Nerve growth factor promotes expression of costimulatory molecules and release of cytokines in dendritic cells involved in Th2 response through LPS-induced p75NTR

Tan, Hongyi; Pan, Pinhua; Zhang, Lemeng; Cao, Zu; Liu, Ben; Li, Haitao; Su, Xiaoli

doi:10.1080/02770903.2016.1185440

Cited by 11 publications

(6 citation statements)

References 44 publications

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“…IL‐1beta and TNF‐alpha stimulate the production of NGF in cultured disc cells . By contrast, Abe et al found that NGF promotes the release of inflammatory cytokines in dendritic cells . These findings indicate that an interaction between macrophage‐derived inflammatory cytokines, including TNF‐alpha and IL‐1beta, and disc resident cell‐derived growth factors, including NGF and VEGF, might explain the pathogenesis of discogenic low back pain (Fig.…”

Section: Discussionmentioning

confidence: 96%

Macrophage‐derived inflammatory cytokines regulate growth factors and pain‐related molecules in mice with intervertebral disc injury

Miyagi

Uchida

Takano

et al. 2018

Journal Orthopaedic Research

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Upregulation of inflammatory cytokines and various growth factors is a significant contributor to discogenic low back pain. The aim of this study was to investigate possible regulation of pain-related molecules by macrophages and the role of macrophage-derived molecules in injured intervertebral disc (IVD)s. C57BL/6J mice were used in this study. We characterized the expression profiles of genes for tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, nerve growth factor (NGF), and vascular endothelial growth factor (VEGF) in both intact and injured IVDs. We examined whether macrophage depletion, induced by systemic injection of clodronate-laden liposomes, affected the expression of these molecules in injured IVDs. The effect of TNF-alpha on cultured F4/80-CD11b-cells in injured IVDs was investigated. Expression of TNF-alpha and IL-1beta was significantly increased in injured IVDs, but decreased by macrophage depletion. Expression of NGF and VEGF was also significantly increased, but by contrast was not decreased by macrophage depletion. TNF-alpha treatment of F4/80-cells from injured IVDs upregulated NGF, VEGF, cyclooxygenase (COX)-2, and microsomal prostaglandin E synthase-1 (mPGES1). IVD injury upregulated inflammatory cytokines and various growth factors. Macrophages in the injured IVDs produced inflammatory cytokines, but not growth factors. Macrophage-derived inflammatory cytokines regulate growth factors and pain-related molecules. These findings demonstrate further complexity in the pathogenesis of discogenic pain. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res.

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Section: Discussionmentioning

confidence: 96%

Macrophage‐derived inflammatory cytokines regulate growth factors and pain‐related molecules in mice with intervertebral disc injury

Miyagi

Uchida

Takano

et al. 2018

Journal Orthopaedic Research

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“…In order to better study the mechanisms of severe asthma, we urgently need to build a neutrophil-predominant severe asthma model. While OVA is a classic asthma model allergen, exposure to LPS is also known to lead to an increased risk of asthma-like symptoms [ 17 ] and the onset of asthma exacerbations [ 18 , 19 ]. Meanwhile, the development of allergic asthma is strongly associated with the exposure to HDM [ 20 , 21 ].…”

Section: Discussionmentioning

confidence: 99%

MBD2 Regulates Th17 Cell Differentiation and Experimental Severe Asthma by Affecting IRF4 Expression

Jia

Wang

Sun

et al. 2017

Mediators of Inflammation

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Th17 cells and IL-17 participate in airway neutrophil infiltration characteristics in the pathogenesis of severe asthma. Methyl-CpG binding domain protein 2 (MBD2) expression increased in CD4+ T cells in peripheral blood samples of asthma patients. However, little is known about that epigenetic regulation of MBD2 in both immunological pathogenesis of experimental severe asthma and CD4+ T cell differentiation. Here, we established a neutrophil-predominant severe asthma model, which was characterized by airway hyperresponsiveness (AHR), BALF neutrophil granulocyte (NEU) increase, higher NEU and IL-17 protein levels, and more Th17 cell differentiation. In the model, MBD2 and IRF4 protein expression increased in the lung and spleen cells. Under overexpression or silencing of the MBD2 and IRF4 gene, the differentiation of Th17 cells and IL-17 secretion showed positive changes. IRF4 protein expression showed a positive change with overexpression or silencing of the MBD2 gene, whereas there was no significant difference in the expression of MBD2 under overexpression or silencing of the IRF4 gene. These data provide novel insights into epigenetic regulation of severe asthma.

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“…3, B and E). This activation of NF-B p65 was blunted by QNZ, a pathway-specific inhibitor for NF-B (58,59), in a dose-dependent manner (Fig. 3F).…”

Section: L489 Il-17a Induces Profibrotic Response In Human Lung Fibromentioning

confidence: 91%

Profibrotic effect of IL-17A and elevated IL-17RA in idiopathic pulmonary fibrosis and rheumatoid arthritis-associated lung disease support a direct role for IL-17A/IL-17RA in human fibrotic interstitial lung disease

Zhang

Wang

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

124

101

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Interleukin (IL)-17 is a T helper 17 cytokine implicated in the pathogenesis of many autoimmune diseases, including rheumatoid arthritis (RA). Although IL-17A has a well-established role in murine pulmonary fibrosis models, its role in the tissue remodeling and fibrosis occurring in idiopathic pulmonary fibrosis (IPF) and RA-associated interstitial lung disease (RA-ILD) is not very well defined. To address this question, we utilized complimentary studies to determine responsiveness of human normal and pathogenic lung fibroblasts to IL-17A and used lung biopsies acquired from patients with IPF and RA-ILD to determine IL-17A receptor (IL-17RA) expression. Both normal and pathogenic IPF lung fibroblasts express functional IL-17RA and respond to IL-17A stimulation with cell proliferation, generation of extracellular matrix (ECM) proteins, and induction of myofibroblast transdifferentiation. Small interfering RNA (siRNA) silencing of IL-17RA attenuated this fibroblast response to IL-17A on ECM production. These fibroblast responses to IL-17A are dependent on NF-κB-mediated signaling. In addition, inhibiting Janus activated kinase (JAK) 2 by either siRNA or a selective pharmacological inhibitor, AZD1480—but not a JAK1/JAK3 selective inhibitor, tofacitinib—also significantly reduced this IL-17A-induced fibrogenic response. Lung biopsies of RA-ILD patients demonstrate significantly higher IL-17RA expression in areas of fibroblast accumulation and fibrosis, compared with either IPF or normal lung tissue. These observations support a direct role for IL-17A in lung fibrosis that may be particularly relevant in the context of RA-ILD.

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Nerve growth factor promotes expression of costimulatory molecules and release of cytokines in dendritic cells involved in Th2 response through LPS-induced p75NTR

Abstract: NGF facilitates OVA with lowLPS-induced maturation of mouse BMDCs through LPS-up-regulated p75 NTR via activation of NF-κB pathways, providing another mechanism for the involvement of NGF in the Th2 response.

Cited by 11 publications

References 44 publications

Macrophage‐derived inflammatory cytokines regulate growth factors and pain‐related molecules in mice with intervertebral disc injury

Macrophage‐derived inflammatory cytokines regulate growth factors and pain‐related molecules in mice with intervertebral disc injury

MBD2 Regulates Th17 Cell Differentiation and Experimental Severe Asthma by Affecting IRF4 Expression

Profibrotic effect of IL-17A and elevated IL-17RA in idiopathic pulmonary fibrosis and rheumatoid arthritis-associated lung disease support a direct role for IL-17A/IL-17RA in human fibrotic interstitial lung disease

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