Interaction of inflammatory cells and oral microorganisms. IX. the bactericidal effects of human polymorphonuclear leukocytes on isolated plaque microorganisms.
Interaction of inflammatory cells and oral microorganisms. IX. the bactericidal effects of human polymorphonuclear leukocytes on isolated plaque microorganisms.
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炎症细胞和口腔微生物的相互作用。
DOI:
10.1111/j.1600-0765.1980.tb00305.x
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发表时间:
1980
影响因子:
3.5
通讯作者:
Taichman,NS
中科院分区:
文献类型:
--
作者:
Passo,SA;Tsai,CC;McArthur,WP;Leifer,C;Taichman,NS
Polymorphonuclear leukocytes (PMNs) come in contact with plaque microorganisms in the gingival sulcus. However, little is known about the ability of PMNs to kill or inhibit the growth of plaque microorganisms. In this study, the bactericidal effects of human PMNs and serum againstS. mutans6715,S. sanguisM5, andA. viscosusT14 virulent and avirulent were examined. Plaque microorganisms grown to stationary phase were incubated with human PMNs and/or serum for 90 minutes at 37°C. The killing and growth inhibition of bacteria were determined by measurement of percent reduction in colony forming units and percent inhibition of3H‐uridine uptake by the microorganisms.A. viscosusT14 virulent was the only microorganism significantly killed by human PMNs in the absence of serum. In the presence of fresh but not heat‐inactivated (56°C, 30 minutes) human serum, human PMNs had a significant bactericidal effect against all of the microorganisms tested. Exposure ofS. mutans6715, but notS. sanguisM5, to sucrose inhibited the bactericidal effect of human PMNs in the presence of fresh human serum but not in the presence of rabbit anti‐S. mutansimmunoglobulin. Cytochalasin B markedly inhibited phagocytosis ofS. mutans6715 by human PMNs in the presence of serum. However, cytochalasin B‐treated PMNs still were significantly bactericidal forS. mutans6715 in the presence of serum. The data suggests that human PMNs may kill or inhibit the growth of certain plaque microorganisms in the gingival crevice. The microbial killing may be influenced by bacterial extracellular polysaccharides and the presence of serum antibodies and complement, both resulting in phagocytosis and extracellular lysosomal release from PMNs.