Adhesion of Candida albicans, but not Candida krusei, to salivary statherin and mimicking host molecules.
Adhesion of Candida albicans, but not Candida krusei, to salivary statherin and mimicking host molecules.
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白色念珠菌（而非克柔念珠菌）对唾液富酪蛋白和模拟宿主分子的粘附。
DOI：
10.1034/j.1399-302x.2000.150207.x
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发表时间：
2000
影响因子：
--
通讯作者：
Strömberg,N
中科院分区：
文献类型：
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作者：
Johansson,I;Bratt,P;Hay,DI;Schluckebier,S;Strömberg,N
本研究的目的是鉴定影响白色念珠菌和克鲁塞念珠菌与唾液膜和上皮细胞粘附的唾液分子。C.白色念珠菌（GDH 18、GDH 3339、CA 1957、ATCC 28366和ATCC 10321），而非念珠菌。krusei（菌株ATCC 14243和Ck 9），结合唾液包被的羟基磷灰石和颊上皮细胞。腮腺唾液组分中含有斯达林、糖基化富脯氨酸蛋白（PRP）和尚未鉴定的组分，这些组分介导了菌株GDH 18的粘附; Fucα1 - 2Galβ1 - 4Glc部分抑制了与不含斯达林组分的粘附。纯的statherin，而不是PRP-1，介导了C的剂量依赖性粘附。相对于ATCC菌株28366和10321，白念珠菌分离株（GDH 18、GDH 3339和CA 1957）稍微更强烈地结合到staterin/唾液，而对于粘附到颊上皮细胞则相反。C.白念珠菌菌株GDH 18对唾液包被的羟基磷灰石和颊上皮细胞的作用分别被嗜酸粒蛋白特异性免疫球蛋白G（IgG）抗体完全（93%）和部分（43%）阻断。对照IgG抗体不阻断粘附。Fucα1 - 2Galβ1 - 4Glc（49%）和N-乙酰葡萄糖胺（38%）也可阻断粘附于上皮细胞，而他汀特异性IgG抗体与Fucα1 - 2Galβ1 - 4Glc联合几乎完全消除粘附（79%）。此外，statherin在溶液中通过诱导细胞聚集来阻断菌株GDH 18与上皮细胞的粘附。
The aim of the present study was to identify salivary molecules affecting adhesion ofCandida albicansandCandida kruseito salivary pellicles and epithelial cells. Strains ofC. albicans(GDH18, GDH3339, CA1957, ATCC 28366 and ATCC 10321), but notC. krusei(strains ATCC 14243 and Ck9), bound to saliva‐coated hydroxyapatite and buccal epithelial cells. Parotid saliva fractions containing statherin, glycosylated proline‐rich proteins (PRP) and as yet unidentified components mediated adhesion of strain GDH18; Fucα1‐2Galβ1‐4Glc partly inhibited the adhesion to those fractions not containing statherin. Pure statherin, but not PRP‐1, mediated dose‐dependent adhesion ofC. albicansstrain GDH18 to hydroxyapatite beads.Candidaisolates (GDH18, GDH3339 and CA1957) bound somewhat more avidly to statherin/saliva relative to ATCC strains 28366 and 10321, while the opposite was true for adhesion to buccal epithelial cells. Adhesion ofC. albicansstrain GDH18 to saliva‐coated hydroxyapatite and buccal epithelial cells was completely (93%) and partly (43%) blocked by statherin‐specific immunoglobulin G (IgG) antibodies, respectively. Control IgG antibodies did not blockCandidaadhesion. Blockage ofCandidaadhesion to epithelial cells also occurred with Fucα1‐2Galβ1‐4Glc (49%) andN‐acetylglucosamine (38%), while statherin specific IgG antibodies in combination with Fucα1‐2Galβ1‐4Glc almost completely eliminatedCandidaadhesion (79%). In addition, statherin in solution blocked the adhesion of strain GDH18 to epithelial cells by inducing aggregation ofCandidacells.