Pathogenesis of Babesia caballi infection in experimental horses

被引:25
作者
Hanafusa, Y
Cho, KO
Kanemaru, T
Wada, R
Sugimoto, C
Onuma, M [1 ]
机构
[1] Hokkaido Univ, Grad Sch Vet Med, Dept Dis Control, Infect Dis Lab, Sapporo, Hokkaido 0600818, Japan
[2] Japan Racing Assoc, Equine Res Inst, Epizoot Res Stn, Tochigi 3290412, Japan
关键词
Babesia caballi; cytokine; nitric oxide; pathogenesis;
D O I
10.1292/jvms.60.1127
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
The present study was designed to investigate the role of cytokines in the pathogenesis of Babesia caballi in experimentally infected horses. The expression of cytokine mRNA was determined by using reverse transcription-polymerase chain reaction in two B. caballi-infected horses for 2 weeks after the infection. In one horse, there was up-regulation of interferon-gamma, tumor necrosis factor-alpha (TNF-alpha) and interleukin-2 mRNAs, while in the second horse, expression of only TNF-alpha mRNA was up-regulated. No change was observed in interleukin-4 mRNA in both of the horses. To know the relation between nitric oxide (NO) production and pathogenesis, NO production was assayed in three dexamethasone treated-B. caballi-infected horses. Production of NO in all 3 horses increased significantly before death, although the parasitemia level remained very low. Treatment with NO inhibitor resulted in the suppression of NO production and increased parasitemia level in a horse, which died of the infection. The pathological examination showed that the main cause of the death was dyspnoea and pulmonary edema. Histopathologically, diffuse global mesangial proliferative glomerulonephritis was also observed. These results suggested that NO may be a critical effector molecule of immune defense against parasite. TNF-alpha and NO might be contributing to the pathogenesis in B. caballi infection.
引用
收藏
页码:1127 / 1132
页数:6
相关论文
共 28 条
[21]  
Rudin W, 1997, AM J PATHOL, V150, P257
[22]  
STEVENSON MM, 1995, J IMMUNOL, V155, P2545
[23]   THE ROLE OF T(H)1 AND T(H)2 CELLS IN A RODENT MALARIA INFECTION [J].
TAYLORROBINSON, AW ;
PHILLIPS, RS ;
SEVERN, A ;
MONCADA, S ;
LIEW, FY .
SCIENCE, 1993, 260 (5116) :1931-1934
[24]   Measurement of nitric oxide and peroxynitrite generation in the postischemic heart - Evidence for peroxynitrite-mediated reperfusion injury [J].
Wang, PH ;
Zweier, JL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (46) :29223-29230
[25]   Effects of prolonged exposure to oxygen-derived free radicals in canine pulmonary arteries [J].
Wiklund, L ;
McGregor, CGA ;
Miller, VM .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1996, 270 (06) :H2184-H2190
[26]  
Wright I G, 1989, Trans R Soc Trop Med Hyg, V83 Suppl, P11, DOI 10.1016/0035-9203(89)90596-8
[27]   Down-regulation of murine susceptibility to cerebral malaria by inoculation with third-stage larvae of the filarial nematode Brugia pahangi [J].
Yan, Y ;
Inuo, G ;
Akao, N ;
Tsukidate, S ;
Fujita, K .
PARASITOLOGY, 1997, 114 :333-338
[28]  
ZWEIER JL, 1994, J BIOL CHEM, V269, P24156