Nicotine inhibits the in vitro production of interleukin 2 and tumour necrosis factor-α by human mononuclear cells

Madretsma, G. S.; Donze, G.J.; Dijk, A. P. M. van; Tak, C. J. A. M.; Wilson, J.H.P.; Zijlstra, Freek J.

doi:10.1016/0162-3109(96)00122-1

Cited by 77 publications

(37 citation statements)

References 16 publications

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“…They attributed the beneficial effects of nicotine to this inhibition. Madretsma et al (32) further corroborated their findings and also documented an inhibition of IL-2 production as well as IL-1p and TNFa. They suggest an immunoregulatory role through modulation of the cytokine production by nonadherent mononuclear cells.…”

Section: Ulcerative Colitis (Smokers Versus Nonsmokers)supporting

confidence: 75%

The influence of cigarette smoking on cytokine levels in patients with inflammatory bowel disease

et al. 2007

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Section: Ulcerative Colitis (Smokers Versus Nonsmokers)supporting

confidence: 75%

The influence of cigarette smoking on cytokine levels in patients with inflammatory bowel disease

et al. 2007

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“…It also modulates the production of various cytokines (Yoshida et al, 1998). Nicotine inhibits the production of IL-2 and TNF-␣ from human mononuclear cells (Madretsma et al, 1996). Recently, Wang et al (2003) reported that the nAChR ␣7 subunit is required for acetylcholine inhibition of macrophage TNF release.…”

Section: Discussionmentioning

confidence: 99%

The Expression and Functional Role of Nicotinic Acetylcholine Receptors in Rat Adipocytes

Liu

Mizuta²,

Matsukura³

2004

J Pharmacol Exp Ther

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To clarify whether nicotine has a direct effect on the function of adipocytes, we evaluated nicotinic acetylcholine receptor (nAChR) expression in adipocytes by reverse transcriptasepolymerase chain reaction (RT-PCR) and immunocytochemistry and the direct effects of nicotine on the production of adipocytokines by enzyme-linked immunosorbent assay and Western blot analysis. Receptor binding assays were performed using [3 H]nicotine. RT-PCR studies revealed that ␣1-7, 9, 10, ␤1-4, ␦, and ⑀ subunit mRNAs are expressed in adipocytes. Immunocytochemical experiments also suggested the presence of ␣7 and ␤2 subunits. The receptor binding assay revealed a binding site for nicotine (K d ϭ 39.2 ϫ 10 Ϫ9

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“…Nicotine has been shown to have T-cell-dependent and -independent effects. Nicotine suppresses antibody-dependent cell-mediated cytotoxicity and lymphokine-activated killer cell activities of normal human lymphocytes (Nair et al, 1990) and also prevents production of inflammatory mediators, such as IL-1, IL-8, and prostaglandin E 2 , from human macrophages (Sugano et al, 1998) and IL-2 and TNF-␣ from human mononuclear cells (Madretsma et al, 1996). An effect that is mediated through modulation of nuclear factor-␤ activation (Sugano et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Nicotine Reduces the Incidence of Type I Diabetes in Mice

Mabley

Pacher

Southan

et al. 2002

J Pharmacol Exp Ther

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Nicotine has been previously shown to have immunosuppressive actions. Type I diabetes is an autoimmune disease resulting from the specific destruction of the insulin-producing pancreatic ␤-cells. Thus, we hypothesized that nicotine may exert protective effects against type I diabetes. The multiple lowdose streptozotocin (MLDS)-induced model and spontaneous nonobese diabetic (NOD) mouse model of type I diabetes were used to assess whether nicotine could prevent this autoimmune disease. Blood glucose levels, diabetes incidence, pancreas insulin content, and cytokine levels were measured in both models of diabetes, both to asses the level of protection exerted by nicotine and to further investigate its mechanism of action. Nicotine treatment reduced the hyperglycemia and incidence of disease in both the MLDS and NOD mouse models of diabetes. Nicotine also protected against the diabetes-induced decrease in pancreatic insulin content observed in both animal models. The pancreatic levels of the Th1 cytokines interleukin (IL)-12, IL-1, tumor necrosis factor (TNF)-␣, and interferon (IFN)-␥ were increased in both MLDS-induced and spontaneous NOD diabetes, an effect prevented by nicotine treatment. Nicotine treatment increased the pancreatic levels of the Th2 cytokines IL-4 and IL-10. Nicotine treatment reduces the incidence of type I diabetes in two animal models by changing the profile of pancreatic cytokine expression from Th1 to Th2.Type I diabetes is a disease characterized by the specific destruction of the insulin-producing ␤-cells of the pancreatic islets of Langerhans by the immune system (Bottazzo and Bonifacio, 1991;Noorchashm et al., 1997). The islet is invaded by immune cells, particularly T-cells that are CD4 ϩ and CD8 ϩ (Rabinovitch, 1994), forming a pancreatic inflammation termed insulitis, with the resulting production of immune cell mediators, such as cytokines and free radicals (including nitric oxide and related radicals such as peroxynitrite), inhibiting ␤-cell function and ultimately inducing ␤-cell death (Rabinovitch and Suarez-Pinzon, 1998). The induction of nitric oxide synthase (iNOS) and the subsequent formation of nitric oxide and related free radicals have been implicated in the destruction of the ␤-cells in diabetes.A variety of cytokines have been found expressed in the insulitis lesion of the animal models of diabetes and in the pancreata of humans with type I diabetes. It has been proposed that the insulitis lesion is ␤-cell destructive when Th1 cytokines (IL-12, IFN-␥, IL-1, and TNF-␣), produced by isletinfiltrating T-cells, dominate over Th2 cytokines (Rabinovitch, 1998). Agents that suppress the immune system, including cyclosporine (Baquerizo et al., 1989) and glucocorticoids (Like et al., 1983), have been shown to reduce the disease incidence in animal models of type I diabetes.There are two murine models of autoimmune diabetes: the multiple low-dose streptozotocin (MLDS) model and the spontaneous NOD mouse model. The MLDS model of diabetes is characterized by progressive hy...

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Nicotine inhibits the in vitro production of interleukin 2 and tumour necrosis factor-α by human mononuclear cells

Cited by 77 publications

References 16 publications

The influence of cigarette smoking on cytokine levels in patients with inflammatory bowel disease

The influence of cigarette smoking on cytokine levels in patients with inflammatory bowel disease

The Expression and Functional Role of Nicotinic Acetylcholine Receptors in Rat Adipocytes

Nicotine Reduces the Incidence of Type I Diabetes in Mice

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