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Adipocytokines leptin and adiponectin function as mast cell activity modulators
Author(s) -
Żelechowska Paulina,
BrzezińskaBłaszczyk Ewa,
Wiktorska Magdalena,
Różalska Sylwia,
Wawrocki Sebastian,
Kozłowska Elżbieta,
Agier Justyna
Publication year - 2019
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.13090
Subject(s) - adipokine , adiponectin , leptin , adiponectin receptor 1 , leptin receptor , medicine , endocrinology , adipose tissue , chemerin , chemistry , chemokine , receptor , microbiology and biotechnology , biology , insulin resistance , insulin , obesity
Summary A growing body of data indicates that adipocytokines, including leptin and adiponectin, are critical components not only of metabolic regulation but also of the immune system, mainly by influencing the activity of cells participating in immunological and inflammatory processes. As mast cells ( MC s) are the key players in the course of those mechanisms, this study aimed to evaluate the impact of leptin and adiponectin on some aspects of MC activity. We documented that in vivo differentiated mature tissue MC s from the rat peritoneal cavity express a receptor for leptin ( OB ‐R), as well as receptors for adiponectin (AdipoR1 and AdipoR2). We established that leptin, but not adiponectin, stimulates MC s to release of histamine as well as to generation of cysteinyl leukotrienes (cys LT s) and chemokine CCL 2. We also found that both adipocytokines affect mRNA expression of various cytokines/chemokines. Leptin and adiponectin also activate MC s to produce reactive oxygen species. Moreover, we documented that leptin significantly augments the surface expression of receptors for cys LT s, i.e. CYSLTR 1, CYSLTR 2, and GPR 17 on MC s, while adiponectin increases only GPR 17 expression, and decreases CYSLTR 2. Finally, we showed that both adipocytokines serve as potent chemoattractants for MC s. In intracellular signaling in MC s activated by leptin Janus‐activated kinase 2, phospholipase C, phosphatidylinositol 3‐kinase ( PI 3K), extracellular signal‐regulated kinase ( ERK 1/2), and p38 molecules play a part whereas the adiponectin‐induced activity of MC s is mediated through PI 3K, p38, and ERK 1/2 pathways. Our observations that leptin and adiponectin regulate MC activity might indicate that adipocytokines modulate the different processes in which MC s are involved.