Riber Ulla, Heegaard Peter M H, Cordes Henriette, Ståhl Marie, Jensen Tim Kåre, Jungersen Gregers
National Veterinary Institute, Technical University of Denmark, Bülowsvej 27, 1870 Frederiksberg C, Denmark.
National Veterinary Institute, Technical University of Denmark, Bülowsvej 27, 1870 Frederiksberg C, Denmark.
Vaccine. 2015 Jan 1;33(1):156-62. doi: 10.1016/j.vaccine.2014.10.084. Epub 2014 Nov 11.
Lawsonia intracellularis causes porcine proliferative enteropathy and is one of the most economically important diseases in modern pig production worldwide. The Enterisol Ileitis vaccine have been shown to reduce clinical disease and to increase weight gain, however, while the natural infection with L. intracellularis can provide complete protection against re-infection, this has not been achieved by this vaccine. We therefore undertook a detailed characterization of immune responses to L. intracellularis infection in vaccinated pigs (VAC) compared to previously infected pigs (RE) in order to pinpoint immunological determinants of protection.
The VAC pigs shed L. intracellularis to the same extent as non-vaccinated pigs after challenge, however less L. intracellularis in ileum and lymph nodes was seen post mortem. In the RE group, challenge did not lead to L. intracellularis shedding and no challenge bacteria were found post mortem. In both VAC and RE the acute phase haptoglobin response was diminished and L. intracellularis specific IgG responses were delayed and reduced compared to non-vaccinated pigs. On the other hand L. intracellularis specific IFN-γ responses tended to develop faster in the VAC group compared to controls.
Although vaccinated and non-vaccinated pigs shed L. intracellularis at similar levels after challenge, a lower number of intestinal L. intracellularis was observed in the vaccinated pigs at post mortem inspection. This might be due to the observed faster CMI responses upon challenge in vaccinated pigs. Complete protection against infection without L. intracellularis shedding, however, was only seen after a previous infection resulting in IFN-γ production predominantly by CD8(+) and CD4(+) CD8(+) cells. Improved protective vaccines against L. intracellularis should therefore target stimulation of these T cell subsets.
胞内劳森菌可引起猪增生性肠炎，是全球现代养猪生产中最具经济重要性的疾病之一。已证明肠内益生素回肠炎疫苗可减少临床疾病并增加体重，然而，虽然自然感染胞内劳森菌可提供针对再次感染的完全保护，但该疫苗尚未实现这一点。因此，我们对接种疫苗的猪（VAC）与先前感染的猪（RE）针对胞内劳森菌感染的免疫反应进行了详细表征，以确定保护的免疫决定因素。
攻毒后，VAC猪排出胞内劳森菌的程度与未接种疫苗的猪相同，但死后在回肠和淋巴结中发现的胞内劳森菌较少。在RE组中，攻毒未导致胞内劳森菌排出，死后未发现攻毒细菌。与未接种疫苗的猪相比，VAC组和RE组的急性期触珠蛋白反应均减弱，胞内劳森菌特异性IgG反应延迟且降低。另一方面，与对照组相比，VAC组中胞内劳森菌特异性IFN-γ反应倾向于更快出现。
尽管接种疫苗和未接种疫苗的猪在攻毒后排出胞内劳森菌的水平相似，但在死后检查中，接种疫苗的猪肠道内的胞内劳森菌数量较少。这可能是由于观察到接种疫苗的猪在攻毒后细胞介导免疫反应更快。然而，只有在先前感染导致主要由CD8(+)和CD4(+)CD8(+)细胞产生IFN-γ后，才能看到对感染的完全保护且无胞内劳森菌排出。因此，针对胞内劳森菌的改进型保护性疫苗应靶向刺激这些T细胞亚群。
