Muir W I, Bryden W L, Husband A J
Department of Veterinary Anatomy and Pathology, Faculty of Veterinary Science, University of Sydney, NSW, Australia.
Poult Sci. 1998 Dec;77(12):1874-83. doi: 10.1093/ps/77.12.1874.
Conventional methods of parenteral immunization with killed bacterin vaccines have met with limited success in protecting the avian intestinal mucosa from pathogens such as Salmonella typhimurium. For mucosal vaccines to be successful they must be evaluated for their ability to stimulate local secretory immunoglobulin (SIgA) at the mucosal surface, which acts as the first line of defense against invading pathogens. Previously we have demonstrated the ability of i.p. immunization with nonreplicating antigen in an appropriate adjuvant to induce a primary immune response, which, after an oral booster immunization, stimulates enhanced intestinal IgA responses in chickens. In the experiments reported here we have applied this immunization protocol to vaccinate against S. typhimurium in chickens, and examined the protection provided against subsequent S. typhimurium challenge by placing vaccinated birds on seeded litter with cohabitant infected birds. Immunized+challenged birds displayed delayed onset of S. typhimurium infection, both at the mucosal surface and within the reticuloendothelial system. Elevated anti-S. typhimurium IgG and IgA titers were detected in serum after vaccination, which markedly increased after challenge, to levels higher than in control+challenged chickens. Anti-S. typhimurium IgA in bile and intestinal scrapings supernatant was also higher in the immunized+challenged birds than in the control+challenged birds 15 d after challenge. This study illustrates the potential for i.p. vaccination to induce a mucosal immune response to S. typhimurium in chickens, which, in the challenge model employed here, provided partial protection against intestinal challenge with the same pathogen and was reflected in deferred onset of bacterial infection and shedding.
用灭活菌苗进行肠胃外免疫的传统方法，在保护禽类肠道黏膜免受鼠伤寒沙门氏菌等病原体侵害方面取得的成功有限。要使黏膜疫苗取得成功，必须评估其在黏膜表面刺激局部分泌型免疫球蛋白（SIgA）的能力，SIgA是抵御入侵病原体的第一道防线。此前我们已经证明，在适当佐剂中用非复制性抗原进行腹腔免疫能够诱导初次免疫反应，经口服加强免疫后，可刺激鸡的肠道IgA反应增强。在本文报道的实验中，我们应用了这种免疫方案对鸡进行鼠伤寒沙门氏菌疫苗接种，并通过将接种疫苗的鸡与同居感染鸡放置在有菌垫料上，来检测对随后鼠伤寒沙门氏菌攻击的保护作用。免疫+攻击组的鸡在黏膜表面和网状内皮系统内，鼠伤寒沙门氏菌感染的发病时间均延迟。接种疫苗后在血清中检测到抗鼠伤寒沙门氏菌IgG和IgA滴度升高，攻击后滴度显著增加，高于对照+攻击组鸡的水平。攻击后15天，免疫+攻击组鸡胆汁和肠道刮取物上清液中的抗鼠伤寒沙门氏菌IgA也高于对照+攻击组鸡。本研究说明了腹腔接种疫苗诱导鸡对鼠伤寒沙门氏菌产生黏膜免疫反应的潜力，在本文采用的攻击模型中，这种免疫反应对同一病原体的肠道攻击提供了部分保护，表现为细菌感染和排菌的延迟。
