Genetic influence on nitric oxide production during Eimeria tenella infections in chickens
Genetic influence on nitric oxide production during Eimeria tenella infections in chickens
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DOI：
10.2307/1592493
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发表时间：
1998-04-01
期刊：
影响因子：
1.4
通讯作者：
Lillehoj, HS
中科院分区：
文献类型：
--
作者：
Allen, PC;Lillehoj, HS
通过用被证明是诱导型一氧化氮合酶有效抑制剂的化合物处理耐药的SC和敏感的TK品系的鸡，评估了体内一氧化氮(NO)产生在抵抗柔嫩艾美耳球虫感染中的重要性。SC品系比TK品系在初次感染时产生更高水平的血浆NO2-+NO3-。在初次感染过程中，S-甲基异硫脲或N-G-甲基L-精氨酸对SC鸡降低NO2-+NO3-水平和增加卵囊产量也有更好的反应。然而，无论药物治疗如何，SC株在初次感染期间始终产生更高的卵囊产量，这表明它可能对更高的寄生虫负担敏感。另一方面，SC品系似乎比TK品系更快地形成免疫力，因为与TK品系相比，未经处理和LNMA处理的雏鸡在攻击感染时卵囊产量都减少了。在攻击感染期间，LNMA处理SC株和TK株的卵囊产量进一步减少，而不是增加，这表明NO的产生在对攻击的免疫反应中的参与很少。这些结果表明，柔嫩E原虫感染过程中产生的NO可能只是几种免疫反应中的一种，而可能不是主要的抗球虫效应。
Studies were carried out to assess the importance of nitric oxide (NO) production in vivo in resistance to Eimeria tenella infections through treatment of resistant SC and susceptible TK strains of chickens with compounds proven to be effective inhibitors of induced nitric oxide synthase. The SC strain produced higher levels of plasma NO2- + NO3- in response to primary infection than did the TK strain. SC chickens were also more responsive in reduction of NO2- + NO3- levels and increased oocyst output in response to treatments with S-methylisothiourea or N-G-methyl-L-arginine (LNMA) during primary infection. However, the SC strain, regardless of drug treatment, consistently yielded higher oocyst output during primary infection, indicating it could be susceptible to a higher parasite burden. On the other hand, the SC strain seemed to develop immunity more rapidly than the TK strain, in that oocyst output was decreased in both untreated and LNMA-treated chicks upon challenge infection compared with that of the TK strain. Oocyst output from both SC and TK strains was further decreased by LNMA treatment during challenge infection rather than increased, suggesting minimal involvement of NO production in the immune response to challenge. These results indicate that NO production during primary E, tenella infection may be only one of several immune responses and may not be the main anticoccidial effector.