Leptin and its soluble receptor in plasma of patients suffering from remitting-relapsing multiple sclerosis (MS) In vitro effects of leptin on type-1 and type-2 cytokine secretion by peripheral blood mononuclear cells, T-cells and monocytes of MS patients.
Leptin is synthesized by adipocytes to regulate appetite. Leptin has also been implicated in the pathogenesis of multiple sclerosis (MS) leading to speculation about a beneficial effect of fasting to autoimmune patients. We measured plasma leptin and its soluble receptor (OB-Rs) in 52 MS patients and 50 controls. We also cultured MS and control peripheral blood mononuclear cells (PBMC), T-cells and monocytes +/- recombinant leptin (rleptin), to assess leptin's direct effect on pro- and anti-inflammatory cytokine secretion. We found similar leptin and OB-Rs plasma levels between patients and controls. Untreated patients in the acute phase or in remission, or patients treated with methylprednisolone, had lower leptin levels than patients in the acute phase or in remission receiving IFN-beta. OB-Rs levels were low in patients refractory to IFN-beta but higher in patients receiving methylprednisolone or patients in remission receiving IFN-beta. PBMC from untreated patients in the acute phase, secreted spontaneously IFN-gamma, TNF-alpha and IL-10. IFN-gamma was contributed by T-cells, TNF-alpha and IL-10 primarily by monocytes and to a lesser extent by T-cells. The overall effect of rleptin on PBMC was a net increase in IL-10 production and a net reduction in IFN-gamma production. These results do not warrant a beneficial effect of fasting to MS patients.
Experimental Hematology & Transfusion Medicine, Medical School & University Hospital, University of Patras, Patras, Greece.
Kokona
K
Chatzantoni
Panagiotis
P
Papathanassopoulos
Euthymia
E
Gourzoulidou
Athanasia
A
Mouzaki
D000328:Adult; D001773:Blood Cells / Q000276:immunology / Q000378:metabolism; D015992:Body Mass Index; D016022:Case-Control Studies; D002478:Cells, Cultured; D016207:Cytokines / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D006801:Humans; D007155:Immunologic Factors / Q000097:blood / Q000494:pharmacology; D007371:Interferon-gamma / Q000096:biosynthesis; D016753:Interleukin-10 / Q000096:biosynthesis; D020738:Leptin / Q000097:blood* / Q000276:immunology / Q000494:pharmacology*; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000097:blood* / Q000209:etiology / Q000276:immunology; D011956:Receptors, Cell Surface / Q000097:blood* / Q000276:immunology; D054411:Receptors, Leptin; D012995:Solubility; D013601:T-Lymphocytes / Q000378:metabolism; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism
D016207:Cytokines; D007155:Immunologic Factors; C515448:LEPR protein, human; D020738:Leptin; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D016753:Interleukin-10; D007371:Interferon-gamma