Eotaxins

Bandeira‐Melo, Christianne; Herbst, Anne; Weller, Peter F.

doi:10.1165/ajrcmb.24.6.f209

Cited by 57 publications

(7 citation statements)

References 51 publications

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“…Recently, greater plasma concentrations of CCL11 have been shown in Brazilian MB leprosy patients, when compared to non infected individuals [20]. CCL11 is a potent chemo attractant for eosinophils and probably other cell types such as Th2 lymphocytes, to inflammatory sites [21,22]. It is possible that CCL11 participates in attracting inflammatory cells to T2R sites.…”

Section: Discussionmentioning

confidence: 99%

Potential plasma markers of type 1 and type 2 leprosy reactions: a preliminary report

et al. 2009

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BackgroundThe clinical management of leprosy Type 1 (T1R) and Type 2 (T2R) reactions pose challenges mainly because they can cause severe nerve injury and disability. No laboratory test or marker is available for the diagnosis or prognosis of leprosy reactions. This study simultaneously screened plasma factors to identify circulating biomarkers associated with leprosy T1R and T2R among patients recruited in Goiania, Central Brazil.MethodsA nested case-control study evaluated T1R (n = 10) and TR2 (n = 10) compared to leprosy patients without reactions (n = 29), matched by sex and age-group (+/- 5 years) and histopathological classification. Multiplex bead based technique provided profiles of 27 plasma factors including 16 pro inflammatory cytokines: tumor necrosis factor-α (TNF-α), Interferon-γ (IFN-γ), interleukin (IL)- IL12p70, IL2, IL17, IL1 β, IL6, IL15, IL5, IL8, macrophage inflammatory protein (MIP)-1 alpha (MIP1α), 1 beta (MIP1β), regulated upon activation normal T-cell expressed and secreted (RANTES), monocyte chemoattractrant protein 1 (MCP1), CC-chemokine 11 (CCL11/Eotaxin), CXC-chemokine 10 (CXCL10/IP10); 4 anti inflammatory interleukins: IL4, IL10, IL13, IL1Rα and 7 growth factors: IL7, IL9, granulocyte-colony stimulating factor (G-CSF), granulocyte macrophage-colony stimulating factor (GM-CSF), platelet-derived growth factor BB (PDGF BB), basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF).ResultsElevations of plasma CXCL10 (P = 0.004) and IL6 (p = 0.013) were observed in T1R patients compared to controls without reaction. IL6 (p = 0.05), IL7 (p = 0.039), and PDGF-BB (p = 0.041) were elevated in T2R. RANTES and GMCSF were excluded due to values above and below detection limit respectively in all samples.ConclusionPotential biomarkers of T1R identified were CXCL10 and IL6 whereas IL7, PDGF-BB and IL6, may be laboratory markers of TR2. Additional studies on these biomarkers may help understand the immunopathologic mechanisms of leprosy reactions and indicate their usefulness for the diagnosis and for the clinical management of these events.

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Section: Discussionmentioning

confidence: 99%

Potential plasma markers of type 1 and type 2 leprosy reactions: a preliminary report

et al. 2009

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“…Specifically, eosinophils may demonstrate increased secretion of granule contents, release of cytokines, respiratory burst, chemotaxis, release of lipid mediators, and cytoskeletal rearrangements with shape change when activated. 27,28 Though a range of soluble factors can activate eosinophils, one prime example is the response of eosinophils to stimulation via the eotaxin receptor, C-C chemokine receptor-3 (CCR3), by the eotaxins. 27 Interestingly, treatment of HES patients with mepolizumab results in the reduced ability of eosinophils to become activated ex vivo as measured by shape change in response to CCR3 stimulation by eotaxin−1, −2, and −3.…”

Section: Eosinophil Biologymentioning

confidence: 99%

“…27,28 Though a range of soluble factors can activate eosinophils, one prime example is the response of eosinophils to stimulation via the eotaxin receptor, C-C chemokine receptor-3 (CCR3), by the eotaxins. 27 Interestingly, treatment of HES patients with mepolizumab results in the reduced ability of eosinophils to become activated ex vivo as measured by shape change in response to CCR3 stimulation by eotaxin−1, −2, and −3. 29 MHC class II, co-stimulatory molecules, and adhesion molecules are upregulated in various disease states in which eosinophils are activated.…”

Section: Eosinophil Biologymentioning

confidence: 99%

Eosinophils and Disease Pathogenesis

Akuthota

Weller

2012

Seminars in Hematology

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“…First, elevated levels of T H 2 cytokines such as IL-13 in the bronchial mucosa increase the expression of CysLT 1 by epithelial cells and, consequently, their responsiveness to cysLTs. When cysLTs are released by activated tissue leucocytes (mast cells and eosinophils), this activate CysLT 1 on airway epithelial cells and, consequently, augment the release of eotaxin-3 induced by IL-13 which then activates pro-inflammatory functions of eosinophils, including the biosynthesis of cysLTs [54]. Further in vivo studies should be performed to confirm if this cycle would amplify and worsen the inflammatory state observed in asthma.…”

Section: Discussionmentioning

confidence: 99%

Leukotriene D4 and Interleukin-13 Cooperate to Increase the Release of Eotaxin-3 by Airway Epithelial Cells

et al. 2012

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IntroductionAirway epithelial cells play a central role in the physiopathology of asthma. They release eotaxins when treated with TH2 cytokines such as interleukin (IL)-4 or IL-13, and these chemokines attract eosinophils and potentiate the biosynthesis of cysteinyl leukotrienes (cysLTs), which in turn induce bronchoconstriction and mucus secretion. These effects of cysLTs mainly mediated by CysLT1 and CysLT2 receptors on epithelial cell functions remain largely undefined. Because the release of inflammatory cytokines, eotaxins, and cysLTs occur relatively at the same time and location in the lung tissue, we hypothesized that they regulate inflammation cooperatively rather than redundantly. We therefore investigated whether cysLTs and the TH2 cytokines would act in concert to augment the release of eotaxins by airway epithelial cells.MethodsA549 cells or human primary bronchial epithelial cells were incubated with or without IL-4, IL-13, and/or LTD4. The release of eotaxin-3 and the expression of cysLT receptors were assessed by ELISA, RT-PCR, and flow cytometry, respectively.ResultsIL-4 and IL-13 induced the release of eotaxin-3 by airway epithelial cells. LTD4 weakly induced the release of eotaxin-3 but clearly potentiated the IL-13-induced eotaxin-3 release. LTD4 had no effect on IL-4-stimulated cells. Epithelial cells expressed CysLT1 but not CysLT2. CysLT1 expression was increased by IL-13 but not by IL-4 and/or LTD4. Importantly, the upregulation of CysLT1 by IL-13 preceded eotaxin-3 release.ConclusionsThese results demonstrate a stepwise cooperation between IL-13 and LTD4. IL-13 upregulates CysLT1 expression and consequently the response to cysLTs This results in an increased release of eotaxin-3 by epithelial cells which at its turn increases the recruitment of leukocytes and their biosynthesis of cysLTs. This positive amplification loop involving epithelial cells and leukocytes could be implicated in the recruitment of eosinophils observed in asthmatics.

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Eotaxins

Cited by 57 publications

References 51 publications

Potential plasma markers of type 1 and type 2 leprosy reactions: a preliminary report

Potential plasma markers of type 1 and type 2 leprosy reactions: a preliminary report

Eosinophils and Disease Pathogenesis

Leukotriene D4 and Interleukin-13 Cooperate to Increase the Release of Eotaxin-3 by Airway Epithelial Cells

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