Leptin Has a Priming Effect on Eotaxin-Induced Human Eosinophil Chemotaxis

Abstract

Background: Tissue eosinophilia is one of the hallmarks of allergic diseases and Th2-type immune responses including asthma. Systemic inflammation caused by adipose tissue in obesity via production of adipokines such as leptin has been attracting attention recently as a contributor to exacerbation of allergic immune reactions. In this study, we examined whether leptin might affect eosinophil chemotactic responses. Methods: Peripheral blood eosinophils were purified, and the effect of leptin on eosinophil migration was investigated using in vitro systems. Results: High concentrations of leptin induced eosinophil chemotaxis and rapid phosphorylation of ERK1/2 and p38 mitogen-activated protein kinase but not calcium mobilization. We also found that pretreatment of eosinophils with physiological concentrations of leptin amplified the chemotactic responses to eotaxin. This leptin-primed chemotaxis appears to be associated with increased calcium mobilization but not with ERK1/2 and p38 pathways. Conclusions: These results indicate that leptin has both direct and indirect effects on eosinophil chemotaxis and intracellular signaling. In physiological settings, leptin may maintain eosinophil accumulation at allergic inflammatory foci.

Adiponectin attenuates human eosinophil adhesion and chemotaxis: implications in allergic inflammation

“…Eosinophils participate in the pathogenesis of asthma not only as final effector cells but also as active regulators for Th2-type immune responses [20]. Eotaxin (CCL11), a CC chemokine, has been known to trigger eosinophil-selective accumulation in keeping with its high affinity for heteromeric G protein-coupled receptor CCR3 [19,21].…”

Correlation of Absolute Eosinophil Count (AEC) and Body Mass Index (BMI) of MBBS Students in an Indian Scenario

“…It activates eosinophils [9] and increases their survival [10]. Again Eotaxin is an eosinophil specific chemokine that is increased in obesity [11].…”

Mediadores de la respuesta inflamatoria en asma y su relación con obesidad

“…Se ha demostrado que la leptina es un factor quimiotáctico para los eosinófilos, que participan en la respuesta asmática tardía, 22 además de activar la producción y secreción de mediadores inflamatorios como TNF-α, IL-6 y proteína C reactiva (PCR). 23,24 El tejido adiposo de los pacientes con obesidad se caracteriza por infiltración de macrófagos (determinada por aumento de la expresión de ARNm de CD68, un marcador especifico de macrófagos) y producción de mediadores inflamatorios.…”