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

Watanabe, K.; Jose, Peter J.; Rankin, Sara M.

doi:10.4049/jimmunol.168.4.1911

Cited by 87 publications

(63 citation statements)

References 64 publications

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“…Moreover, MMP-9 and eotaxin-2 were decreased in the peritoneal cavity of Thy-1 À/À mice upon induction of inflammation by thioglycollate. As shown by other groups, we also detected these products in granulocytes or monocytes by RT-PCR [33][34][35][36][37]. Thus, the decreased number of granulocytes and macrophages in Thy-1 À/À mice might be directly responsible for the reduced levels of these cytokines, chemokines, and protease in the BAL or peritoneal fluid of Thy-1 À/À mice.…”

Section: Discussionsupporting

confidence: 78%

“…Data from Furusho et al, describing an association of the number of eosinophils and the level of IL-4 and IL-5 concentrations in BAL in an murine model of toluene diisocyanate-induced asthma [32], support our findings. Our own PCR data and Watanabe et al show that peripheral monocytes generate eotaxin-2 constitutively [35]. Furthermore, IL-4 augmented eotaxin-2 expression in allergic lung inflammation [38].…”

Section: Discussionsupporting

confidence: 65%

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Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

et al. 2011

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Human Thy-1 (CD90) has been shown to mediate adhesion of inflammatory cells to activated microvascular endothelial cells via interaction with Mac-1 (CD11b/CD18) in vitro. Since there are no data showing the physiological relevance of Thy-1 for the recruitment of inflammatory cells in vivo, different inflammation models were investigated in Thy-1-deficient mice and littermate controls. In thioglycollate-induced peritonitis, the number of neutrophils and monocytes was significantly diminished in Thy-1-deficient mice. During acute lung inflammation, the extravasation of eosinophils and monocytes into the lung was significantly reduced in Thy-1-deficient mice. Moreover, during chronic lung inflammation, the influx of eosinophils and monocytes was also strongly decreased. These effects were independent of Thy-1 expression on T cells, as shown by the transplantation of WT BM into the Thy-1-deficient mice. In spite of the strong Thy-1 expression on T cells in the chimeric mice, the extravasation of the inflammatory cells in these mice was significantly diminished, compared to control mice. Finally, the altered number and composition of infiltrating leukocytes in Thy-1-deficient mice modified the chemokine/cytokine and protease expression at the site of inflammation. In conclusion, Thy-1 is involved in the control of inflammatory cell recruitment and, thus, also in conditioning the inflammatory microenvironment.Key words: Extravasation . Inflammation . Thy-1 Supporting Information available online IntroductionThe recruitment of inflammatory cells to sites of inflammation plays an important role in the pathogenesis of several inflammatory diseases. Leukocyte adhesion to endothelial cells (ECs) follows a multistep process, including the capture of free leukocytes out of the blood stream, rolling, firm adhesion, and transendothelial diapedesis. The importance of several adhesion molecules in this series of events has been described previously [1]. In ICAM-1-deficient mice, neutrophil recruitment was significantly reduced, but it was not completely blocked in a chemical peritonitis model or in a lipopolysaccharide 645(LPS)-induced airway inflammation model, indicating the involvement of additional adhesion molecules [2,3]. Furthermore, leukocyte recruitment in experimental colitis was not affected by blocking ICAM-1 or MadCAM, whereas the blocking of VCAM-1 resulted in a significant attenuation of colitis [4]. Thus, under specific inflammatory conditions, certain adhesion molecules mediate adhesion and transmigration of leukocytes into the perivascular tissue.Recently, human Thy-1 expressed on ECs was identified as an adhesion molecule mediating the binding of neutrophils and monocytes to activated microvascular ECs [5]. Thy-1 is a highly glycosylated GPI-anchored surface protein and a member of the immunoglobulin superfamily [6,7,8]. In humans, Thy-1 is expressed on ECs at sites of inflammation or in tumours whereas ECs do not express Thy-1 in healthy tissue [5,9]. Thy-1 is also expressed on fibroblasts, neurons, and a su...

