Leptin in Immunology

Matarese, Giuseppe; Moschos, Stergios J.; Mantzoros, Christos S.

doi:10.4049/jimmunol.174.6.3137

Cited by 516 publications

(476 citation statements)

References 88 publications

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“…However, Karul, et al did not adjust results for socio‐economic status, adiposity and age of the participants, which are well‐known factors affecting leptin concentrations and parasitic infection 41. The findings of the present study might be related to role of leptin as a hormone in the gut 42. Leptin has shown to prevent epithelial apoptosis and promoting tissue repair, which are required for mucosal defence against pathogens 43.…”

Section: Discussionmentioning

confidence: 60%

Intestinal parasites: Associations with intestinal and systemic inflammation

Zavala

García

Camacho

et al. 2018

Parasite Immunology

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SummaryThe aim of the present study was to evaluate associations between intestinal parasitic infection with intestinal and systemic inflammatory markers in school‐aged children with high rates of obesity. Plasma concentrations of C‐Reactive Protein (CRP), leptin, TNF‐α, IL‐6 and IL‐10 were measured as systemic inflammation markers and count of stool leukocytes as marker of intestinal inflammation in 291 children (6‐10 years). Intestinal parasitic infection was measured by stool examination. Logistic regression analyses were performed to determine the odds of having high inflammatory markers for each parasite or group of parasites as compared to parasite‐free children while adjusting for sex, age, mother's educational level and percentage of body fat. The prevalence of soil‐transmitted helminths and intestinal protozoa infections was 12% and 36%, respectively. Parasitic infection was not associated with CRP, IL‐6, IL‐10 or TNF‐α. Children infected with Ascaris lumbricoides (aOR: 5.91, 95% CI: 1.97‐17.70) and Entamoeba coli (aOR: 8.46, 95% CI: 2.85‐25.14) were more likely to have higher stool leucocytes than parasite‐free children. Children with multiple infections (aOR: 10.60, 95% CI: 2.85‐25.14) were more likely to have higher leptin concentrations than parasite‐free children. Intestinal parasitic infection was not associated with systemic inflammation, but was associated with intestinal inflammation. Having multiple infections were associated with higher leptin concentrations.

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Section: Discussionmentioning

confidence: 60%

Intestinal parasites: Associations with intestinal and systemic inflammation

Zavala

García

Camacho

et al. 2018

Parasite Immunology

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“…A histological observation of the colon revealed marked inflammation in mice injected with wild-type cells, whereas no inflammation was observed in mice receiving db/db cells. 44,89 Serum leptin levels are not altered in human inflammatory bowel diseases, although they might increase during the acute stages of ulcerative colitis. Furthermore, leptin mRNA is upregulated in mesenteric adipose tissue of these patients.…”

Section: Leptin Connective Tissue Diseases and Organ-specific Autoimmentioning

confidence: 99%

“…This receptor lacks intrinsic tyrosine kinase activity, is involved in several downstream signal transduction pathways, and has been identified in immune cells of both animals and humans. 43,44 OB-Rb has been shown to have the signaling capabilities of IL-6-type cytokine receptors, activating janus kinases and signal transducers and activators of transcription (STAT), phosphatidylinositol 3-kinase and the mitogen-activated protein kinase (MAPK) signaling pathways. 36,41,45 Like other cytokine receptor family members, OB-Rb is internalized upon ligand binding via …”

Section: Leptin Inflammation and Immune Responsementioning

confidence: 99%

“…Leptin alone is unable to induce the proliferation and activation of mature human peripheral blood lymphocytes unless it is co-administered with other nonspecific immunostimulants, in which case leptin results in the induction of early (CD69) and late activation markers (CD25 and CD71) in both CD4 and CD8 lymphocytes. 16,44,55 Figure 1 Leptin functions in humans. Leptin, mainly secreted by white adipose tissue, travels through the blood, crossing the hematoencephalic barrier.…”

Section: Leptin and Autoimmunity M Vadacca Et Al 204mentioning

confidence: 99%

“…5,82 During the active phase of EAE, leptin is secreted by both macrophages and T cells that have infiltrated the central nervous system, and leptin secretion by activated T cells appears to constitute an autocrine loop, sustaining their proliferation. 5,44,82 MS is a chronic, immune-mediated disorder of the central nervous system. The disease is characterized by autoreactive T cells that traffic to the brain and spinal cord and injure the myelin sheaths of the central nervous system, resulting in chronic or relapsing-remitting paralysis.…”

Section: Leptin and Multiple Sclerosis (Ms)mentioning

confidence: 99%

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Leptin in immuno-rheumatological diseases

et al. 2011

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Leptin is one of the most important hormones secreted by adipocytes, with a variety of physiological roles related to the control of metabolism and energy homeostasis. Since its discovery in 1994, leptin has attracted increasing interest in the scientific community for its pleiotropic actions. One of these functions is the relationship between nutritional status and immune competence. It structurally resembles proinflammatory cytokines, such as IL-6 and IL-12. The cytokine-like structural characteristic of leptin is implicative of its function in regulating immune responses. The role of leptin in regulating immune responses has been assessed in vitro as well as in clinical studies. It has been shown that disease conditions of reduced leptin production are associated with increased infection susceptibility. Conversely, immune-mediated disorders, such as autoimmune diseases, are associated with the increased secretion of leptin and the production of proinflammatory pathogenic cytokines. In this paper, we review the most recent advances of the role of leptin in immune-rheumatological diseases, and we discuss whether strategies aimed at modifying leptin levels could represent innovative and therapeutic tools for autoimmune disorders. Keywords: adipokines; autoimmune diseases; leptin; rheumatic diseases INTRODUCTIONThe existence of a factor secreted by white adipose tissue (WAT), which acts to control feeding, weight and WAT mass, was first proposed by Kennedy 1 and is supported by monogenic mutations resulting in obesity. [2][3][4] WAT is composed of adipocytes filled mainly with triacylglycerol and embedded in loose connective tissue containing adipocyte precursors, fibroblasts, immune and other cells. Obesity, the condition that originally motivated the research on WAT, is characterized by low-grade systemic inflammation. It is thought that excess WAT can contribute to the maintenance of obesity through inflammation-inducing lipotoxicity by secreting factors that stimulate the synthesis of inflammatory agents in other organs and by secreting inflammatory agents itself. 5 The current view of WAT states that it is an active contributor to body homeostasis by sending out and responding to signals that modulate appetite, energy expenditure, insulin sensitivity, the endocrine and reproductive systems, bone metabolism, inflammation and immunity. 6 Several findings have converged to indicate that adipocytes share certain properties with immune cells, such as complement activation 7 and proinflammatory cytokine production. 8 Fat cell precursors also share features with macrophages. Numerous genes that code for transcription factors, cytokines, inflammatory signaling molecules, and fatty acid transporters are essential for adipocyte biology and are also expressed and functional in macrophages. 9 Adipose tissue secrets a variety of factors: the term 'adipokine' is generally given to any protein that can be synthesized and secreted by adipocytes. Among these factors, only leptin and adiponectin (and possibly resistin, adipsi...

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