Neuropeptide Y and its receptor subtypes specifically modulate rat peritoneal macrophage functions in vitro: counter regulation through Y1 and Y2/5 receptors

Dimitrijević, Mirjana; Stanojević, Stanislava; Vujić, Vesna; Beck‐Sickinger, Annette G.; Hörsten, Stephan von

doi:10.1016/j.regpep.2004.07.012

Cited by 54 publications

(51 citation statements)

References 41 publications

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“…One mechanism by which NPY may affect virus levels is by limiting the recruitment and/or infiltration of virus-infected macrophages into the brain. NPY has multiple reported effects on macrophages, including inhibiting chemotaxis and modulating phagocytosis, oxidative burst, and tumor growth factor beta production (11,13,38). It is possible that NPY expression in the periphery affects macrophage activation and limits the migration of infected cells to the brain.…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y Has a Protective Role during Murine Retrovirus-Induced Neurological Disease

Butchi

Woods

et al. 2010

J Virol

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Viral infections in the central nervous system (CNS) can lead to neurological disease either directly by infection of neurons or indirectly through activation of glial cells and production of neurotoxic molecules.Understanding the effects of virus-mediated insults on neuronal responses and neurotrophic support is important in elucidating the underlying mechanisms of viral diseases of the CNS. In the current study, we examined the expression of neurotrophin-and neurotransmitter-related genes during infection of mice with neurovirulent polytropic retrovirus. In this model, virus-induced neuropathogenesis is indirect, as the virus predominantly infects macrophages and microglia and does not productively infect neurons or astrocytes. Virus infection is associated with glial cell activation and the production of proinflammatory cytokines in the CNS. In the current study, we identified increased expression of neuropeptide Y (NPY), a pleiotropic growth factor which can regulate both immune cells and neuronal cells, as a correlate with neurovirulent virus infection. Increased levels of Npy mRNA were consistently associated with neurological disease in multiple strains of mice and were induced only by neurovirulent, not avirulent, virus infection. NPY protein expression was primarily detected in neurons near areas of virus-infected cells. Interestingly, mice deficient in NPY developed neurological disease at a faster rate than wild-type mice, indicating a protective role for NPY. Analysis of NPY-deficient mice indicated that NPY may have multiple mechanisms by which it influences virus-induced neurological disease, including regulating the entry of virus-infected cells into the CNS.

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Section: Discussionmentioning

confidence: 99%

Neuropeptide Y Has a Protective Role during Murine Retrovirus-Induced Neurological Disease

Butchi

Woods

et al. 2010

J Virol

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“…Stimulation of immune cells using receptor-specific peptides indicates that the activating effects of NPY are mediated primarily by Y1R, while the inhibitory effects are mediated by Y2R and Y5R (20,48). In agreement with this, the expression of DPP4, which cleaves NPY to a form that preferentially binds Y2R over Y1R, by monocytes also contributes to the anti-inflammatory effects of NPY (49).…”

Section: Discussionmentioning

confidence: 69%

“…NPY is also upregulated in the cerebrospinal fluid of patients with HIV encephalopathy, although the effect of this upregulation remains unknown (18). Recent studies with macrophage-like cell lines or isolated macrophages have demonstrated that NPY can influence macrophage activation (19)(20)(21)(22)(23)(24). Additionally, NPY has been found to inhibit interleukin 1␤ (IL-1␤)-induced activation of microglia (25,26), the primary resident myeloid cell type in the CNS.…”

mentioning

confidence: 99%

Neuropeptide Y Negatively Influences Monocyte Recruitment to the Central Nervous System during Retrovirus Infection