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Section: Discussionsupporting

confidence: 78%

Section: Discussionsupporting

confidence: 65%

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

et al. 2011

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“…Second, eotaxin-1 is known to be involved in the early phase (6-24 h) of allergic inflammation (37)(38)(39)(40), and our protocol (sacrifice 24 or 48 h after the final challenge) may have failed to evaluate ALN's effect on the production of eotaxin-1 in the lung. According to previous in vitro reports, eotaxin-1 production is limited to airway smooth muscle cells, epithelial cells, and fibroblasts (43,50,51). We could not detect eotaxin-1 from pleural macrophages under any conditions (with LPS and/or IL-4, -17, -33) in vitro (data not shown); therefore, we could not fully confirm ALN's effect on the production of eotaxin-1 by macrophages.…”

Section: Discussioncontrasting

confidence: 50%

Alendronate Attenuates Eosinophilic Airway Inflammation Associated with Suppression of Th2 Cytokines, Th17 Cytokines, and Eotaxin-2

Sasaki

Imamura

Yamazumi

et al. 2013

The Journal of Immunology

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Bisphosphonates (BPs) have been widely used to treat osteoporosis. They act by inhibiting farnesyl diphosphate synthase in the mevalonate pathway. This resembles the action of statins, whose immune-modulating effect has recently been highlighted. In contrast, the effect of BPs on immune responses has not been elucidated well. In this study, we examined the effect of alendronate (ALN), a nitrogen-containing BP, on allergic airway inflammation in a mouse model. BALB/c mice were sensitized twice with OVA and challenged three times with nebulized OVA to induce eosinophilic airway inflammation. ALN was administered by an intragastric tube before each inhalation. ALN strongly suppressed airway eosinophilia and Th2, as well as Th17 cytokine production in the lung. ALN also attenuated eotaxin-2 production in the lung. Immunohistochemistry demonstrated that the major cell source of eotaxin-2 was peribronchial/perivascular macrophages, and flow cytometrical studies confirmed that ALN decreased eotaxin-2 expression in these macrophages. Furthermore, ALN attenuated eotaxin-2 production from mouse pleural macrophages and human monocyte/macrophage-like THP-1 cells in vitro. These results suggest that ALN suppressed Ag-induced airway responses in the mouse model. The suppression of eotaxin-2 production from macrophages appears to be one of ALN’s immunomodulatory effects, whereas the mechanism by which ALN suppressed Th2 and Th17 responses could not be fully elucidated in this study. Although a clinical study should be conducted, ALN could be a novel therapeutic option for asthma.

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“…Eotaxin-1-deficient mice are able to develop airway eosinophilia and airway hyperresponsiveness in a model of experimental asthma [19,20], implying that other eosinophil-active chemoattractants are also involved in eosinophil recruitment into the airways. Th2 cytokines differentially regulate eotaxin-2 expression in monocytes and macrophages [21]. Recent studies of eotaxin-2-deficient mice have revealed an eotaxin-2-dependent mechanism in IL-13-induced airway eosinophilia [22].…”

Section: Introductionmentioning

confidence: 99%

Membrane‐bound eotaxin‐3 mediates eosinophil transepithelial migration in IL‐4‐stimulated epithelial cells

et al. 2006

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Epithelial cells play an important role in orchestrating mucosal immune responses. In allergic‐type inflammation, epithelial cells control the recruitment of eosinophils into the mucosa. Th2‐type cytokine‐driven release of eosinophil‐active chemokines from epithelial cells directs eosinophil migration into the mucosal epithelium. CCR3, the main eosinophil chemokine receptor, regulates this process; however, the respective contribution of individual CCR3 ligands in eosinophil transepithelial migration is less well understood. Using an in vitro transepithelial chemotaxis system, we found that eotaxin‐3 produced by IL‐4‐stimulated airway epithelial cells and CCR3 on eosinophils exclusively mediate eosinophil transepithelial migration. Eotaxin‐3 protein levels were also increased in the nasal mucosal epithelium recovered from allergic patients as compared to non‐allergic patients. Surprisingly, eotaxin‐3 in IL‐4‐stimulated airway epithelial cells was predominantly cell surface bound, and the cell surface form was critical for eosinophil transepithelial migration. Eotaxin‐3 cell surface association was partially glycosaminoglycan (GAG) dependent, but was completely protein dependent, suggesting that eotaxin‐3 associates with both GAG and cell surface proteins. We thus provide evidence that cell surface‐associated eotaxin‐3 is the critical IL‐4‐dependent chemotactic signal mediating eosinophil transepithelial migration in the setting of allergic inflammation.

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

Cited by 87 publications

References 64 publications

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

Alendronate Attenuates Eosinophilic Airway Inflammation Associated with Suppression of Th2 Cytokines, Th17 Cytokines, and Eotaxin-2

Membrane‐bound eotaxin‐3 mediates eosinophil transepithelial migration in IL‐4‐stimulated epithelial cells

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