Eotaxin Expression and Eosinophilic Inflammation in Asthma

Mattoli, Sabrina; Stacey, Martin; Sun, Guo Ying; Bellini, Alberto; Marini, Maurizio

doi:10.1006/bbrc.1997.6958

Cited by 129 publications

(89 citation statements)

References 22 publications

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“…The first eotaxin was discovered using a guinea pig model of allergic airway disease characterised by marked lung eosinophilia [26,27]. In humans, MATTOLI et al [28] showed that the numbers of cells expressing mRNA for eotaxin-1 correlated significantly with the number of eosinophils, bronchial hyperreactivity and symptom score in asthmatics. Furthermore, increased eotaxin-1 protein has been detected in the BAL fluid of asthmatic subjects [29].…”

Section: Discussionmentioning

confidence: 99%

Eotaxin-2 in sputum cell culture to evaluate asthma inflammation

Scheicher¹,

Teixeira²,

Cunha³

et al. 2006

Eur Respir J

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The aim of the present study was to elucidate whether the culture of cells recovered from induced sputum may represent a suitable model to evaluate cytokine and chemokine production by airway inflammatory cells.Sputum induction was performed in 21 normal subjects and 30 asthmatic patients. A total of 21 out of the 30 asthmatic patients were taking inhaled corticosteroids, while the remaining nine were steroid-naive asthmatics. The steroid-naive group was evaluated before and after a 14-day treatment with oral prednisone (40 mg?day -1). The supernatant of lysed and centrifuged sputum and the supernatant of sputum cell culture were analysed. Tumour necrosis factor-a, interleukin (IL)-8 (CXCL8), IL-1b, IL-13 and eotaxin-2 (CCL24) concentrations were determined by specific ELISA.Eotaxin-2 production by cell culture was higher in the asthma group (131¡108 pg?mL) than in the control group (36¡41 pg?mL -1 ) and treatment with oral corticosteroids eliminated this difference. In addition, reduction of eotaxin-2 levels by corticosteroid treatment was greater in cell culture (81.3% reduction) than in sputum (26.4%). There was correlation between the decrease in eotaxin-2 production and the decrease in blood eosinophil number and between eotaxin-2 and eosinophils in sputum.Eotaxin-2 may play an important role in asthma and the response to corticosteroid treatment suggests that analysis of sputum cell culture is relevant as an inflammatory parameter.

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Section: Discussionmentioning

confidence: 99%

Eotaxin-2 in sputum cell culture to evaluate asthma inflammation

Scheicher¹,

Teixeira²,

Cunha³

et al. 2006

Eur Respir J

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“…Eotaxin plays an important part in the pathophysiology of eosinophilic airway inflammation. A variety of cell types are responsible for eotaxin production, including macrophages, T lymphocytes, bronchial epithelial cells, endothelial cells, and fibroblasts (31)(32)(33)(34)(35). However, fibroblasts are considered the major source of eotaxin (34 -36).…”

Section: Discussionmentioning

confidence: 99%

Up-Regulation of Cysteinyl Leukotriene 1 Receptor by IL-13 Enables Human Lung Fibroblasts to Respond to Leukotriene C4 and Produce Eotaxin

Chibana

Ishii

Asakura

et al. 2003

The Journal of Immunology

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Cysteinyl leukotrienes (CysLTs) play an important role in eosinophilic airway inflammation. In addition to their direct chemotactic effects on eosinophils, indirect effects have been reported. Eotaxin is a potent eosinophil-specific chemotactic factor produced mainly by fibroblasts. We investigated whether CysLTs augment eosinophilic inflammation via eotaxin production by fibroblasts. Leukotriene (LT)C4 alone had no effect on eotaxin production by human fetal lung fibroblasts (HFL-1). However, LTC4 stimulated eotaxin production by IL-13-treated fibroblasts, thereby indirectly inducing eosinophil sequestration. Unstimulated fibroblasts did not respond to LTC4, but coincubation or preincubation of fibroblasts with IL-13 altered the response to LTC4. To examine the mechanism(s) involved, the expression of CysLT1R in HFL-1 was investigated by quantitative real-time PCR and flow cytometry. Only low levels of CysLT1R mRNA and no CysLT1R protein were expressed in unstimulated HFL-1. In contrast, stimulation with IL-13 at a concentration of 10 ng/ml for 24 h significantly up-regulated both CysLT1R mRNA and protein expression in HFL-1. The synergistic effect of LTC4 and IL-13 on eotaxin production was abolished by CysLT1R antagonists pranlukast and montelukast. These findings suggest that IL-13 up-regulates CysLT1R expression, which may contribute to the synergistic effect of LTC4 and IL-13 on eotaxin production by lung fibroblasts. In the Th2 cytokine-rich milieu, such as that in bronchial asthma, CysLT1R expression on fibroblasts might be up-regulated, thereby allowing CysLTs to act effectively and increase eosinophilic inflammation.

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“…Among these, eotaxin and RANTES have been shown to induce eosinophil migration both in vitro and in vivo in humans and various animal models (7,(12)(13)(14)(15)(16). In addition, expression of most of these ligands has been associated with asthma, and recent studies in human asthmatics make CCR3 an attractive target for therapeutic intervention (17)(18)(19)(20).…”

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confidence: 99%

The murine CCR3 receptor regulates both the role of eosinophils and mast cells in allergen-induced airway inflammation and hyperresponsiveness

Humbles

Liu

Friend

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

357

277

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CCR3 is a chemokine receptor initially thought specific to eosinophils but subsequently identified on TH2 cell subsets, basophils, mast cells, neural tissue, and some epithelia. Because of the prominent role of these cells in allergic disease, including asthma, we generated mice deficient in CCR3 to determine its contribution in a model of allergic airway disease. Here we show that CCR3 is important for the basal trafficking of eosinophils to the intestinal mucosa but not the lung. In contrast, CCR3 disruption significantly curtails eosinophil recruitment to the lung after allergen challenge, with the majority of the eosinophils being arrested in the subendothelial space. Further, a role for CCR3 in mast cell homing has been identified; after sensitization and allergen challenge, we find increased numbers of intraepithelial mast cells in the trachea of knockout mice. Physiologically, we find that the net result of these complex cell fates after sensitization and allergen challenge is a paradoxical increase in airway responsiveness to cholinergic stimulation. These data underscore a more complex role for CCR3 in allergic disease than was anticipated.

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Eotaxin Expression and Eosinophilic Inflammation in Asthma

Cited by 129 publications

References 22 publications

Eotaxin-2 in sputum cell culture to evaluate asthma inflammation

Eotaxin-2 in sputum cell culture to evaluate asthma inflammation

Up-Regulation of Cysteinyl Leukotriene 1 Receptor by IL-13 Enables Human Lung Fibroblasts to Respond to Leukotriene C4 and Produce Eotaxin

The murine CCR3 receptor regulates both the role of eosinophils and mast cells in allergen-induced airway inflammation and hyperresponsiveness

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