Herman R, Nolan T J, Fahey J R
Am J Trop Med Hyg. 1982 Jul;31(4):730-9. doi: 10.4269/ajtmh.1982.31.730.
Female hamsters, infected intracardially (i.c.) with 1.0--2.0 x 10(5) amastigotes of Leishmania donovani produced offspring, following mating, which, when immunized subcutaneously with 1.0 x 10(7) amastigotes at 8 weeks of age, were more resistant to i.c. challenge 6 weeks later than were hamsters born to non-infected mothers. Offspring of mothers infected with as many as 6.0 x 10(6) amastigotes demonstrated no greater capacity for immunization than did those of mothers infected with 1.0 x 10(5) amastigotes. Sensitization of offspring of infected mothers apparently is transplacental since the effect could only be seen in offspring of infected mothers and not in those of normal mothers weaned by infected dams. Offspring of female hamsters immunized by footpad inoculation of 1.0 x 10(7) amastigotes exhibited reduced spleen parasite burdens when challenged at 8.5 weeks of age and reduced spleen and liver parasite burdens when challenged at 16 weeks of age, compared to offspring of nonimmunized hamsters; this effect was not noted following challenge of offspring of the two groups within 1 day of weaning. The passage of parasites from mother to young during gestation and/or nursing apparently does not occur since, at 125 days of age, no parasites were observed in spleen or liver impression smears of offspring of hamsters infected i.c. with 6.0 x 10(6) amastigotes while parasites were seen in such smears of hamsters infected, 120 days previously, with 10 amastigotes i.c. Thus, sensitization to immunization in offspring of infected hamsters and to challenge of offspring of immunized hamsters is apparently transplacental, effected either by soluble leishmanial antigen, soluble lymphocyte (or transfer) factor, or by cells.
雌性仓鼠经心内注射1.0--2.0×10⁵杜氏利什曼原虫无鞭毛体后受孕产仔。这些仔鼠在8周龄时经皮下注射1.0×10⁷无鞭毛体进行免疫,6周后经心内攻击时,比未感染母亲所生的仓鼠更具抵抗力。感染多达6.0×10⁶无鞭毛体的母亲所生的仔鼠,其免疫能力并不比感染1.0×10⁵无鞭毛体的母亲所生的仔鼠更强。感染母亲的仔鼠的致敏显然是经胎盘的,因为这种效应只在感染母亲的仔鼠中可见,而在由感染母鼠哺育的正常母亲的仔鼠中则未见。与未免疫仓鼠的后代相比,经足垫接种1.0×10⁷无鞭毛体免疫的雌性仓鼠的后代在8.5周龄时受到攻击时脾脏寄生虫负荷降低,在16周龄时受到攻击时脾脏和肝脏寄生虫负荷降低;在两组后代断奶后1天内进行攻击时,未观察到这种效应。在妊娠和/或哺乳期间,寄生虫显然不会从母亲传给幼仔,因为在125日龄时,经心内注射6.0×10⁶无鞭毛体感染的仓鼠的后代的脾脏或肝脏印片涂片中未观察到寄生虫,而在120天前经心内注射10个无鞭毛体感染的仓鼠的此类涂片中可见寄生虫。因此,感染仓鼠的后代对免疫的致敏以及免疫仓鼠的后代对攻击的反应显然是经胎盘的,可能是由可溶性利什曼原虫抗原、可溶性淋巴细胞(或转移)因子或细胞引起的。