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The role of TLR2/JNK/NF-κB pathway in amyloid β peptide-induced inflammatory response in mouse NG108-15 neural cells.
Int Immunopharmacol. 2013 Nov; 17(3):880-4.II

Abstract

The TLR2-mediated neuroinflammatory activation has been involved in the pathogenesis of Alzheimer's disease (AD) associated with amyloid β(Aβ) deposition. In neuronal damage, JNK and NF-κB pathways contribute to TLR2-dependent secretion of proinflammatory cytokines. However, the role of TLR2/JNK/NF-κB pathway on Aβ-induced inflammatory response in nerve cell damage remains unclear. In the present study, Aβ1-42 was used to induce mouse NG108-15 neural cell injury. The cell viability was detected by methylthiazolyldiphenyl-tetrazolium bromide (MTT). The levels of tumor necrosis factor (TNF)-α, monocyte chemoattractant protein(MCP)-1 and interleukin (IL)-10 in culture supernatant were measured by ELISA. western blot analysis was performed to detect the expressions of JNK and p-65 NF-κB proteins. Immunofluorescence assay was also performed to examine the p-JNK and p-65 NF-κB activation. As a result, Aβ1-42 incubation for 36 h inhibited remarkedly the cell viability of NG108-15, and increased significantly the levels of inflammatory cytokines TNF-α, MCP-1 and IL-10, as well as enhanced the expressions of JNK and p-65 NF-κB in western blot analysis and immunofluorescence assay. However, the pre-incubation with anti-TLR2 (OPN301, 1 μg/ml) or JNK inhibitor SP600125 (10 μg/ml) prior to Aβ1-42 administration, these upregulation events were all reduced. These results suggested that the induction of Aβ1-42 on proinflammatory cytokine generation might be associated with TLR2-dependent JNK/NF-κB signal pathway, at least partially. Our findings indicated that blockade of TLR2/JNK/NF-κB pathway could be beneficial in the pathogenesis of AD.

Authors+Show Affiliations

Department of Neurology, Jintan People's Hospital, Jiangsu, Jintan 213200, PR China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24126115

Citation

Lin, Wei, et al. "The Role of TLR2/JNK/NF-κB Pathway in Amyloid Β Peptide-induced Inflammatory Response in Mouse NG108-15 Neural Cells." International Immunopharmacology, vol. 17, no. 3, 2013, pp. 880-4.
Lin W, Ding M, Xue J, et al. The role of TLR2/JNK/NF-κB pathway in amyloid β peptide-induced inflammatory response in mouse NG108-15 neural cells. Int Immunopharmacol. 2013;17(3):880-4.
Lin, W., Ding, M., Xue, J., & Leng, W. (2013). The role of TLR2/JNK/NF-κB pathway in amyloid β peptide-induced inflammatory response in mouse NG108-15 neural cells. International Immunopharmacology, 17(3), 880-4. https://doi.org/10.1016/j.intimp.2013.09.016
Lin W, et al. The Role of TLR2/JNK/NF-κB Pathway in Amyloid Β Peptide-induced Inflammatory Response in Mouse NG108-15 Neural Cells. Int Immunopharmacol. 2013;17(3):880-4. PubMed PMID: 24126115.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The role of TLR2/JNK/NF-κB pathway in amyloid β peptide-induced inflammatory response in mouse NG108-15 neural cells. AU - Lin,Wei, AU - Ding,Ming, AU - Xue,Jianqin, AU - Leng,Wenhui, Y1 - 2013/10/12/ PY - 2013/06/21/received PY - 2013/09/09/revised PY - 2013/09/11/accepted PY - 2013/10/16/entrez PY - 2013/10/16/pubmed PY - 2014/9/25/medline KW - AD KW - Alzheimer's disease KW - Aβ KW - Aβ deposition KW - ECL KW - ELISA KW - IL-10 KW - IPP KW - Image pro plus KW - JNK KW - MCP-1 KW - MTT KW - NF-κB KW - Neuroinflammatory KW - OD KW - TLR2 KW - TLR2/JNK/NF-κB KW - TNF-α KW - amyloid-beta KW - c-Jun N-terminal kinase KW - enhanced chemiluminescence KW - enzyme linked immunosorbent assay KW - interleukin-10 KW - methylthiazolyldiphenyl-tetrazolium bromide KW - monocyte chemoattractant protein-1 KW - nuclear factor-κB KW - optical density KW - toll-like receptor-2 KW - tumor necrosis factor-α SP - 880 EP - 4 JF - International immunopharmacology JO - Int. Immunopharmacol. VL - 17 IS - 3 N2 - The TLR2-mediated neuroinflammatory activation has been involved in the pathogenesis of Alzheimer's disease (AD) associated with amyloid β(Aβ) deposition. In neuronal damage, JNK and NF-κB pathways contribute to TLR2-dependent secretion of proinflammatory cytokines. However, the role of TLR2/JNK/NF-κB pathway on Aβ-induced inflammatory response in nerve cell damage remains unclear. In the present study, Aβ1-42 was used to induce mouse NG108-15 neural cell injury. The cell viability was detected by methylthiazolyldiphenyl-tetrazolium bromide (MTT). The levels of tumor necrosis factor (TNF)-α, monocyte chemoattractant protein(MCP)-1 and interleukin (IL)-10 in culture supernatant were measured by ELISA. western blot analysis was performed to detect the expressions of JNK and p-65 NF-κB proteins. Immunofluorescence assay was also performed to examine the p-JNK and p-65 NF-κB activation. As a result, Aβ1-42 incubation for 36 h inhibited remarkedly the cell viability of NG108-15, and increased significantly the levels of inflammatory cytokines TNF-α, MCP-1 and IL-10, as well as enhanced the expressions of JNK and p-65 NF-κB in western blot analysis and immunofluorescence assay. However, the pre-incubation with anti-TLR2 (OPN301, 1 μg/ml) or JNK inhibitor SP600125 (10 μg/ml) prior to Aβ1-42 administration, these upregulation events were all reduced. These results suggested that the induction of Aβ1-42 on proinflammatory cytokine generation might be associated with TLR2-dependent JNK/NF-κB signal pathway, at least partially. Our findings indicated that blockade of TLR2/JNK/NF-κB pathway could be beneficial in the pathogenesis of AD. SN - 1878-1705 UR - https://www.unboundmedicine.com/medline/citation/24126115/The_role_of_TLR2/JNK/NF_κB_pathway_in_amyloid_β_peptide_induced_inflammatory_response_in_mouse_NG108_15_neural_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1567-5769(13)00361-5 DB - PRIME DP - Unbound Medicine ER -