Yong-Ning Deng1, Wen-Bin Zhou. 1. Department of Neurology, Xiang Ya Hospital, Central South University, Chang Sha, People's Republic of China.
Abstract
OBJECTIVE: Experimental autoimmune neuritis (EAN) is a T cell-mediated animal model of the Guillain-Barré syndrome characterized by inflammation and demyelination of the peripheral nervous system (PNS). The key pathogenesis of EAN is the imbalance between Th1- and Th2-type immune response. Toll-like receptor (TLR) is a receptor of the innate immune system. It can recognize the antigen by pathogen-associated molecular patterns, and activate the antigen-presenting cells, producing costimulating molecules to activate T cells. In this study, we observed the expression of mRNA of TLR4 and TLR9 in EAN rats. METHODS: Male Lewis rats were immunized with the component of PNS myelin sheath protein P0 180-199 (100 microg) and Freund's complete adjuvant (CFA). The clinical signs of rats and the pathological changes in the sciatic nerves were observed. The rats in the immunized group and the control group were sacrificed on day 7, 16, 24 and 33 after immunization. To observe the histopathological changes, sciatic nerve was embedded in paraffin, sectioned and stained with HE and Weil's stain. The mRNA expression of TLR4 and TLR9 in spleen, sciatic nerve, peripheral blood monocytes and lymph nodes was detected by reverse transcriptase PCR dynamically. RESULTS: The EAN group reached the peak of the clinical score at day 16 after the immunization, and the clinical manifestation obviously improved at day 33 after the immunization. The mRNA expression of TLR4 peaked at day 16, then decreased gradually, but at day 33, it was still higher than that of the CFA control group (p < 0.05); there were significant differences among the four time points (p < 0.05). The mRNA expression of TLR9 was upregulated during the entire course of EAN compared to the CFA and the control group (p < 0.05). CONCLUSIONS: TLR4 and TLR9 may play a role in the pathogenesis of EAN by taking part in the activation phage and effector phage. (c) 2008 S. Karger AG, Basel.
OBJECTIVE: Experimental autoimmune neuritis (EAN) is a T cell-mediated animal model of the Guillain-Barré syndrome characterized by inflammation and demyelination of the peripheral nervous system (PNS). The key pathogenesis of EAN is the imbalance between Th1- and Th2-type immune response. Toll-like receptor (TLR) is a receptor of the innate immune system. It can recognize the antigen by pathogen-associated molecular patterns, and activate the antigen-presenting cells, producing costimulating molecules to activate T cells. In this study, we observed the expression of mRNA of TLR4 and TLR9 in EAN rats. METHODS: Male Lewis rats were immunized with the component of PNS myelin sheath protein P0 180-199 (100 microg) and Freund's complete adjuvant (CFA). The clinical signs of rats and the pathological changes in the sciatic nerves were observed. The rats in the immunized group and the control group were sacrificed on day 7, 16, 24 and 33 after immunization. To observe the histopathological changes, sciatic nerve was embedded in paraffin, sectioned and stained with HE and Weil's stain. The mRNA expression of TLR4 and TLR9 in spleen, sciatic nerve, peripheral blood monocytes and lymph nodes was detected by reverse transcriptase PCR dynamically. RESULTS: The EAN group reached the peak of the clinical score at day 16 after the immunization, and the clinical manifestation obviously improved at day 33 after the immunization. The mRNA expression of TLR4 peaked at day 16, then decreased gradually, but at day 33, it was still higher than that of the CFA control group (p < 0.05); there were significant differences among the four time points (p < 0.05). The mRNA expression of TLR9 was upregulated during the entire course of EAN compared to the CFA and the control group (p < 0.05). CONCLUSIONS:TLR4 and TLR9 may play a role in the pathogenesis of EAN by taking part in the activation phage and effector phage. (c) 2008 S. Karger AG, Basel.
Authors: Israt Jahan; Rijwan U Ahammad; Mir M Khalid; Mohammad I Rahman; Shoma Hayat; Badrul Islam; Quazi D Mohammad; Zhahirul Islam Journal: Ann Clin Transl Neurol Date: 2019-03-03 Impact factor: 4.511