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Spinal toll like receptor 3 is involved in chronic pancreatitis-induced mechanical allodynia of rat.
Mol Pain. 2011 Feb 22; 7:15.MP

Abstract

BACKGROUND

Mechanisms underlying pain in chronic pancreatitis (CP) are incompletely understood. Our previous data showed that astrocytes were actively involved. However, it was unclear how astrocytic activation was induced in CP conditions. In the present study, we hypothesized that toll-like receptors (TLRs) were involved in astrocytic activation and pain behavior in CP-induced pain.

RESULTS

To test our hypothesis, we first investigated the changes of TLR2-4 in the rat CP model induced by intrapancreatic infusion of trinitrobenzene sulfonic acid (TNBS). Western blot showed that after TNBS infusion, TLR3, but not TLR2 or TLR4, was increased gradually and maintained at a very high level for up to 5 w, which correlated with the changing course of mechanical allodynia. Double immunostaining suggested that TLR3 was highly expressed on astrocytes. Infusion with TLR3 antisense oligodeoxynucleotide (ASO) dose-dependently attenuated CP-induced allodynia. CP-induced astrocytic activation in the spinal cord was also significantly suppressed by TLR3 ASO. Furthermore, real-time PCR showed that IL-1β, TNF-α, IL-6 and monocyte chemotactic protein-1 (MCP-1) were significantly increased in spinal cord of pancreatic rats. In addition, TLR3 ASO significantly attenuated CP-induced up-regulation of IL-1β and MCP-1.

CONCLUSIONS

These results suggest a probable "TLR3-astrocytes-IL-1β/MCP-1" pathway as a positive feedback loop in the spinal dorsal horn in CP conditions. TLR3-mediated neuroimmune interactions could be new targets for treating persistent pain in CP patients.

Authors+Show Affiliations

Department of Hepatobiliary Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, PR China.No affiliation info availableNo affiliation info availableNo 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

21342497

Citation

Qian, Nian-Song, et al. "Spinal Toll Like Receptor 3 Is Involved in Chronic Pancreatitis-induced Mechanical Allodynia of Rat." Molecular Pain, vol. 7, 2011, p. 15.
Qian NS, Liao YH, Feng QX, et al. Spinal toll like receptor 3 is involved in chronic pancreatitis-induced mechanical allodynia of rat. Mol Pain. 2011;7:15.
Qian, N. S., Liao, Y. H., Feng, Q. X., Tang, Y., Dou, K. F., & Tao, K. S. (2011). Spinal toll like receptor 3 is involved in chronic pancreatitis-induced mechanical allodynia of rat. Molecular Pain, 7, 15. https://doi.org/10.1186/1744-8069-7-15
Qian NS, et al. Spinal Toll Like Receptor 3 Is Involved in Chronic Pancreatitis-induced Mechanical Allodynia of Rat. Mol Pain. 2011 Feb 22;7:15. PubMed PMID: 21342497.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Spinal toll like receptor 3 is involved in chronic pancreatitis-induced mechanical allodynia of rat. AU - Qian,Nian-Song, AU - Liao,Yong-Hui, AU - Feng,Quan-Xing, AU - Tang,Yu, AU - Dou,Ke-Feng, AU - Tao,Kai-Shan, Y1 - 2011/02/22/ PY - 2010/09/02/received PY - 2011/02/22/accepted PY - 2011/2/24/entrez PY - 2011/2/24/pubmed PY - 2011/6/23/medline SP - 15 EP - 15 JF - Molecular pain JO - Mol Pain VL - 7 N2 - BACKGROUND: Mechanisms underlying pain in chronic pancreatitis (CP) are incompletely understood. Our previous data showed that astrocytes were actively involved. However, it was unclear how astrocytic activation was induced in CP conditions. In the present study, we hypothesized that toll-like receptors (TLRs) were involved in astrocytic activation and pain behavior in CP-induced pain. RESULTS: To test our hypothesis, we first investigated the changes of TLR2-4 in the rat CP model induced by intrapancreatic infusion of trinitrobenzene sulfonic acid (TNBS). Western blot showed that after TNBS infusion, TLR3, but not TLR2 or TLR4, was increased gradually and maintained at a very high level for up to 5 w, which correlated with the changing course of mechanical allodynia. Double immunostaining suggested that TLR3 was highly expressed on astrocytes. Infusion with TLR3 antisense oligodeoxynucleotide (ASO) dose-dependently attenuated CP-induced allodynia. CP-induced astrocytic activation in the spinal cord was also significantly suppressed by TLR3 ASO. Furthermore, real-time PCR showed that IL-1β, TNF-α, IL-6 and monocyte chemotactic protein-1 (MCP-1) were significantly increased in spinal cord of pancreatic rats. In addition, TLR3 ASO significantly attenuated CP-induced up-regulation of IL-1β and MCP-1. CONCLUSIONS: These results suggest a probable "TLR3-astrocytes-IL-1β/MCP-1" pathway as a positive feedback loop in the spinal dorsal horn in CP conditions. TLR3-mediated neuroimmune interactions could be new targets for treating persistent pain in CP patients. SN - 1744-8069 UR - https://www.unboundmedicine.com/medline/citation/21342497/Spinal_toll_like_receptor_3_is_involved_in_chronic_pancreatitis_induced_mechanical_allodynia_of_rat_ L2 - https://journals.sagepub.com/doi/10.1186/1744-8069-7-15?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -