Jarillo-Luna A, Moreno-Fierros L, Campos-Rodríguez R, Rodríguez-Monroy M A, Lara-Padilla E, Rojas-Hernández S
Departamento de Investigación y Postgrado, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luís y Díaz Mirón, México, D.F., Mexico.
Parasite Immunol. 2008 Jan;30(1):31-8. doi: 10.1111/j.1365-3024.2007.00999.x.
According to previous reports, intranasal administration of the Cry1Ac protein alone or with amoebic lysates increases protection against Naegleria fowleri meningoencephalitis in mice, apparently by eliciting IgA responses in the nasal mucosa. In the current study, we performed an immunohistochemical analysis of IgA in the nasal mucosa of mice immunized intranasally with Cry1Ac, and amoebic lysates or a combination of both. The animals were sacrificed 24 h after the last immunization or after an intranasal lethal challenge with N. fowleri. Our results indicate that all of the intranasal immunizations provoked an increase in areas with metaplasia in the olfactory epithelium, allowing for secretion of IgA. As a result, IgA antibodies were found interacting with trophozoites in the nasal lumen, and there was a marked increase of IgA in the metaplasic epithelium. On the other hand in nonimmunized mice trophozoites were observed invading the nasal mucosa, which was not the case for immunized mice. Our results suggest that intranasal immunization provokes cellular changes in the olfactory epithelium, leading to greater protection against N. fowleri that is probably caused by an increased secretion of IgA. The increased IgA response induced in the nasal mucosa by immunization probably impedes both amoebic adhesion and subsequent invasion of the parasite to the nasal epithelium.
根据先前的报道,单独经鼻内给予Cry1Ac蛋白或与阿米巴裂解物一起给予时,可增强小鼠对福氏耐格里阿米巴脑膜脑炎的抵抗力,这显然是通过在鼻黏膜中引发IgA反应实现的。在本研究中,我们对经鼻内用Cry1Ac、阿米巴裂解物或两者组合免疫的小鼠鼻黏膜中的IgA进行了免疫组织化学分析。在最后一次免疫后24小时或经鼻内用福氏耐格里阿米巴进行致死性攻击后,处死动物。我们的结果表明,所有经鼻内免疫均引发嗅上皮化生区域增加,从而允许IgA分泌。结果,发现IgA抗体与鼻腔内的滋养体相互作用,并且化生上皮中的IgA显著增加。另一方面,在未免疫的小鼠中观察到滋养体侵入鼻黏膜,而免疫小鼠则未出现这种情况。我们的结果表明,经鼻内免疫引发嗅上皮的细胞变化,从而对福氏耐格里阿米巴产生更大的抵抗力,这可能是由于IgA分泌增加所致。免疫在鼻黏膜中诱导的IgA反应增加可能会阻碍阿米巴的黏附以及随后寄生虫对鼻上皮的侵袭。