Differential effects of neuropeptide Y (NPY) on leukocyte subsets in the blood: mobilization of B-1-like B-lymphocytes and activated monocytes

Bedoui, Sammy; Kuhlmann, Susanne; Nave, Heike; Drube, Jens; Pabst, Reinhard; Hörsten, Stephan von

doi:10.1016/s0165-5728(01)00328-9

Cited by 57 publications

(44 citation statements)

References 34 publications

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“…Intravenous application of NPY to rats quickly increases the number of CD4 pos T cells, monocytes, and NK cells in the central blood stream (4). NPY appears to inhibit the interaction of these leukocytes with endothelial cells, resulting in their mobilizing from the so-called marginal pool.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous publications already underline the pivotal role of NPY in the regulation of the innate and the adaptive immune system (3,4,(21)(22)(23). Intravenous application of NPY to rats quickly increases the number of CD4 pos T cells, monocytes, and NK cells in the central blood stream (4).…”

Section: Discussionmentioning

confidence: 99%

“…Among other functions, NPY strongly regulates T cell function, Ag presentation, blood leukocyte adhesion to endothelia, and leukocyte transmigration (2)(3)(4)(5).…”

Section: N Europeptide Y (Npy)mentioning

confidence: 99%

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Neuropeptide Y Is Expressed by Rat Mononuclear Blood Leukocytes and Strongly Down-Regulated during Inflammation

Holler

Zakrzewicz²,

Kaufmann

et al. 2008

The Journal of Immunology

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Neuropeptide Y (NPY), a classical sympathetic comediator, regulates immunological functions including T cell activation and migration of blood leukocytes. A NPY-mediated neuroimmune cross-talk is well conceivable in sympathetically innervated tissues. In denervated, e.g., transplanted organs, however, leukocyte function is not fundamentally disturbed. Thus, we hypothesized that NPY is expressed by blood leukocytes themselves and regulated during inflammation. NPY mRNA and peptide expression were analyzed in mononuclear leukocytes isolated from the blood vessels of healthy rat kidneys, as well as from the blood vessels of isogeneic and allogeneic renal grafts transplanted in the Dark Agouti to Lewis or in the Fischer 344 to Lewis rat strain combination. Depending on the donor strain, acute allograft rejection is either fatal or reversible but both experimental models are characterized by massive accumulation of intravascular leukocytes. Leukocytes, predominantly monocytes, isolated from the blood vessels of untreated kidneys and isografts expressed high amounts of NPY mRNA and peptide, similar to expression levels in sympathetic ganglia. During acute allograft rejection, leukocytic NPY expression drastically dropped to ∼1% of control levels in both rat strain combinations. In conclusion, NPY is an abundantly produced and tightly regulated cytokine of mononuclear blood leukocytes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Neuropeptide Y Is Expressed by Rat Mononuclear Blood Leukocytes and Strongly Down-Regulated during Inflammation

Holler

Zakrzewicz²,

Kaufmann

et al. 2008

The Journal of Immunology

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“…on alternate days from the day of immunization (day 0) until the termination of the experiments. The selection of NPY dosages is based on previous studies (29). We found that the continuous, alternate day treatment with NPY inhibits the clinical severity of EAE in a dose-dependent manner (Fig.…”

Section: Npy Inhibits Actively Induced Eae In a Dose-dependent Mannermentioning

confidence: 91%

Neuropeptide Y (NPY) Suppresses Experimental Autoimmune Encephalomyelitis: NPY1 Receptor-Specific Inhibition of Autoreactive Th1 Responses In Vivo

Bedoui

Miyake

Lin

et al. 2003

The Journal of Immunology

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Prior studies have revealed that the sympathetic nervous system regulates the clinical and pathological manifestations of experimental autoimmune encephalomyelitis (EAE), an autoimmune disease model mediated by Th1 T cells. Although the regulatory role of catecholamines has been indicated in the previous works, it remained possible that other sympathetic neurotransmitters like neuropeptide Y (NPY) may also be involved in the regulation of EAE. Here we examined the effect of NPY and NPY receptor subtype-specific compounds on EAE, actively induced with myelin oligodendrocyte glycoprotein 35–55 in C57BL/6 mice. Our results revealed that exogenous NPY as well as NPY Y1 receptor agonists significantly inhibited the induction of EAE, whereas a Y5 receptor agonist or a combined treatment of NPY with a Y1 receptor antagonist did not inhibit signs of EAE. These results indicate that the suppression of EAE by NPY is mediated via Y1 receptors. Furthermore, treatment with the Y1 receptor antagonist induced a significantly earlier onset of EAE, indicating a protective role of endogenous NPY in the induction phase of EAE. We also revealed a significant inhibition of myelin oligodendrocyte glycoprotein 35–55-specific Th1 response as well as a Th2 bias of the autoimmune T cells in mice treated with the Y1 receptor agonist. Ex vivo analysis further demonstrated that autoimmune T cells are directly affected by NPY via Y1 receptors. Taken together, we conclude that NPY is a potent immunomodulator involved in the regulation of the Th1-mediated autoimmune disease EAE.

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“…In addition, determination of blood leukocyte subsets by FACS analysis (Figure 4B; presented in percentage in Table 2) revealed a significant increase of NK cells wF(1,7)s11.06, ps0.007x, Bcells wF(1,7)s6.2, ps0.03x, and CD5 positive B1-like cells wF(1,7)s8.6, ps0.03x in DP4 deficient rats. In previous studies, we have shown that, especially, these leukocyte subpopulations are mobilized by NPY infusions (39), suggesting that apart from altered local chemokine metabolism also DP4 mediated N-terminal truncation of the noradrenergic co-transmitter NPY at the local level of sympathetic innervated immune organs, such as the spleen, might be involved in this phenomenon. A similar mechanism may also lead to an NPY potentiated noradrenalin-mediated increase of the splenic IL-6 outflow (25) (Figure 4G).…”

Section: Differential Immune Cell Distribution Diminished Immune Celmentioning

confidence: 88%

Phenotyping of congenic dipeptidyl peptidase 4 (DP4) deficient Dark Agouti (DA) rats suggests involvement of DP4 in neuro-, endocrine, and immune functions

Frerker

Raber²,

Bode³

et al. 2009

Clinical Chemistry and Laboratory Medicine

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Differential effects of neuropeptide Y (NPY) on leukocyte subsets in the blood: mobilization of B-1-like B-lymphocytes and activated monocytes

Cited by 57 publications

References 34 publications

Neuropeptide Y Is Expressed by Rat Mononuclear Blood Leukocytes and Strongly Down-Regulated during Inflammation

Neuropeptide Y Is Expressed by Rat Mononuclear Blood Leukocytes and Strongly Down-Regulated during Inflammation

Neuropeptide Y (NPY) Suppresses Experimental Autoimmune Encephalomyelitis: NPY1 Receptor-Specific Inhibition of Autoreactive Th1 Responses In Vivo

Phenotyping of congenic dipeptidyl peptidase 4 (DP4) deficient Dark Agouti (DA) rats suggests involvement of DP4 in neuro-, endocrine, and immune functions

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