Objective To characterize platelet activation and its correlations with parasitemia in peripheral blood of mice infected by Babesia microti. Methods BALB/c mice were intraperitoneally inoculated with B. microti infected blood, which was collected, heparinized, and diluted with sterile saline to achieve a 30% RBC parasitic infection rate. Following the infection, anti-coagulated peripheral blood was collected from the mice at each day. The blood was stained with anti-CD61 and anti-CD62P antibodies, and then used to analyze the activation of platelet with flow cytometry. Furthermore, the percentage of parasitized red blood cells was determined via Giemsa-stained thin blood films. Finally, Pearson correlation analysis was used to evaluate the correlation of platelet activation and parasitemia. Results The percentage of platelet activation started to increase on the second day post infection, reached the peak on the third day[(15.50±0.17)%], and declined from the fourth day, but was absence of obvious regularities. The percentage of parasitized red blood cells gradually ascended post infection and reached the peak at the eighth day[(63.10±3.43)%], and then declined. However, there was no significant difference between the percentage of platelet activation and parasitized red blood cells, which was characterized by Pearson correlation analysis (P>0.05). Conclusion The platelet activation can be induced by B. microti infection, but it has no significant correlation with parasitemia.
[1] Vannier E, Krause PJ. Human babesiosis[J]. N Engl J Med, 2012,366(25):2397-2407.
[2] Vannier E, Krause PJ. Babesiosis in China, an emerging threat[J]. Lancet Infect Dis,2015,15(2):137-139.
[3] Fang LQ, Liu K, Li XL, et al. Emerging tick-borne infections in mainland China:an increasing public health threat[J]. Lancet Infect Dis,2015,15(12):1467-1479.
[4] Lemieux JE,Tran AD,Freimark L,et al. A global map of genetic diversity in Babesia microti reveals strong population structure and identifies variants associated with clinical relapse[J]. Nat Microbiol,2016,1(7):16079.
[5] Obiegala A, Pfeffer M, Pfister K, et al. Molecular examinations of Babesia microti in rodents and rodent-attached ticks from urban and sylvatic habitats in Germany[J]. Ticks Tick Borne Dis,2015,6(4):445-449.
[6] Bullard JM, Ahsanuddin AN, Perry AM, et al. The first case of locally acquired tick-borne Babesia microti infection in Canada[J]. Can J Infect Dis Med Microbiol,2014,25(6):e87-89.
[7] Tuvshintulga B, Sivakumar T, Battsetseg B, et al. The PCR detection and phylogenetic characterization of Babesia microti in questing ticks in Mongolia[J]. Parasitol Int,2015,64(6):527-532.
[8] Smyth SS, McEver RP, Weyrich AS, et al. Platelet functions beyond hemostasis[J]. J Thromb Haemost,2009,7(11):1759-1766.
[9] Czapiga M, Kirk AD, Lekstrom-Himes J, et al. Platelets deliver costimulatory signals to antigen-presenting cells:a potential bridge between injury and immune activation[J]. Exp Hematol, 2004,32(2):135-139.
[10] Sharma J, Eickhoff CS, Hoft DF, et al. Absence of calcium-independent phospholipase A2β impairs platelet-activating factor production and inflammatory cell recruitment in Trypanosoma cruzi-infected endothelial cells[J]. Physiol Rep, 2014,2(1):e00196.
[11] Goncalves R,Zhang X,Cohen H,et al. Platelet activation attracts a subpopulation of effector monocytes to sites of Leishmania major infection[J]. J Exp Med,2011,208(6):1253-1265.
[12] McMorran BJ, Wieczorski L, Drysdale KE, et al. Platelet factor 4 and Duffy antigen required for platelet killing of Plasmodium falciparum[J]. Science,2012,338(6112):1348-1351.
[13] McMorran BJ, Marshall VM, de Graaf C, et al. Platelets kill intraerythrocytic malarial parasites and mediate survival to infection[J]. Science,2009,323(5915):797-800.
[14] Aggrey AA, Srivastava K, Ture S, et al. Platelet induction of the acute-phase response is protective in murine experimental cerebral malaria[J]. J Immunol,2013,190(9):4685-4691.
[15] Goddard A,Leisewitz AL,Kristensen AT,et al. Platelet activation and platelet-leukocyte interaction in dogs naturally infected with Babesia rossi[J]. Vet J,2015,205(3):387-392.
[16] Michelson AD, Barnard MR, Krueger LA, et al. Circulating monocyte-platelet aggregates are a more sensitive marker of in vivo platelet activation than platelet surface P-selection:studies in baboons, human coronary intervention, and human acute myocardial infarction[J]. Circulation,2001,104(13):1533-1537.
[17] Moritz A, Walcheck BK, Weiss DJ. Flow cytometric detection of activated platelets in the dog[J]. Vet Clin Pathol,2003,32(1):6-12.
[18] 张加,司晨晨, 蔡玉春,等. 田鼠巴贝虫可溶性抗原组分分析及其初步应用[J]. 中国人兽共患病学报,2014,30(5):469-478.
[19] Zhou X,Xia S,Huang JL, et al. Human babesiosis, an emerging tick-borne disease in the people's republic of China[J]. Parasit Vectors,2014,7:509.
[20] Emuchay CI, Usanga EA. Increased platelet factor 3 activity in Plasmodium falciparum malaria[J]. East Afr Med J,1997,74(8):527-529.
[21] Pain A,Ferguson DJP, Kai O, et al. Platelet-mediated clumping of Plasmodium falciparum-infected erythrocytes is a common adhesive phenotype and is associated with severe malaria[J]. Proc Natl Acad Sci USA,2001,98(4):1805-1810.
[22] Chotivanich K, Sritabal J, Udomsangpetch R, et al. Platelet-induced autoagglutination of Plasmodium falciparum-infected red blood cells and disease severity in Thailand[J]. J Infect Dis, 2004,189(6):1052-1055.
[23] 魏金龙,周勇志,龚海燕,等. 田鼠巴贝斯虫感染对宿主凝血系统的影响[J]. 中国兽医科学,2015,45(4):390-394.
[24] Piguet PF, Kan CD, Vesin C. Thrombocytopenia in an animal model of malaria is associated with an increased caspase-mediated death of thrombocytes[J]. Apoptosis,2002,7(2):91-98.
[25] Gramaglia I,Sahlin H,Nolan JP,et al. Cell-rather than antibody-mediated immunity leads to the development of profound thrombocytopenia during experimental Plasmodium berghei malaria[J]. J Immunol,2005,175(11):7699-7707.
[26] Evelyn ME, Ezeiruaku F, Ukaji DC. Experiential relationship between malaria parasite density and some haematological parameters in malaria infected male subjects in Port Harcourt, Nigeria[J]. Glob J Health Sci,2012,4(4):139-148.
