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致病性鼠伤寒沙门氏菌引起鸡淋巴细胞耗竭和免疫抑制。

Virulent Salmonella typhimurium-induced lymphocyte depletion and immunosuppression in chickens.

作者信息

Hassan J O, Curtiss R

机构信息

Department of Biology, Washington University, St. Louis, Missouri 63130.

出版信息

Infect Immun. 1994 May;62(5):2027-36. doi: 10.1128/iai.62.5.2027-2036.1994.

Abstract

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.

摘要

在给1日龄雏鸡口服接种或给4周龄鸡进行气囊肿内接种有毒的鼠伤寒沙门氏菌野生型chi 3761或无毒的鼠伤寒沙门氏菌cya缺失crp缺失疫苗株chi 3985后,评估了实验性沙门氏菌感染对鸡淋巴器官、免疫反应以及沙门氏菌粪便排出的影响。给一些经气囊肿内接种chi 3761或chi 3985的4周龄鸡用禽博德特氏菌进行攻毒,以确定沙门氏菌感染对禽博德特氏菌继发感染的影响。鼠伤寒沙门氏菌chi 3761在1日龄雏鸡和4周龄鸡感染后2天导致淋巴细胞减少、淋巴器官萎缩和免疫抑制。观察到的淋巴细胞减少或淋巴器官萎缩是短暂的且呈剂量依赖性。淋巴细胞减少和免疫抑制与鼠伤寒沙门氏菌chi 3761粪便排出时间延长有关。在经口或气囊肿内接种chi 3985的鸡群中未观察到淋巴细胞减少、免疫抑制或沙门氏菌排出时间延长。在用禽博德特氏菌攻毒前用沙门氏菌感染鸡并未抑制对禽博德特氏菌的特异性抗体反应。然而,在接种chi 3761并用禽博德特氏菌攻毒的鸡的内脏器官中,禽博德特氏菌的分离率高于仅感染禽博德特氏菌的鸡。用chi 3985感染鸡减少了禽博德特氏菌的定植。我们报道了沙门氏菌发病机制中的一个新因素,并揭示了一种可能在鸡沙门氏菌带菌状态发展中起关键作用的现象。我们还表明,我们确定的鸡口服疫苗剂量10⁸CFU的chi 3985不会导致免疫抑制或促进鸡沙门氏菌带菌状态的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf0/186462/0791dc478651/iai00005-0537-a.jpg

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