Chemokine production by the BEAS-2B human bronchial epithelial cells: Differential regulation of eotaxin, IL-8, and RANTES by TH2- and TH1-derived cytokines

Fujisawa, Takao; Kato, Yoshiko; Atsuta, Jun; Terada, Akihiko; Iguchi, Kosei; Kamiya, Hitoshi; Yamada, Hirokazu; Nakajima, Toshiharu; Miyamasu, Misato; Hirai, Koichi

doi:10.1016/s0091-6749(00)90187-8

Cited by 125 publications

(76 citation statements)

References 31 publications

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“…Furthermore, in vitro studies show that certain cell types, including human dermal fibroblasts (HDF) and the epithelial cell lines BEAS2B and A549, generate eotaxin-1 protein when stimulated with IL-4 and IL-13 (31)(32)(33). Therefore, these reports are consistent with a role for eotaxin-1 in allergic inflammatory reactions.…”

mentioning

confidence: 64%

Eotaxin-2 Generation Is Differentially Regulated by Lipopolysaccharide and IL-4 in Monocytes and Macrophages

Watanabe

Jose

Rankin

2002

The Journal of Immunology

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The eotaxins are a family of CC chemokines that coordinate the recruitment of inflammatory cells, in particular eosinophils, to sites of allergic inflammation. The cDNA for eotaxin-2 (CC chemokine ligand 24) was originally isolated from an activated monocyte library. In this study, we show for the first time that peripheral blood monocytes generate bioactive eotaxin-2 protein constitutively. Eotaxin-2 production was significantly up-regulated when monocytes were stimulated with the proinflammatory cytokine IL-1β and the microbial stimuli, LPS and zymosan. In contrast, the Th2 cytokines, IL-4 and IL-13, and the proinflammatory cytokine, TNF-α, acting alone or in combination, did not enhance the generation of eotaxin-2 by monocytes. Indeed, IL-4 suppressed the generation of eotaxin-2 by LPS-stimulated monocytes. Although other chemokines, including macrophage-inflammatory protein-1α, monocyte chemoattractant protein-1, macrophage-derived chemokine, and IL-8 were generated by monocytes, eotaxin-1 (CC chemokine ligand 11) could not be detected in the supernatants of monocytes cultured in the presence or absence of any of the stimuli used in the above experiments. Furthermore, human dermal fibroblasts that produce eotaxin-1 did not generate eotaxin-2 under basal conditions or when stimulated with specific factors, including IL-4, IL-13, TNF-α, and LPS. When monocytes were differentiated into macrophages, their constitutive generation of eotaxin-2 was suppressed. Moreover, IL-4, but not LPS, up-regulated the production of eotaxin-2 by macrophages. Taken as a whole, these results support a role for macrophage-derived eotaxin-2 in adaptive immunity, with a Th2 bias. In contrast, a role for monocyte-derived eotaxin-2 is implicated in innate immunity.

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confidence: 64%

Eotaxin-2 Generation Is Differentially Regulated by Lipopolysaccharide and IL-4 in Monocytes and Macrophages

Watanabe

Jose

Rankin

2002

The Journal of Immunology

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“…This inhibitory effect of IL-17 on RANTES secretion stands in opposition to its stimulatory effects on TNF-␣-induced IL-6, IL-8, and MCP-1 secretion in these cells (11). In many cells, the regulation of RANTES secretion has been reported to be coupled to that of IL-8 and MCP-1 secretion through the NF-B signaling pathway (3,14,19,20). Based on this viewpoint, IL-17 may be a cytokine of a novel class which exerts a counterregulatory action on chemokine (IL-8, MCP-1, and RANTES) secretion.…”

Section: Discussionmentioning

confidence: 99%

IL-17 Selectively Down-Regulates TNF-α-Induced RANTES Gene Expression in Human Colonic Subepithelial Myofibroblasts

Andoh

Fujino

Bamba

et al. 2002

The Journal of Immunology

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IL-17 enhances the TNF-α-induced IL-6 and IL-8 secretion in human colonic subepithelial myofibroblasts. In this study, we investigated how IL-17 modulates RANTES secretion in these cells. TNF-α potently induced RANTES secretion, but IL-17 dose-dependently inhibited the TNF-α-induced RANTES secretion. This was also observed at the mRNA level. Even after pretreatment with TNF-α for 12 h, the inhibitory effect of IL-17 was detectable. IL-17 did not affect the TNF-α-induced stability of the RANTES gene. IL-17 significantly decreased the TNF-α-induced increase in RANTES promoter activity, and IL-17 actually blocked the TNF-α-induced RANTES gene transcription. EMSAs demonstrated that IL-17 did not modulate the TNF-α-induced NF-κB DNA-binding activity, but markedly decreased TNF-α-induced IFN regulatory factor-1 (IRF-1) DNA-binding activity. Because cooperation between NF-κB and IRF-1 is important in the TNF-α-induced RANTES gene expression, the major mechanism mediating the inhibitory effect of IL-17 may be achieved by the inhibition of IRF-1 DNA-binding activity.

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“…Chemokines are a crucial facet of the interaction between eosinophils and the airway epithelium in asthmatic inflammation (Lukacs 2001). Only eotaxin is eosinophil-specific and its production by the airway epithelium is well established, being regulated by cytokines implicated in asthmatic inflammation including IL-13, IL-4, tumour necrosis factor-and IL-1 (Lamkhioued et al 1997, Lilly et al 1997, Fujisawa et al 2000, Jedrzkiewicz et al 2000. It is interesting to note that the lung epithelium itself expresses functional CCR3 , the receptor for RANTES (regulated upon activation, normal T cell expressed and secreted), eotaxin, eotaxin 2 and 3, monocyte chemotactic protein MCP-3 and MCP-4.…”

Section: Bronchial Epithelial Cellsmentioning

confidence: 99%

Corticosteroids, eosinophils and bronchial epithelial cells: new insights into the resolution of inflammation in asthma

Walsh¹,

Sexton²,

Blaylock³

2003

Journal of Endocrinology

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Anti-inflammatory therapy in asthma is reliant on corticosteroids, particularly in their inhaled form. However, steroids are rather non-specific in their actions and they also raise concerns regarding compliance and side-effect issues. Furthermore, a small proportion of patients with asthma fail to respond to oral glucocorticoids even at high doses. This article will review the role that steroids and membrane receptor ligation play in the induction of eosinophil apoptosis together with the mechanisms by which corticosteroids enhance the disposal of apoptotic eosinophils by both professional and non-professional phagocytes. Eosinophils are thought to be the major pro-inflammatory effector cell in asthma and their persistence in the airways is probably enhanced by the presence of several asthma-relevant cytokines that prolong eosinophil survival by inhibition of apoptosis (interleukin (IL)-3, IL-5, granulocyte-macrophage colony-stimulating factor,

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Chemokine production by the BEAS-2B human bronchial epithelial cells: Differential regulation of eotaxin, IL-8, and RANTES by TH2- and TH1-derived cytokines

Cited by 125 publications

References 31 publications

Eotaxin-2 Generation Is Differentially Regulated by Lipopolysaccharide and IL-4 in Monocytes and Macrophages

Eotaxin-2 Generation Is Differentially Regulated by Lipopolysaccharide and IL-4 in Monocytes and Macrophages

IL-17 Selectively Down-Regulates TNF-α-Induced RANTES Gene Expression in Human Colonic Subepithelial Myofibroblasts

Corticosteroids, eosinophils and bronchial epithelial cells: new insights into the resolution of inflammation in asthma

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