Effect of aging on the modulation of macrophage functions by neuropeptides

Fuente, Mónica De la; Medina, Sonia; Rı́o, M. Del; Ferrández, M.D.; Hernánz, Ángel

doi:10.1016/s0024-3205(00)00799-2

Cited by 54 publications

(24 citation statements)

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“…Further, in the present study we have found a greater chemotaxis in macrophages from aged (72-week-old) mice than in those from adult (22-week-old) animals. This is in agreement with previous work carried out by Wustrow et al (1982) and by De la Fuente et al (2000b), who reported a greater chemotactic capacity in old age in B6 and in SJLjJ mice, and in BALB/c mice, respectively. This fact could be due to the release of chemokines induced by higher proinflammatory cytokines such as TNFa and IL-1{3 released in old animals (Rink et al 1998).…”

Section: Discussionsupporting

confidence: 94%

“…Moreover, since these cells carry out a collal:\oration with the lymphocytes responsible for the antigenic response, their altered function could contribute to the decline in functionality of the lymphocytes in old age (Makinodan & Kay, 1980;Solana et al 1991;McArthur, 1998). In fact, it has been reported that the more highly differentiated functions of macrophages requiring cell-to-cell signalling would be adversely affected by age (Solana et al 1991), whereas there is evidence that other functions, namely phagocytosis, could be more active in the elderly (Kay, 1996;~cArthur, 1998;De la Fuente et al 2000b). It is possible that an adequate function of the nonspecific immune response mediated by macrophages is essential in order to avoid infections in situations, such as ageing, in which lymphocyte-specific responses are decreased.…”

Section: Discussionmentioning

confidence: 99%

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Ageing Modulates some Aspects of the Non‐Specific Immune Response of Murine Macrophages and Lymphocytes

Ortega

Garcı́a

Fuente

2000

Experimental Physiology

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The deterioration of the immune system with ageing, which leads to an increased morbidity and mortality from infections, appears to be related to decreases in specific lymphocyte functions. However, the alteration of non-specific immunity is a more controversial subject. Our purpose was to investigate the age-related changes of different functions of the non-specific immune response in peritoneal macrophages (adherence to tissues, mobility directed to a chemical gradient from an infectious focus or chemotaxis, phagocytosis of foreign agents and destruction of these agents by superoxide anion production) and in lymphocytes (adherence and chemotaxis) from peritoneum, axillary lymph nodes, spleen and thymus. We used young (12 weeks), adult (22 weeks), mature (48 weeks) and old (72 weeks) female BALB/c mice. The adherence capacity of macrophages and lymphocytes was greater in adult and old mice than in young animals. The chemotaxis of macrophages showed higher values in cells from young mice than in those from adult mice, increasing again in macrophages from mature and old animals. A similar behaviour was shown by phagocytosis, which reached its highest values in old animals. Anion superoxide production increased with age and again the highest values were obtained in the oldest mice. Conversely, chemotaxis of lymphocytes was higher in the adult and mature animals than in the young and old animals. We conclude that, although there is a decrease in lymphocyte chemotaxis in old animals, the non-specific immune response of macrophages instead of decreasing, may increase in aged mice with respect to the values seen in adult mice. Experimental Physiology (2000) 85.5, 519-525.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Ageing Modulates some Aspects of the Non‐Specific Immune Response of Murine Macrophages and Lymphocytes

Ortega

Garcı́a

Fuente

2000

Experimental Physiology

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“…It also remains to be seen whether gastrin induces specific immunomodulatory effects on the lymphocytes that it recruits, and particularly in addition to its chemotactic influence evidenced both here (Figs. 4 and 5) and earlier by de la Fuente et al (2000).…”

Section: Discussionsupporting

confidence: 54%

Gastrin Significantly Modifies the Migratory Abilities of Experimental Glioma Cells

Lefranc

Camby

Belot

et al. 2002

Laboratory Investigation

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SUMMARY:Malignant astrocytic tumors are characterized by the pronounced and diffuse migration of tumor astrocytes into the brain parenchyma. The present study shows that gastrin is a brain neuropeptide that is able to significantly modulate astrocytic tumor migration at both invasion and motility levels. In the matter of invasion, gastrin severely reduces the in vitro invasive abilities of C6 rat glioma, 9L rat gliosarcoma, and U373 human glioma cells in a collagen matrix. In vitro, gastrin also markedly modifies the motility features in both C6 and U373 cells, at least partly through a decrease in the expression of the RhoA small GTPase, and so brings about some dramatic modifications to the organization in the actin cytoskeleton. The in vitro preincubation of C6 tumor cells with gastrin significantly increases the life spans of rats stereotactically implanted with these cells as compared with the survival periods of rats implanted with gastrin-untreated C6 cells. As suggested by our in vitro experiments, these effects, observed in vivo cannot relate to only the gastrin-induced decrease in tumor astrocyte migratory abilities. Indeed, gastrin also induces immunomodulatory effects, because we observed a marked gastrin-induced recruitment of lymphocytes into C6 gliomas and 9L gliosarcomas. These data all suggest that gastrin can act as an endogenous modulator of glioma progression. (Lab Invest 2002, 82:1241-1252.

