Morchón R, Roca F, López-Belmonte J, Genchi M, Venco L, Rodríguez-Barbero A, Simón F
Laboratorio de Parasitología, Facultad de Farmacia, Universidad de Salamanca, Avda. Campo Charro s/n, 37007 Salamanca, Spain.
Vet Parasitol. 2007 Jul 20;147(3-4):271-5. doi: 10.1016/j.vetpar.2007.04.010. Epub 2007 Jun 1.
Feline heartworm (Dirofilaria immitis) infection is a severe, life-threatening disease. The eicosanoids are lipid mediators derived from the metabolism of the arachidonic acid, involved in the regulation of the immune response and of inflammatory reactions. In this study, naturally infected cats showed significant higher levels of prostaglandin E(2) (PGE2), thromboxane B(2) (TXB(2)) and leukotriene B(4) (LTB4) than uninfected cats. Changes in the levels of eicosanoids during the infection were observed in experimentally infected cats. PGE2 increased significantly during the first 60 days post-infection, then progressively decreased until day 180 post-infection. At this time, PGE2 values are still significantly higher than those observed before the infection. TxB2 and LTB4 increased progressively from the beginning of infection and reached their maximum levels 180 days post-infection. In experimentally infected, ivermectin-treated cats, 15 days after treatment (45 days after infection) both PGE2 and LTB4 levels were similar to those observed in experimentally infected, untreated cats. No significant differences of PGE2 levels were found before the infection and at the end of the experiment (165 days post-treatment, 195 days post-infection). Increased levels of LTB4 were found 15 days post-treatment, afterward they progressively decreased. These data show that D. immitis infection influences the production of intravascular eicosanoids in cats. The high levels of PGE2 observed in the early phase of infection could be related to the survival of the worms, while those of TxB2 and LTB4 detected at the end of the study could mediate the inflammatory reactions and thrombi formation during the feline dirofilariosis.
猫心丝虫（恶丝虫）感染是一种严重的、危及生命的疾病。类花生酸是由花生四烯酸代谢产生的脂质介质，参与免疫反应和炎症反应的调节。在本研究中，自然感染的猫体内前列腺素E2（PGE2）、血栓素B2（TXB2）和白三烯B4（LTB4）的水平显著高于未感染的猫。在实验感染的猫中观察到感染期间类花生酸水平的变化。感染后前60天PGE2显著升高，然后逐渐下降直至感染后180天。此时，PGE2值仍显著高于感染前观察到的值。TXB2和LTB4从感染开始逐渐升高，并在感染后180天达到最高水平。在实验感染并接受伊维菌素治疗的猫中，治疗后15天（感染后45天），PGE2和LTB4水平与实验感染但未治疗的猫中观察到的水平相似。在感染前和实验结束时（治疗后165天，感染后195天）未发现PGE2水平有显著差异。治疗后15天发现LTB4水平升高，之后逐渐下降。这些数据表明，恶丝虫感染会影响猫体内血管内类花生酸的产生。感染早期观察到的高PGE2水平可能与虫体的存活有关，而研究结束时检测到的TXB2和LTB4水平可能介导了猫心丝虫病期间的炎症反应和血栓形成。
