induction of profibrotic factors and the recruitment of fibrocytes. Our data complement existing human and animal data supporting the hypothesis that gherpesviruses can serve as initiating cofactors in the pathogenesis of pulmonary fibrosis.

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Leukotriene D₄‐induced, epithelial cell‐derived transforming growth factor β1 in human bronchial smooth muscle cell proliferation

Abstract: In conclusion, elevated expression of cys-LTs in asthmatic airways might contribute to BSMC hyperplasia and concomitant clinical features of asthma such as airway hyperresponsiveness via a paracrine loop involving TGF-beta1 production by airway epithelial cells.

Cited by 45 publications

References 59 publications

Leukotriene D4 Stimulates the Migration but Not Proliferation of Endothelial Cells Mediated by the Cysteinyl Leukotriene CysLT1 Receptor via the Extracellular Signal-Regulated Kinase Pathway

Leukotriene D4 Stimulates the Migration but Not Proliferation of Endothelial Cells Mediated by the Cysteinyl Leukotriene CysLT1 Receptor via the Extracellular Signal-Regulated Kinase Pathway

GM‐CSF– and M‐CSF–primed macrophages present similar resolving but distinct inflammatory lipid mediator signatures

Latent Herpesvirus Infection Augments Experimental Pulmonary Fibrosis

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Leukotriene D4‐induced, epithelial cell‐derived transforming growth factor β1 in human bronchial smooth muscle cell proliferation

Abstract: In conclusion, elevated expression of cys-LTs in asthmatic airways might contribute to BSMC hyperplasia and concomitant clinical features of asthma such as airway hyperresponsiveness via a paracrine loop involving TGF-beta1 production by airway epithelial cells.

Cited by 45 publications

References 59 publications

Leukotriene D4 Stimulates the Migration but Not Proliferation of Endothelial Cells Mediated by the Cysteinyl Leukotriene CysLT1 Receptor via the Extracellular Signal-Regulated Kinase Pathway

Leukotriene D4 Stimulates the Migration but Not Proliferation of Endothelial Cells Mediated by the Cysteinyl Leukotriene CysLT1 Receptor via the Extracellular Signal-Regulated Kinase Pathway

GM‐CSF– and M‐CSF–primed macrophages present similar resolving but distinct inflammatory lipid mediator signatures

Latent Herpesvirus Infection Augments Experimental Pulmonary Fibrosis

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Leukotriene D₄‐induced, epithelial cell‐derived transforming growth factor β1 in human bronchial smooth muscle cell proliferation