Durand Jorge L, Mukherjee Shankar, Commodari Fernando, De Souza Andrea P, Zhao Dazhi, Machado Fabiana S, Tanowitz Herbert B, Jelicks Linda A
Department of Physiology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Am J Trop Med Hyg. 2009 May;80(5):782-7.
Trypanosoma cruzi infection results in an increase in myocardial NO and intense inflammation. NO modulates the T. cruzi-induced myocardial inflammatory reaction. NO synthase (NOS)1-, NOS2-, and NOS3-null mice were infected with T. cruzi (Brazil strain). Infected NOS1-null mice had increased parasitemia, mortality, and left ventricular inner diameter (LVID). Chronically infected NOS1- and NOS2-null and wild-type mice (WT) exhibited increased right ventricular internal diameter (RVID), although the fold increase in the NOS2-null mice was smaller. Infected NOS3-null mice exhibited a significant reduction both in LVID and RVID. Reverse transcriptase-polymerase chain reaction showed expression of NOS2 and NOS3 in hearts of infected NOS1-null and WT mice, whereas infected NOS2-null hearts showed little change in expression of other NOS isoforms. Infected NOS3-null hearts showed an increase only in NOS1 expression. These results may indicate different roles for NOS isoforms in T. cruzi-induced cardiomyopathy.
克氏锥虫感染会导致心肌一氧化氮（NO）增加以及强烈的炎症反应。NO调节克氏锥虫诱导的心肌炎症反应。将一氧化氮合酶（NOS）1、NOS2和NOS3基因敲除的小鼠感染克氏锥虫（巴西株）。感染的NOS1基因敲除小鼠的寄生虫血症、死亡率和左心室内径（LVID）增加。慢性感染的NOS1和NOS2基因敲除小鼠以及野生型小鼠（WT）的右心室内径（RVID）增加，尽管NOS2基因敲除小鼠的增加倍数较小。感染的NOS3基因敲除小鼠的LVID和RVID均显著降低。逆转录聚合酶链反应显示，感染的NOS1基因敲除小鼠和WT小鼠的心脏中NOS2和NOS3表达，而感染的NOS2基因敲除心脏中其他NOS同工型的表达变化不大。感染的NOS3基因敲除心脏仅显示NOS1表达增加。这些结果可能表明NOS同工型在克氏锥虫诱导的心肌病中具有不同作用。
