Henry-Stanley Michelle J, Hess Donavon J, Erickson Elizabeth A, Garni Robb M, Wells Carol L
Department of Laboratory Medicine & Pathology, Minneapolis, Minnesota 55455, USA.
J Surg Res. 2003 Jul;113(1):42-9. doi: 10.1016/s0022-4804(03)00156-2.
Candida albicans is a polymorphic fungus that frequently causes systemic infection in postsurgical and trauma patients. Others have reported that Escherichia coli lipopolysaccharide (LPS) acts as a copathogen to enhance the virulence of parenteral C. albicans. Experiments were designed to clarify the effect of parenteral LPS on systemic candidiasis initiated via the oral route.
Antibiotic-treated mice were orally inoculated with C. albicans CAF2 (wild-type) or mutant HLC54 (defective in filament formation), and were given 100 microg parenteral LPS 16 h before sacrifice. Separate groups of mice were additionally exposed to intermittent hypoxia prior to LPS. At sacrifice, cecal flora and microbial translocation to the mesenteric lymph nodes were quantified. C. albicans adherence to cultured HT-29 and Caco-2 enterocytes (pretreated with LPS, or calcium-free medium to expose the enterocyte lateral surface, or both) was quantified by enzyme-linked immunoabsorbent assay.
All mice had high numbers of cecal C. albicans, and LPS was associated with an additional increase in cecal concentrations of HLC54 but not CAF2. Translocation of HLC54, but not CAF2, appeared facilitated by hypoxia, but LPS did not facilitate translocation in any treatment group. Exposure of the lateral surface of cultured enterocytes had no effect on C. albicans adherence, although LPS consistently decreased adherence of both C. albicans strains.
In contrast to experiments where systemic candidiasis was initiated by the parenteral route, parenteral LPS did not act as a copathogen in mice with systemic candidiasis initiated by the oral route, and these results might be related to LPS-induced alterations in C. albicans adherence to host enterocytes.
白色念珠菌是一种多态性真菌，常导致外科手术和创伤患者发生全身感染。其他人报告称，大肠杆菌脂多糖（LPS）作为一种协同病原体可增强肠外白色念珠菌的毒力。本实验旨在阐明肠外LPS对经口途径引发的全身念珠菌病的影响。
用抗生素处理的小鼠经口接种白色念珠菌CAF2（野生型）或突变体HLC54（丝状形成缺陷型），并在处死前16小时给予100微克肠外LPS。另外，在给予LPS之前，将单独的几组小鼠暴露于间歇性低氧环境。处死时，对盲肠菌群以及向肠系膜淋巴结的微生物易位进行定量分析。通过酶联免疫吸附测定法定量分析白色念珠菌对培养的HT - 29和Caco - 2肠上皮细胞（用LPS预处理，或用无钙培养基暴露肠上皮细胞侧面，或两者皆用）的黏附情况。
所有小鼠盲肠中的白色念珠菌数量都很高，LPS与盲肠中HLC54浓度的进一步增加相关，但与CAF2无关。低氧似乎促进了HLC54而非CAF2的易位，但LPS在任何治疗组中均未促进易位。培养的肠上皮细胞侧面的暴露对白色念珠菌的黏附没有影响，尽管LPS持续降低了两种白色念珠菌菌株的黏附。
与通过肠外途径引发全身念珠菌病的实验不同，肠外LPS在经口途径引发全身念珠菌病的小鼠中不作为协同病原体，这些结果可能与LPS诱导的白色念珠菌对宿主肠上皮细胞黏附的改变有关。
