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A cholinergic agonist attenuates endotoxin-induced uveitis in rats.
Invest Ophthalmol Vis Sci 2007; 48(6):2719-25IO

Abstract

PURPOSE

Investigation of physiological anti-inflammatory mechanisms can contribute to the treatment of inflammatory disorders. The purpose of the present study was to investigate the effect of nicotine, a selective cholinergic agonist, on endotoxin-induced uveitis (EIU) in rats and the underlying molecular mechanism.

METHODS

Lipopolysaccharide (LPS; endotoxin) and nicotine were injected intraperitoneally. Clinical scores were evaluated by slit lamp. Intracameral protein content and the number of cells were determined. Immunohistochemical reactivity of alpha7 nicotine acetylcholine receptor (alpha7nAChR) was examined in the iris and ciliary body (ICB). mRNA and protein levels of cytokines and chemokines were measured by real-time PCR and enzyme-linked immunosorbent assay.

RESULTS

After LPS injection, clinical scores, as well as protein content and number of cells in the aqueous humor increased during 18 to 36 hours. Nicotine inhibited the endotoxin-induced elevation of these levels. mRNA and protein of alpha7nAChR expression levels were significantly increased by LPS and/or nicotine injection. Nicotine showed no effects on endotoxin-induced elevation of mRNA levels in ICB. However, nicotine decreased the endotoxin-induced elevation of interleukin (IL)-6, IL-1beta, tumor necrosis factor (TNF)-alpha, cytokine-induced neutrophil chemoattractant (CINC)-1, and monocyte chemotactic protein (MCP)-1, but did not affect IL-10 in the serum and aqueous humor.

CONCLUSIONS

Nicotine attenuated endotoxin-induced uveitis through directly decreasing the levels of multiple cytokines and chemokines in the aqueous humor, but did not affect the mRNA levels of these factors. The findings suggest that the nicotinic anti-inflammatory pathway may be involved in the pathogenesis of EIU.

Authors+Show Affiliations

Department of Ophthalmology, Graduate School of Medicine, University of Toyama, Toyama, Japan. ophthal@med.u-toyama.ac.jpNo 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

17525204

Citation

Chi, Zai-Long, et al. "A Cholinergic Agonist Attenuates Endotoxin-induced Uveitis in Rats." Investigative Ophthalmology & Visual Science, vol. 48, no. 6, 2007, pp. 2719-25.
Chi ZL, Hayasaka S, Zhang XY, et al. A cholinergic agonist attenuates endotoxin-induced uveitis in rats. Invest Ophthalmol Vis Sci. 2007;48(6):2719-25.
Chi, Z. L., Hayasaka, S., Zhang, X. Y., Cui, H. S., & Hayasaka, Y. (2007). A cholinergic agonist attenuates endotoxin-induced uveitis in rats. Investigative Ophthalmology & Visual Science, 48(6), pp. 2719-25.
Chi ZL, et al. A Cholinergic Agonist Attenuates Endotoxin-induced Uveitis in Rats. Invest Ophthalmol Vis Sci. 2007;48(6):2719-25. PubMed PMID: 17525204.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A cholinergic agonist attenuates endotoxin-induced uveitis in rats. AU - Chi,Zai-Long, AU - Hayasaka,Seiji, AU - Zhang,Xue-Yun, AU - Cui,Hu-Shan, AU - Hayasaka,Yoriko, PY - 2007/5/26/pubmed PY - 2007/7/3/medline PY - 2007/5/26/entrez SP - 2719 EP - 25 JF - Investigative ophthalmology & visual science JO - Invest. Ophthalmol. Vis. Sci. VL - 48 IS - 6 N2 - PURPOSE: Investigation of physiological anti-inflammatory mechanisms can contribute to the treatment of inflammatory disorders. The purpose of the present study was to investigate the effect of nicotine, a selective cholinergic agonist, on endotoxin-induced uveitis (EIU) in rats and the underlying molecular mechanism. METHODS: Lipopolysaccharide (LPS; endotoxin) and nicotine were injected intraperitoneally. Clinical scores were evaluated by slit lamp. Intracameral protein content and the number of cells were determined. Immunohistochemical reactivity of alpha7 nicotine acetylcholine receptor (alpha7nAChR) was examined in the iris and ciliary body (ICB). mRNA and protein levels of cytokines and chemokines were measured by real-time PCR and enzyme-linked immunosorbent assay. RESULTS: After LPS injection, clinical scores, as well as protein content and number of cells in the aqueous humor increased during 18 to 36 hours. Nicotine inhibited the endotoxin-induced elevation of these levels. mRNA and protein of alpha7nAChR expression levels were significantly increased by LPS and/or nicotine injection. Nicotine showed no effects on endotoxin-induced elevation of mRNA levels in ICB. However, nicotine decreased the endotoxin-induced elevation of interleukin (IL)-6, IL-1beta, tumor necrosis factor (TNF)-alpha, cytokine-induced neutrophil chemoattractant (CINC)-1, and monocyte chemotactic protein (MCP)-1, but did not affect IL-10 in the serum and aqueous humor. CONCLUSIONS: Nicotine attenuated endotoxin-induced uveitis through directly decreasing the levels of multiple cytokines and chemokines in the aqueous humor, but did not affect the mRNA levels of these factors. The findings suggest that the nicotinic anti-inflammatory pathway may be involved in the pathogenesis of EIU. SN - 0146-0404 UR - https://www.unboundmedicine.com/medline/citation/17525204/A_cholinergic_agonist_attenuates_endotoxin_induced_uveitis_in_rats_ L2 - http://iovs.arvojournals.org/article.aspx?doi=10.1167/iovs.06-0644 DB - PRIME DP - Unbound Medicine ER -