Leptin stimulates tissue rat mast cell pro-inflammatory activity and migratory response

Żelechowska, Paulina; Agier, Justyna; Różalska, Sylwia; Wiktorska, Magdalena; Brzezińska‐Błaszczyk, Ewa

doi:10.1007/s00011-018-1171-6

Cited by 19 publications

(14 citation statements)

References 41 publications

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“…established that this adipocytokine directly induces histamine release as well as IL‐13, IFN‐ γ , and CCL2 synthesis, but reduces IL‐4, IL‐6, IL‐10, and CCL3 production by murine bone‐marrow‐derived MCs. Besides, we previously indicated that leptin induces Ca 2+ ‐dependent MC degranulation as well as cysLTs and CCL3 production . Our present findings provided further information on leptin impact on MC activity.…”

Section: Discussionsupporting

confidence: 77%

“…Besides, we previously indicated that leptin induces Ca 2+dependent MC degranulation as well as cysLTs and CCL3 production. 59 Our present findings provided further information on leptin impact on MC activity. Moreover, our observations that adiponectin affects tissue MC response are entirely innovative as, to our best knowledge, there is no information about the direct impact of adiponectin on MC activity.…”

Section: Discussionsupporting

confidence: 68%

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Adipocytokines leptin and adiponectin function as mast cell activity modulators

et al. 2019

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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 (MCs) 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 MCs 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 MCs to release of histamine as well as to generation of cysteinyl leukotrienes (cysLTs) and chemokine CCL2. We also found that both adipocytokines affect mRNA expression of various cytokines/chemokines. Leptin and adiponectin also activate MCs to produce reactive oxygen species. Moreover, we documented that leptin significantly augments the surface expression of receptors for cysLTs, i.e. CYSLTR1, CYSLTR2, and GPR17 on MCs, while adiponectin increases only GPR17 expression, and decreases CYSLTR2. Finally, we showed that both adipocytokines serve as potent chemoattractants for MCs. In intracellular signaling in MCs activated by leptin Janus‐activated kinase 2, phospholipase C, phosphatidylinositol 3‐kinase (PI3K), extracellular signal‐regulated kinase (ERK1/2), and p38 molecules play a part whereas the adiponectin‐induced activity of MCs is mediated through PI3K, p38, and ERK1/2 pathways. Our observations that leptin and adiponectin regulate MC activity might indicate that adipocytokines modulate the different processes in which MCs are involved.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionsupporting

confidence: 68%

Adipocytokines leptin and adiponectin function as mast cell activity modulators

et al. 2019

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“…Adipocytes release adipocytokines that may induce a series of immune responses in surrounding cells within AT. For instance, leptin acts on the leptin receptor expressed by MCs and triggers the release of mediators including cysLTs and CCL3 [30,72]. MC mediators including IFN-γ, MMP-9, and phospholipase A2 regulate activation of macrophages [24].…”

Section: Crosstalk With Cells Of Adipose Tissuementioning

confidence: 99%

Crosstalk Between Mast Cells and Adipocytes in Physiologic and Pathologic Conditions

Komi

Shafaghat

Christian

2020

Clinic Rev Allerg Immunol

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Excessive fatty acids and glucose uptake support the infiltration of adipose tissue (AT) by a variety of immune cells including neutrophils, pro-inflammatory M1 macrophages, and mast cells (MCs). These cells promote inflammation by releasing proinflammatory mediators. The involvement of MCs in AT biology is supported by their accumulation in the AT of obese individuals along with significantly higher serum levels of MC-derived tryptase. AT-resident MCs under the influence of locally derived adipokines such as leptin become activated and release pro-inflammatory cytokines including TNFα that worsens the inflammatory state. MCs support angiogenesis in AT by releasing chymase and inducing preadipocyte differentiation and also the proliferation of adipocytes through 15-deoxy-delta PGJ2/PPARγ interaction. Additionally, they contribute to the remodeling of the AT extracellular matrix (ECM) and play a role in the recruitment and activation of leukocytes. MC degranulation has been linked to brown adipocyte activation, and evidence indicates an important link between MCs and the appearance of BRITE/beige adipocytes in white AT. Cell crosstalk between MCs and AT-resident cells, mainly adipocytes and immune cells, shows that these cells play a critical role in the regulation of AT homeostasis and inflammation.

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“…Leptin either enhances or reduces the expression of some adhesion molecules in eosinophils and induces the migration of monocytes, macrophages, granulocytes, mast cells and dendritic cells. 11,[44][45][46][47][48] Resistin augments endothelial permeability, up-regulates the expression of several adhesion molecules in monocytes and induces endothelial cell migration. [49][50][51] Visfatin can serve as a chemotactic factor facilitating the motility of monocytes as well.…”

Section: Adipokines Modulate the Activity Of Cells Engaged In Innatmentioning

confidence: 99%

“…Leptin enhances the secretion of pro-inflammatory cytokines, chemokines and other mediators from monocytes/macrophages, eosinophils, basophils and mast cells. 11,44,47,75 Interestingly, leptin is also able to down-regulate or even inhibit the production of certain anti-inflammatory cytokines by macrophages, mast cells and dendritic cells. 10,76 Resistin mainly stimulates macrophages and endothelial cells to produce cytokines/chemokines exhibiting pro-inflammatory properties.…”

Section: Adipokines Modulate the Activity Of Cells Engaged In Innatmentioning

confidence: 99%

The role of adipokines in the modulation of lymphoid lineage cell development and activity: An overview

2020

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Summary Adipokines are predominantly known to play a vital role in the control of food intake, energy homeostasis and regulation of glucose and lipid metabolism. However, evidence supporting the concept of their extensive involvement in immune system defence mechanisms and inflammatory processes continues to grow. Some of the adipokines, that is, leptin and resistin, have been recognized to exhibit mainly pro‐inflammatory properties, whereas others such as visfatin, chemerin, apelin and vaspin have been found to exert regulatory effects. In contrast, adiponectin or omentin are known for their anti‐inflammatory activities. Hence, adipokines influence the activity of various cells engaged in innate immune response and inflammatory processes mainly by affecting adhesion molecule expression, chemotaxis, apoptosis and phagocytosis, as well as mediators production and release. However, much less is known about the role of adipokines in processes involving lymphoid lineage cells. This review summarizes the current knowledge regarding the importance of different adipokines in the lymphopoiesis, recirculation, differentiation and polarization of lymphoid lineage cells. It also provides insight into the influence of selected adipokines on the activity of those cells in tissues.

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Leptin stimulates tissue rat mast cell pro-inflammatory activity and migratory response

Cited by 19 publications

References 41 publications

Adipocytokines leptin and adiponectin function as mast cell activity modulators

Adipocytokines leptin and adiponectin function as mast cell activity modulators

Crosstalk Between Mast Cells and Adipocytes in Physiologic and Pathologic Conditions

The role of adipokines in the modulation of lymphoid lineage cell development and activity: An overview

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