Wing E J, Remington J S
Infect Immun. 1978 Aug;21(2):398-404. doi: 10.1128/iai.21.2.398-404.1978.
To determine whether activated macrophages are important in resistance against the intestinal phase of nematode parasites, we studied Trichinella spiralis infections in mice with normal macrophages and in mice with macrophages activated by either chronic Toxoplasma gondii or acute Listeria monocytogenes infections. The peak T. spiralis adult worm burden in the intestines of normal C57BL/6 or Swiss Webster mice occurred from 6 to 14 days after infection. Subsequent expulsion of worms from the intestines occurred from 8 to 20 days after infection. C57BL/6 mice chronically infected with T. gondii and then challenged with T. spiralis larvae had significantly lower peak intestinal worm burdens (P < 0.05) than normal C57BL/6 mice similarly challenged. Swiss Webster mice infected 7 or 13 days earlier with L. monocytogenes and then challenged with T. spiralis larvae had significantly lower peak worm burdens (P < 0.01) than uninfected mice. The time of expulsion of adult worms was not affected by either infection. Swiss Webster mice infected 42 days earlier with L. monocytogenes (i.e., possessing lymphocytes sensitized to L. monocytogenes but not possessing activated macrophages) did not have a lower worm burden than uninfected mice. Serum factors (e.g., antibody) did not appear to play a role because normal mice injected with serum from L. monocytogenes-infected mice had worm burdens similar to those of mice injected with normal serum. The histopathology of intestines of mice infected with T. gondii or L. monocytogenes was the same as that of normal mice. When T. spiralis larvae were incubated with normal macrophages or macrophages from T. spiralis-infected mice in vitro for 24 h, the number of larvae with adherent T. spiralis macrophages was significantly (P < 0.005) greater than the number of larvae with adherent normal macrophages. These studies suggest a role for activated macrophages in resistance to T. spiralis.
为了确定活化的巨噬细胞在抵抗线虫寄生虫肠道期感染中是否重要,我们研究了正常巨噬细胞的小鼠以及巨噬细胞被慢性弓形虫感染或急性单核细胞增生李斯特菌感染激活的小鼠中的旋毛虫感染情况。正常C57BL/6或瑞士韦伯斯特小鼠肠道内旋毛虫成虫负荷高峰出现在感染后6至14天。随后在感染后8至20天出现肠道内蠕虫排出。慢性感染弓形虫后再用旋毛虫幼虫攻击的C57BL/6小鼠,其肠道蠕虫负荷高峰显著低于(P<0.05)同样受到攻击的正常C57BL/6小鼠。7天或13天前感染单核细胞增生李斯特菌后再用旋毛虫幼虫攻击的瑞士韦伯斯特小鼠,其蠕虫负荷高峰显著低于(P<0.01)未感染小鼠。成虫排出时间不受任何一种感染的影响。42天前感染单核细胞增生李斯特菌的瑞士韦伯斯特小鼠(即拥有对单核细胞增生李斯特菌致敏的淋巴细胞但不拥有活化巨噬细胞),其蠕虫负荷并不低于未感染小鼠。血清因子(如抗体)似乎不起作用,因为注射来自单核细胞增生李斯特菌感染小鼠血清的正常小鼠的蠕虫负荷与注射正常血清的小鼠相似。感染弓形虫或单核细胞增生李斯特菌的小鼠肠道组织病理学与正常小鼠相同。当旋毛虫幼虫在体外与正常巨噬细胞或旋毛虫感染小鼠的巨噬细胞孵育24小时时,附着有旋毛虫巨噬细胞的幼虫数量显著(P<0.005)多于附着有正常巨噬细胞的幼虫数量。这些研究表明活化的巨噬细胞在抵抗旋毛虫感染中发挥作用。