INFLUENCE OF THE ESCHERICHIA-COLI CAPSULE ON COMPLEMENT-FIXATION AND ON PHAGOCYTOSIS AND KILLING BY HUMAN PHAGOCYTES
INFLUENCE OF THE ESCHERICHIA-COLI CAPSULE ON COMPLEMENT-FIXATION AND ON PHAGOCYTOSIS AND KILLING BY HUMAN PHAGOCYTES
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DOI：
10.1172/jci109663
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发表时间：
1980-01-01
影响因子：
15.9
通讯作者：
SILVERSTEIN, SC
中科院分区：
文献类型：
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作者：
HORWITZ, MA;SILVERSTEIN, SC
为了确定多糖荚膜增强革兰氏阴性菌毒力的机制，研究了E。大肠杆菌荚膜对细菌表面补体结合以及小鼠巨噬细胞和人多形核白细胞（PMN）和单核细胞对这些细菌的吞噬和杀伤作用进行了研究。当E.用刀豆球蛋白（Con）A将大肠杆菌粘附在小鼠巨噬细胞上，巨噬细胞能吞噬未被包囊的细菌，但不能吞噬包囊的大肠杆菌。除非加入抗细菌或抗ConA抗体[Ab]，否则不存在任何抗ConA抗体。当这些细菌附着于人PMN与ConA，PMN摄取未封装的，但不封装E。杆菌中性粒细胞吞噬并杀死包裹的抗血清E.在补体[C]和抗细菌抗体存在的情况下，PMN吞噬并杀死未被包囊的大肠杆菌。大肠杆菌的同一菌株在单独的C的存在下。荧光显微镜显示，包封的E.大肠杆菌将C固定在其表面。探讨人中性粒细胞和单核细胞C受体在吞噬和杀伤微囊化大肠杆菌中的作用。用人和兔抗细菌免疫球蛋白（IG）M固定C。中性粒细胞和单核细胞吞噬并杀死E.在IgM和C的存在下，但不存在单独的血清调理素。在抗细菌IgG存在下，PMN和单核细胞需要C才能有效地吞噬和杀死E。杆菌附着本身导致摄入未包封但未包封的E。杆菌在生理条件下，E.除非C被固定在它们的表面，否则大肠杆菌不能被PMN或单核细胞有效地吞噬或杀死。在缺乏Ab的情况下，E.大肠杆菌荚膜可能通过掩蔽能够激活C途径的表面成分（如脂多糖）来阻断C固定到细菌表面。急诊大肠杆菌荚膜对C固定的特异性抗细菌抗体提出了要求。人PMN和单核细胞的C受体介导C包被的包囊细菌的吞噬作用，并且是吞噬和杀死这些细菌的主要介质。
To define mechanisms by which polysaccharide capsules confer enhanced virulence on gram-negative bacteria, the effect of E. coli capsule on complement fixation to the bacterial surface and on phagocytosis and killing of these bacteria by mouse macrophages and human polymorphonuclear leukocytes (PMN) and monocytes was examined. When E. coli were attached to mouse macrophages with concanavalin(Con)A, the macrophages readily phagocytosed unencapsulated but not encapsulated bacteria even in the presence of fresh mouse serum; macrophages did not phagocytose encapsulated E. coli unless anti-bacterial or anti-Con A antibody [Ab] was added. When these bacteria were attached to human PMN with Con A, PMN ingested unencapsulated but not encapsulated E. coli. PMN phagocytosed and killed encapsulated serum-resistant E. coli only in the presence of complement [C] and anti-bacterial Ab; PMN phagocytosed and killed unencapsulated E. coli of the same strain in the presence of C alone. Fluorescence microscopy showed that Ab had to be present for encapsulated but not unencapsulated E. coli to fix C to its surface. To examine the role of the C receptors of human PMN and monocytes in phagocytosis and killing of encapsulated E. coli, human and rabbit anti-bacterial immunoglobulin (Ig)M were used to fix C to the bacteria. PMN and monocytes phagocytosed and killed encapsulated E. coli in the presence of IgM and C but not in the presence of either serum opsonin alone. In the presence of anti-bacterial IgG, PMN and monocytes required C to effectively phagocytose and kill the E. coli. Attachment by itself results in ingestion of unencapsulated but not encapsulated E. coli. Under physiologic conditions E. coli are not phagocytosed or killed effectively by PMN or monocytes unless C is fixed to their surface. In the absence of Ab, the E. coli capsule blocks C fixation to the bacterial surface probably by masking surface components, such as lipopolysaccharide, capable of activating the C pathway. The E. coli capsule imposes a requirement for specific anti-bacterial Ab for C fixation. The C receptor of human PMN and monocytes mediates phagocytosis of C-coated encapsulated bacteria and is the primary mediator of phagocytosis and killing of these bacteria.