Macrophages express neurotrophins and neurotrophin receptors

Barouch, Rina; Appel, Elena; Kazimirsky, Gila; Brodie, Chaya

doi:10.1016/s0165-5728(00)00408-2

Cited by 91 publications

(72 citation statements)

References 29 publications

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“…An- other potential mechanism for colocalization is the selective recruitment of catecholaminergic fibers by cellular processes associated with SIV replication. Activated leukocytes produce neurotropic factors and cytokines that could support the growth or maintenance of neural fibers (1,19). This hypothesis might account for the localized association between catecholaminergic varicosities and SIV replication within a given lymph node, but it is not consistent with the strong inverse relationship observed between SIV replication frequencies and overall innervation density across different lymph nodes.…”

Section: Discussionmentioning

confidence: 99%

Enhanced Replication of Simian Immunodeficiency Virus Adjacent to Catecholaminergic Varicosities in Primate Lymph Nodes

Sloan¹,

Tarara

Capitanio

et al. 2006

J Virol

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Clinical and in vitro studies have shown that activity of the autonomic nervous system (ANS) can stimulate lentivirus replication. To define the potential anatomical basis for this effect, we analyzed the spatial relationship between catecholaminergic neural fibers and sites of simian immunodeficiency virus (SIV) replication in lymph nodes from rhesus macaques experimentally infected with SIVmac251. Viral replication was mapped by in situ hybridization for SIV env, gag, and nef RNA, and catecholaminergic varicosities from the ANS were mapped by sucrose phosphate glyoxylic acid chemofluorescence. Spatial statistical analyses showed that the likelihood of active SIV replication increased by 3.9-fold in the vicinity of catecholaminergic varicosities (P < 0.0001). The densities of both ANS innervation and SIV replication differed across cortical, paracortical, and medullary regions of the lymph node, but analyses of each region separately continued to show increased replication of SIV adjacent to catecholaminergic varicosities. Ancillary analyses ruled out the possibility that SIV-induced alterations in lymph node architecture might create a spurious spatial association. These data support human clinical studies and in vitro molecular analyses showing that catecholamine neurotransmitters from the ANS can increase lentiviral replication by identifying a specific anatomic context for interactions between ANS neural fibers and replication of SIV in lymphoid tissue.

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Section: Discussionmentioning

confidence: 99%

Enhanced Replication of Simian Immunodeficiency Virus Adjacent to Catecholaminergic Varicosities in Primate Lymph Nodes

Sloan¹,

Tarara

Capitanio

et al. 2006

J Virol

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“…The reason for this unexpected result remains unclear. Several studies have shown that NGF seems to have not just an islet regulatory role [19][20][21][22] but also pro-inflammatory properties, [27][28][29][30] mediating effects such as lymphocyte [31][32][33][34][35] and macrophage activation, 32,36,37 eosinophil chemotaxis, 38 and mast cell survival and degranulation. 39 One possible explanation for the discrepancy in our results is that NGF-treated islets may stimulate immunocompetent cells after intraportal islet transplantation.…”

Section: Do Not Distributementioning

confidence: 99%

“…45 As described above, several studies suggest that NGF can activate immunocompetent cells such as lymphocytes, macrophages and granulocytes. [27][28][29][30][31][32][33][34][35][36][37][38][39] Although several reports show the relationship between VEGF and inflammation, 46,47 to our knowledge there is no compelling evidence that VEGF directly activates immunocompetent cells. This difference in pro-inflammatory properties of growth factors might be one of the reasons for the discrepancy in transplant outcome.…”

Section: Do Not Distributementioning

confidence: 99%

Nerve growth factor is associated with islet graft failure following intraportal transplantation

Saito

Chan

Sakata

et al. 2012

Islets

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Nerve growth factor (NGF) has recently been recognized as an angiogenic factor with an important regulatory role in pancreatic b-cell function. We previously showed that treatment of pancreatic islets with NGF improved their quality and viability. Revascularization and survival of islets transplanted under the kidney capsule were improved by NGF. However, the usefulness of NGF in intraportal islet transplantation was not previously tested. To resolve this problem, we transplanted syngeneic islets (360 islet equivalents per recipient) cultured with or without NGF into the portal vein of streptozotocin-induced diabetic BALB/c mice. Analysis revealed that 44.4% (4/9) of control and 12.5% (1/8) of NGF-treated mice attained normoglycemia (# 200 mg/dL) (p = 0.195). NGF-treated islets led to worse graft function (area under the curve of intraperitoneal glucose tolerance tests (IPGTT) on post-operative day (POD) 30, control; 35,800 ± 3,960 min*mg/dl, NGF-treated; 47,900 ± 3,220 min*mg/dl: *p = 0.0348). NGF treatment of islets was also associated with increased graft failure [the percentage of TdT-mediated dUTP-biotin nick-end labeling (TUNEL)-positive and necrotic transplanted islets on POD 5, control; 23.8% (5/21), NGF-treated; 52.9% (9/17): p = 0.0650] following intraportal islet transplantation. Nonviable (TUNEL-positive and necrotic) islets in both groups expressed vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1a (HIF-1a). On the other hand, viable (TUNEL-negative and not necrotic) islets in both groups did not express VEGF and HIF-1a. In the present study, pre-transplant NGF treatment was associated with impaired survival and angiogenesis of intraportal islet grafts. The effect of NGF on islet transplantation may significantly vary according to the transplant site.

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“…Brain macrophages and microglia express a variety of neurotrophins and neurotrophin receptors (Barouch et al, 2001;Elkabes et al, 1998;Gilad and Gilad, 1995;Miwa et al, 1997). The expressed repertoire varies with the cell type, the activation state and the location in vivo.…”

Section: Neurotrophin Expression Defines Complex Interactions Betweenmentioning

confidence: 99%

Macrophages and HIV-1: dangerous liaisons

Verani¹,

Gras

Pancino

2005

Molecular Immunology

102

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Macrophages express neurotrophins and neurotrophin receptors

Cited by 91 publications

References 29 publications

Enhanced Replication of Simian Immunodeficiency Virus Adjacent to Catecholaminergic Varicosities in Primate Lymph Nodes

Enhanced Replication of Simian Immunodeficiency Virus Adjacent to Catecholaminergic Varicosities in Primate Lymph Nodes

Nerve growth factor is associated with islet graft failure following intraportal transplantation

Macrophages and HIV-1: dangerous liaisons

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