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“…The mechanisms of the effects of NPY on macrophages and lipid deposition remain to be determined. Previously, however, NPY was shown to activate monocyte migration and phagocytosis 44 and also to promote lipid storage in adipocytes. 45 The latter action is not only of central origin 46 but results from the strong antilipolytic action of NPY in adipocytes.…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y–Induced Acceleration of Postangioplasty Occlusion of Rat Carotid Artery

Lee

et al. 2003

ATVB

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Objective-Attempts to restore blood flow through atherosclerotic vessels by angioplasty often result in restenosis. Because the role of nerves in this process is unclear, we investigated whether neuropeptide Y (NPY), a sympathetic cotransmitter with vascular mitogenic activities, contributes to postangioplasty restenosis. Methods and Results-Carotid artery balloon angioplasty upregulated vascular expression of NPY and its processing enzyme (DPPIV/cd26) and receptors (Y1, Y2, Y5 mRNA and protein) within 6 to 24 hours and stimulated neointima formation and accumulation of NPY in platelets after 14 days. NPY pellets (1 to 10 g/pellet for 14 days) inserted next to the injured artery elevated platelet and vascular NPY immunoreactivity to stress-like levels and dose-dependently augmented angioplasty-induced neointima. Strikingly, 10 g NPY for 14 days led to vessel occlusion with an atherosclerotic-like lesion, with thrombus and neointima containing neovessels, macrophages, matrix, and lipids. Y1 or Y5 receptor antagonist completely prevented the effect of NPY and reduced angioplasty-induced neointima by 50%. Conclusions-Angioplasty See page 1137Multiple growth factors have been implicated in restenosis, 4 most of them thought to derive from mesenchymal cells. Surprisingly, the role of perivascular sympathetic nerves that richly innervate these vessels is less known. Sympathetic activity has been believed to promote atherosclerosis indirectly, either by its vasoconstrictive effects 5 or by stimulating platelet aggregation or insulin resistance. 6 However, these views have been rapidly changing in recent years because both norepinephine 7 and its cotransmitter, ATP, 8 have been found to exert direct trophic actions on vascular smooth muscle cells (VSMCs) both in vivo and in vitro.NPY is also a sympathetic and central cotransmitter, mediating pleiotropic activities such as stimulation of appetite and anxiolysis by activating multiple G i/o -coupled Y1-Y5 receptors. 9 -11 In the cardiovascular system, NPY cooperates with norepinephrine (NE) and causes, via Y1 receptors, a slow-onset, long-lasting vasoconstriction in many arteries, including coronary and cerebral. 9 -12 Plasma NPY levels are elevated by stress, such as cold exposure or treadmill exercise 9,12,13 and, in patients with myocardial ischemia, congestive heart failure and hypertension. 9,12,13 Recently, the vasoconstrictive Y1 receptor has also been identified as mediating proliferation of VSMCs in vitro. 14,15 In addition to neurogenic, extraneuronal NPY synthesis has been identified in endothelial 16 and immune cells 17 and megakaryocytes/platelets. 9,18 -20 Similar to VSMCs, NPY potently promotes growth of endothelial and immune cells, 14,16 but specific receptor subtypes mediating its effects appear to differ. For example, the angiogenic activity of NPY seems to be mediated not by Y1 but by Y2/Y5 receptors. The switch from the Y1-receptor-mediated vasoconstriction and VSMC mitogenesis to non-Y1-receptor-mediated angiogenic actions of NPY is provided by DPP...

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Effect of aging on the modulation of macrophage functions by neuropeptides

Cited by 54 publications

References 0 publications

Ageing Modulates some Aspects of the Non‐Specific Immune Response of Murine Macrophages and Lymphocytes

Ageing Modulates some Aspects of the Non‐Specific Immune Response of Murine Macrophages and Lymphocytes

Gastrin Significantly Modifies the Migratory Abilities of Experimental Glioma Cells

Neuropeptide Y–Induced Acceleration of Postangioplasty Occlusion of Rat Carotid Artery

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