Nerve growth factor and its receptors in asthma and inflammation

Frossard, Nelly; Freund, Véronique; Advenier, C.

doi:10.1016/j.ejphar.2004.07.044

Cited by 90 publications

(89 citation statements)

References 174 publications

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“…This raises the possibility that reduced neurotrophin expression following SIV infection might be a consequence of denervation, rather than a cause, since neurotrophins may derive from both immune and neural sources (Kuruvilla, et al, 2004;Bronzetti, et al, 2006;Edling, et al, 2004;Frossard, et al, 2004;Levi-Montalcini, 1987). However, two findings argue against the hypothesis that changes in neurotrophin expression are solely a consequence of denervation.…”

Section: Discussioncontrasting

confidence: 45%

“…Members of the neurotrophin family, including nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT3) and neurotrophin-4/5 (NT4), are critical in shaping patterns and density of innervation, both centrally and in the periphery. NGF was first characterized as an essential factor for neuronal development and survival (Levi-Montalcini, 1987) and is expressed in a wide range of neuronal and non-neuronal celltypes (Levi-Montalcini, 1987;Frossard, et al, 2004). Target-derived NGF is essential for guiding developing sympathetic neurons to peripheral organs (Kuruvilla, et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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SIV infection decreases sympathetic innervation of primate lymph nodes: The role of neurotrophins

Sloan

Nguyen

Cox

et al. 2008

Brain, Behavior, and Immunity

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The sympathetic nervous system regulates immune responses in part through direct innervation of lymphoid organs. Recent data indicate that viral infections can alter the structure of lymph node innervation. To determine the molecular mechanisms underlying sympathetic denervation during Simian Immunodeficiency Virus (SIV) infection, we assessed the expression of neurotrophic factors and neuromodulatory cytokines within lymph nodes from experimentally infected rhesus macaques. Transcription of nerve growth factor (NGF), brain derived neurotropic factor (BDNF) and neurotrophin-4 (NT4) decreased significantly in vivo during chronic SIV infection, whereas expression of the neuro-inhibitory cytokine interferon-γ (IFNγ) was up-regulated. Acute SIV infection of macaque leukocytes in vitro induced similar changes in the expression of neurotrophic and neuro-inhibitory factors, indicative of an innate immune response. Statistical mediation analyses of data from in vivo lymph node gene expression suggested that coordinated changes in expression of multiple neuromodulatory factors may contribute to SIV-induced depletion of catecholaminergic varicosities within lymphoid tissue. Given previous evidence that lymph node catecholaminergic varicosities can enhance SIV replication in vivo, these results are consistent with the hypothesis that reduced expression of neurotrophic factors during infection could constitute a neurobiological component of the innate immune response to viral infection.

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Section: Discussioncontrasting

confidence: 45%

Section: Introductionmentioning

confidence: 99%

SIV infection decreases sympathetic innervation of primate lymph nodes: The role of neurotrophins

Sloan

Nguyen

Cox

et al. 2008

Brain, Behavior, and Immunity

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“…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%

“…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%

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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“…NGF has been shown to synergize with granulocyte-macrophage CSF (GM-CSF) to promote human basophilic cells differentiation (14) and synergize with stem cell factor to support hemopoietic stem cell development (15,16). NGF was found to be increased during inflammatory responses (17), autoimmune disorders (18,19), allergic diseases (20) and stress (21). Thus, NGF is also regarded as an important factor involved in the immune responses and pathogenesis of autoimmune diseases.…”

mentioning

confidence: 99%

Nerve Growth Factor Promotes TLR4 Signaling-Induced Maturation of Human Dendritic Cells In Vitro through Inducible p75NTR 1

Jiang

Chen

Zhang

et al. 2007

The Journal of Immunology

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Nerve growth factor (NGF) has been shown to play important roles in the differentiation, function, and survival of immune cells, contributing to immune responses and pathogenesis of autoimmune diseases. Dendritic cells (DCs) are a potent initiator for immune and inflammatory responses upon recognition of pathogens via Toll-like receptors (TLR). However, expression of NGF and its receptors on human monocyte-derived DCs (MoDCs) and the role of NGF in the response of DCs to TLR ligands remain to be investigated. In the present study, we demonstrate that there were weak expressions of NGF and no expression of NGF receptors p140TrkA and p75NTR on human immature MoDCs, however, the expression of NGF and p75NTR on MoDCs could be significantly up-regulated by LPS in a dose- and time-dependent manner. NGF could markedly promote LPS-induced expression of HLA-DR, CD40, CD80, CD83, CD86, CCR7, secretion of IL-12p40 and proinflammatory cytokines IL-1, IL-6, TNF-α, and the T cell-stimulating capacity of MoDCs, indicating that NGF can promote LPS-induced DC maturation. The promoting effect of NGF on LPS-induced MoDCs maturation could be completely abolished by pretreatment of MoDCs with p75NTR antagonist, suggesting that LPS-induced p75NTR mediates the effect. Furthermore, increased activation of the p38MAPK and NF-κB pathways has been shown to be responsible for the NGF-promoted DC maturation. Therefore, NGF facilitates TLR4 signaling-induced maturation of human DCs through LPS-up-regulated p75NTR via activation of p38 MAPK and NF-κB pathways, providing another mechanism for the involvement of NGF in the immune responses and pathogenesis of autoimmune diseases.

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Nerve growth factor and its receptors in asthma and inflammation

Cited by 90 publications

References 174 publications

SIV infection decreases sympathetic innervation of primate lymph nodes: The role of neurotrophins

SIV infection decreases sympathetic innervation of primate lymph nodes: The role of neurotrophins

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

Nerve Growth Factor Promotes TLR4 Signaling-Induced Maturation of Human Dendritic Cells In Vitro through Inducible p75NTR 1

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