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首页> 外文期刊>Infection and immunity >Virulent Salmonella typhimurium-induced lymphocyte depletion and immunosuppression in chickens.
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Virulent Salmonella typhimurium-induced lymphocyte depletion and immunosuppression in chickens.

机译:鸡伤寒沙门氏菌引起的淋巴细胞耗竭和免疫抑制。

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摘要

The effect of experimental Salmonella infection on chicken lymphoid organs, immune responses, and fecal shedding of salmonellae were assessed following oral inoculation of 1-day-old chicks or intra-air-sac infection of 4-week-old chickens with virulent S. typhimurium wild-type chi 3761 or avirulent S. typhimurium delta cya delta crp vaccine strain chi 3985. Some 4-week-old chickens infected intra-air-sac with chi 3761 or chi 3985 were challenged with Bordetella avium to determine the effect of Salmonella infection on secondary infection by B. avium. S. typhimurium chi 3761 caused lymphocyte depletion, atrophy of lymphoid organs, and immunosuppression 2 days after infection in 1-day-old chicks and 4-week-old chickens. The observed lymphocyte depletion or atrophy of lymphoid organs was transient and dose dependent. Lymphocyte depletion and immunosuppression were associated with prolonged fecal shedding of S. typhimurium chi 3761. No lymphocyte depletion, immunosuppression, or prolonged Salmonella shedding was observed in groups of chickens infected orally or intra-air-sac with chi 3985. Infection of chickens with salmonellae before challenge with B. avium did not suppress the specific antibody response to B. avium. However, B. avium isolation was higher in visceral organs of chickens infected with chi 3761 and challenged with B. avium than in chickens infected with B. avium only. Infection of chickens with chi 3985 reduced B. avium colonization. We report a new factor in Salmonella pathogenesis and reveal a phenomenon which may play a critical role in the development of Salmonella carrier status in chickens. We also showed that 10(8) CFU of chi 3985, which is our established oral vaccination dose for chickens, did not cause immunosuppression or enhance the development of Salmonella carrier status in chickens.
机译:在口服接种1日龄小鸡或4周龄强毒鼠伤寒沙门氏菌气内感染后,评估了实验性沙门氏菌感染对鸡淋巴器官,免疫反应和排泄沙门氏菌的影响。野生型chi 3761或无毒鼠伤寒沙门氏菌del cya delta crp疫苗株chi3985。用气孔博德特氏菌攻击一些感染了chi 3761或chi 3985的气囊内4周龄的鸡,以确定沙门氏菌感染的效果禽双歧杆菌继发感染。感染鼠伤寒沙门氏菌chi 3761在1日龄雏鸡和4周龄雏鸡感染后2天导致淋巴细胞耗竭,淋巴器官萎缩和免疫抑制。所观察到的淋巴细胞耗竭或淋巴器官萎缩是短暂的并且是剂量依赖性的。淋巴细胞耗竭和免疫抑制与鼠伤寒沙门氏菌chi 3761的粪便排泄时间延长有关。口服或在气囊内感染chi 3985的鸡群中未观察到淋巴细胞耗竭,免疫抑制或沙门氏菌排放时间延长。沙门氏菌感染的鸡在用禽双歧杆菌攻击之前,未抑制对禽双歧杆菌的特异性抗体应答。但是,在感染了chi 3761并感染了B. avium的鸡的内脏器官中,B。avium的分离度要高于仅感染B. avium的鸡。感染chi 3985的鸡减少了禽双歧杆菌的定殖。我们报告了沙门氏菌发病机理中的一个新因素,并揭示了一种现象,该现象可能在鸡中沙门氏菌携带者地位的发展中发挥关键作用。我们还显示,chi 3985的10(8)CFU(这是我们为鸡确定的口服疫苗接种剂量)不会引起免疫抑制或增强鸡中沙门氏菌携带者的状态。

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