Thakur A, Kyd J, Xue M, Willcox M D, Cripps A
Cooperative Research Center for Eye Research and Technology, The University of New South Wales, Sydney, New South Wales 2052, Australia.
Infect Immun. 2001 May;69(5):3295-304. doi: 10.1128/IAI.69.5.3295-3304.2001.
Pseudomonas aeruginosa is an opportunistic pathogen which causes sight-threatening corneal infections in humans. The purpose of this study was to evaluate various immunization routes that may provide protection against Pseudomonas keratitis and to define the molecular mechanisms involved in the protection. Sprague-Dawley rats (10 to 12 weeks old) were immunized using paraformaldehyde-killed P. aeruginosa (strain 6206) via oral, nasal, and intra-Peyer's patch (IPP) routes followed by an ocular topical booster dose. Scratched corneas were challenged with an infective dose of P. aeruginosa. Following clinical examination, eyes were enucleated for histology, polymorphonuclear leukocyte (PMN) quantitation, bacterial count, enzyme-linked immunosorbent assay, and RNase protection assay. PMN infiltration was higher early (4 h) during the infection in immunized rats than in nonimmunized rats. Later during the infection, the number of PMNs diminished in immunized rats while in nonimmunized animals the number of PMNs continued to increase. Bacteria were cleared much faster from immunized groups than from the nonimmunized group, and the nasally immunized group had the most efficacious response among the immunized groups. Nasal and IPP immunization groups had increased cytokine expression of interleukin-2 (IL-2) and IL-5 and differed from each other for IL-6. All three immunized groups had significantly reduced IL-1 beta levels when compared with the nonimmunized rats and a significantly altered profile for CINC-1 expression. This study has shown that the route of immunization modulates the inflammatory response to ocular P. aeruginosa infection, thus affecting the severity of keratitis and adverse pathology, with nasal immunization being the most effective.
铜绿假单胞菌是一种机会致病菌,可导致人类发生威胁视力的角膜感染。本研究的目的是评估可能提供针对铜绿假单胞菌性角膜炎保护作用的各种免疫途径,并确定参与保护作用的分子机制。选用10至12周龄的Sprague-Dawley大鼠,通过口服、鼻腔和经派伊尔结内注射(IPP)途径,用甲醛灭活的铜绿假单胞菌(菌株6206)进行免疫,随后给予眼部局部加强剂量。用感染剂量的铜绿假单胞菌对划痕角膜进行攻击。临床检查后,摘除眼球进行组织学检查、多形核白细胞(PMN)定量、细菌计数、酶联免疫吸附测定和核糖核酸酶保护测定。在感染早期(4小时),免疫大鼠角膜中的PMN浸润高于未免疫大鼠。在感染后期,免疫大鼠角膜中的PMN数量减少,而未免疫动物角膜中的PMN数量继续增加。与未免疫组相比,免疫组细菌清除速度更快,且鼻腔免疫组在免疫组中反应最为有效。鼻腔免疫组和IPP免疫组白细胞介素-2(IL-2)和IL-5的细胞因子表达增加,IL-6表达两者有所不同。与未免疫大鼠相比,所有三个免疫组的IL-1β水平均显著降低,趋化因子CINC-1的表达谱也有显著改变。本研究表明,免疫途径可调节对眼部铜绿假单胞菌感染的炎症反应,从而影响角膜炎的严重程度和不良病理变化,其中鼻腔免疫最为有效。