Toll-like receptors participate in Naegleria fowleri recognition

被引:13
作者
Martinez-Castillo, Moises [1 ]
Santos-Argumedo, Leopoldo [2 ]
Manuel Galvan-Moroyoqui, Jose [3 ]
Serrano-Luna, Jesus [4 ]
Shibayama, Mineko [1 ]
机构
[1] Natl Polytech Inst, Ctr Res & Adv Studies, Dept Infect & Mol Pathogenesis, Av IPN 2508, Mexico City 07360, DF, Mexico
[2] Natl Polytech Inst, Ctr Res & Adv Studies, Dept Mol Biomed, Av IPN 2508, Mexico City 07360, DF, Mexico
[3] Univ Sonora, Dept Med & Hlth Sci, Blvd Luis Donaldo Colosio, Hermosillo 83000, Sonora, Mexico
[4] Natl Polytech Inst, Ctr Res & Adv Studies, Dept Cell Biol, Av IPN 2508, Mexico City 07360, DF, Mexico
关键词
Naegleria fowleri; Toll-like receptors; Pro-inflammatory cytokines; Antimicrobial peptides; Mucoepithelial cells; Primary amoebic meningoencephalitis; NF-KAPPA-B; PRIMARY AMEBIC MENINGOENCEPHALITIS; IMMUNE-RESPONSE; BINDING PROTEIN; INNATE IMMUNITY; EXPRESSION; ACTIVATION; CELLS; TLR; LIPOPOLYSACCHARIDE;
D O I
10.1007/s00436-017-5666-9
中图分类号
R38 [医学寄生虫学]; Q [生物科学];
学科分类号
07 ; 0710 ; 09 ; 100103 ;
摘要
Naegleria fowleri is a protozoan that invades the central nervous system and causes primary amoebic meningoencephalitis. It has been reported that N. fowleri induces an important inflammatory response during the infection. In the present study, we evaluated the roles of Toll-like receptors in the recognition of N. fowleri trophozoites by human mucoepithelial cells, analyzing the expression and production of innate immune response mediators. After amoebic interactions with NCI-H292 cells, the expression and production levels of IL-8, TNF-alpha, IL-1 beta, and human beta defensin-2 were evaluated by RT-PCR, ELISA, immunofluorescence, and dot blot assays, respectively. To determine whether the canonical signaling pathways were engaged, we used different inhibitors, namely, IMG-2005 for MyD88 and BAY 11-7085 for the nuclear factor NFkB. Our results showed that the expression and production of the pro-inflammatory cytokines and beta defensin-2 were induced by N. fowleri mainly through the canonical TLR4 pathway in a time-dependent manner.
引用
收藏
页码:75 / 87
页数:13
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