Woods

Carmody

et al. 2016

J Virol

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Monocyte infiltration into the CNS is a hallmark of several viral infections of the central nervous system (CNS), including retrovirus infection.Understanding the factors that mediate monocyte migration in the CNS is essential for the development of therapeutics that can alter the disease process. In the current study, we found that neuropeptide Y (NPY) suppressed monocyte recruitment to the CNS in a mouse model of polytropic retrovirus infection. NPY ؊/؊ mice had increased incidence and kinetics of retrovirus-induced neurological disease, which correlated with a significant increase in monocytes in the CNS compared to wildtype mice. Both Ly6C hi inflammatory and Ly6C lo alternatively activated monocytes were increased in the CNS of NPY ؊/؊ mice following virus infection, suggesting that NPY suppresses the infiltration of both cell types. Ex vivo analysis of myeloid cells from brain tissue demonstrated that infiltrating monocytes expressed high levels of the NPY receptor Y2R. Correlating with the expression of Y2R on monocytes, treatment of NPY ؊/؊ mice with a truncated, Y2R-specific NPY peptide suppressed the incidence of retrovirus-induced neurological disease. These data demonstrate a clear role for NPY as a negative regulator of monocyte recruitment into the CNS and provide a new mechanism for suppression of retrovirus-induced neurological disease. IMPORTANCEMonocyte recruitment to the brain is associated with multiple neurological diseases. However, the factors that influence the recruitment of these cells to the brain are still not well understood. In the current study, we found that neuropeptide Y, a protein produced by neurons, affected monocyte recruitment to the brain during retrovirus infection. We show that mice deficient in NPY have increased influx of monocytes into the brain and that this increase in monocytes correlates with neurological-disease development. These studies provide a mechanism by which the nervous system, through the production of NPY, can suppress monocyte trafficking to the brain and reduce retrovirus-induced neurological disease. The recruitment of monocytes into the central nervous system (CNS) is associated with a number of neurological diseases. Monocyte recruitment to the CNS has been reported for traumatic brain injury (TBI), misfolded-protein diseases, and multiple sclerosis (MS), as well as many different viral infections, including West Nile virus (WNV), herpes simplex virus (HSV), and retroviruses, such as HIV (1-4). Monocyte trafficking is particularly important for retrovirus-induced neurological diseases, as monocytes are susceptible to retrovirus infection (5, 6).Monocytes recruited to the CNS may contribute to pathogenesis in these neurological diseases. Decreased cognitive performance correlated with increased monocyte infiltration in HIVassociated neurocognitive disorders (HAND) (1). Additionally, infiltration of monocytes was found to be important for seizure development in a mouse model of Theiler's murine encephalitis (7). Recent studies in a mouse mo...

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“…Az NPY az immunfolyamatok lecsengéséért felelős, mert gátolja a T-sejtek migrációját, fokozza a makrofá-gok funkcióját [12], csökkenti az IL-1β, IL-2 és a TNF-α szekrécióját peritonealis makrofágokban [13], csökkenti a fagocitózist és a NO termelését. A gyulladásos folyamatokban nemcsak az SP-tartalmú idegrostok mennyisége emelkedik meg, hanem az NPY idegrostok száma is [14].…”

Section: Npy Hatása Gyulladásos Folyamatokbanunclassified

Neuropeptid Y és P anyag immunreaktív idegrostok és immunkompetens sejtek változása hepatitisben

Fehér

2015

Orvosi Hetilap

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A neuropeptid Y és a P anyag olyan neuropeptidek, amelyek fontos szerepet játszanak az immunsejtek működésében és a gyulladásos folyamatok fenntartásában és eliminálásában. Hepatitisben mindkét neuropeptidet tartalmazó idegrost mennyisége megnövekszik, a neuropeptid Y immunreaktív rostok növekedése szignifi káns. Számos lymphocytá-ban és hízósejtben szintén neuropeptid Y és a P anyag mutatható ki. Gyakran fi gyelhető meg közeli kapcsolat (kevesebb mint 1 μm) a neuropeptid Y immunreaktív idegrostok és a neuropeptid Y pozitív immunsejtek között. Az immunsejtek egy részében tumornekrózis-faktor-α és nukleáris faktor kappa-B-jelölődés is megfi gyelhető. Néhány P anyagot tartalmazó immunsejtben kolokalizációban fi gyelhető meg a tumornekrózis-faktor-α. Feltételezhető, hogy hepatitisben az idegrostokból és immunsejtekből felszabaduló neuropeptid Y és P anyag részt vesz a gyulladásos folyamatokban és azok eliminálásában. Orv. Hetil., 2015, 156(47), 1892-1897. Kulcsszavak: hepatitis, neuropeptid Y, P anyag, neuroimmun-moduláció Changes in neuropeptide Y and substance P immunoreactive nerve fi bres and immune competent cells in hepatitisNeuropeptide Y and substance P were thought to play a role in the function of immune cells and in amplifi cation or elimination of the infl ammatory processes. In hepatitis the number of both neuropeptide Y and substance P immunoreactive nerve fi bres are increased, where the increase of neoropeptide Y is signifi cant. A large number of lymphocytes and mast cells are also stained for neuropeptide Y and substance P. Very close associations (less than 1 μm) were observed between neuropeptide Y immunoreactive nerve fi bres and immune cells stained also with neuropeptide Y. Some immune cells were also found to be immunoreactive for tumor necrosis factor-α and NF-κB. Some of the SP IR immunocells were also stained for TNF-α and nuclear factor kappaB. Based on these data it is hypothesized that neuropeptid Y and substance P released from nerve fi bres and immune cells play a role in infl ammation and elimination of infl ammation in hepatitis.

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Neuropeptide Y and its receptor subtypes specifically modulate rat peritoneal macrophage functions in vitro: counter regulation through Y1 and Y2/5 receptors

Cited by 54 publications

References 41 publications

Neuropeptide Y Has a Protective Role during Murine Retrovirus-Induced Neurological Disease

Neuropeptide Y Has a Protective Role during Murine Retrovirus-Induced Neurological Disease

Neuropeptide Y Negatively Influences Monocyte Recruitment to the Central Nervous System during Retrovirus Infection

Neuropeptid Y és P anyag immunreaktív idegrostok és immunkompetens sejtek változása hepatitisben

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