Lactoferrin effects on phagocytic cell function. I. Increased uptake and killing of an intracellular parasite by murine macrophages and human monocytes.
Lactoferrin effects on phagocytic cell function. I. Increased uptake and killing of an intracellular parasite by murine macrophages and human monocytes.
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DOI：
10.4049/jimmunol.134.6.4176
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发表时间：
1985-06
影响因子：
4.4
通讯作者：
M. Lima;F. Kierszenbaum
中科院分区：
文献类型：
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作者：
M. Lima;F. Kierszenbaum
小鼠腹腔巨噬细胞（MPM）或人血单核细胞（HBM）与细胞内（无鞭毛体; AMA）形式的克氏锥虫在人乳铁蛋白（LF）的存在下共培养的生物体数量比在LF的情况下更多;吞噬细胞摄取AMA的比例也显着增加。用LF预处理MPM或AMA也增强了细胞-寄生虫缔合。通过免疫荧光，HBM，MPM和AMA被发现结合LF。通过使用125 I标记的LF，确定每个AMA具有平均1.1 × 10（6）个LF表面受体。当在MPM或AMA与LF孵育期间存在兔抗LF IgG或α-甲基甘露糖苷（α-MM）时，或当用LF预处理的AMA然后与LF阻断剂中的任一种孵育时，LF对细胞-寄生虫协会的增强作用被抑制。尽管这些发现似乎表明LF通过桥接这些细胞增加了MPM-AMA的结合，但当用LF预处理的MPM随后与α-MM或抗LF孵育时，LF效应未受到抑制。此外，LF刺激吞噬作用，表示由LF处理后的MPM的胶乳颗粒摄取的显着增加。HBM或MPM的细胞内杀伤能力也被LF刺激，并表示LF处理后AMA破坏增加。LF似乎只是通过简单地促进吞噬更多数量的AMA，然后在细胞内被破坏来增加AMA杀死率的可能性似乎不太可能，因为已经吸收了未经处理的AMA的未经处理的MPM在随后与LF孵育时杀死了更多数量的AMA。氧还原中间体清除剂实验和氮蓝四唑还原实验结果表明，LF处理的MPM对AMA的杀灭作用与H_2O_2、O_2 ~-和~ 1O_2有关。这些结果表明，LF，一种糖蛋白分泌的中性粒细胞在炎症过程中超过正常量，可能有助于巨噬细胞清除AMA从感染的宿主细胞释放。
Mouse peritoneal macrophages (MPM) or human blood monocytes (HBM) co-cultured with intracellular (amastigote; AMA) forms of Trypanosoma cruzi in the presence of human lactoferrin (LF) took up greater numbers of organisms than in the absence of LF; the proportion of phagocytes taking up AMA was also significantly increased. Pretreatment of either MPM or AMA with LF also enhanced cell-parasite association. By immunofluorescence, HBM, MPM, and AMA were found to bind LF. By using 125I-labeled LF, each AMA was determined to have an average 1.1 X 10(6) surface receptors for LF. The enhancing effect of LF on cell-parasite association was inhibited when either rabbit anti-LF IgG or alpha-methyl mannoside (alpha-MM) was present during the incubation of MPM or AMA with LF, or when AMA pretreated with LF were then incubated with either of the LF blocking agents. Although these findings seemed to suggest that LF increased MPM-AMA association by bridging these cells, the LF effect was not inhibited when MPM pretreated with LF were subsequently incubated with either alpha-MM or anti-LF. Furthermore, LF stimulated phagocytosis, as denoted by a significant increase in latex particle uptake after LF treatment of MPM. The intracellular killing capacity of HBM or MPM was also stimulated by LF and was denoted by increased AMA destruction after LF treatments. The possibility that LF only appeared to increase the rate of AMA killing by simply promoting the engulfment of greater numbers of AMA that would then be destroyed intracellularly seemed unlikely because untreated MPM that had already taken up untreated AMA killed greater numbers of AMA when they were subsequently incubated with LF. The results of experiments with scavengers of oxygen reduction intermediates and of nitroblue tetrazolium reduction tests indicated that H2O2, O2- and 1O2 were involved in the killing of AMA by LF-treated MPM. These results suggest that LF, a glycoprotein secreted by neutrophils in greater than normal amounts during inflammation, may contribute to macrophage clearance of AMA released from infected host cells.