Adherence of nontypeable Streptococcus pneumoniae to human conjunctival epithelial cells

被引:22
|
作者
Williamson, Yulanda M. [1 ]
Gowrisankar, Rajam [1 ]
Longo, Dana L. [1 ]
Facklam, Richard [1 ]
Gipson, Ilene K. [2 ]
Ades, Edwin P. [1 ]
Carlone, George M. [1 ]
Sampson, Jacquelyn S. [1 ]
机构
[1] Ctr Dis Control & Prevent, Atlanta, GA 30333 USA
[2] Harvard Univ, Sch Med, Schepens Eye Inst, Boston, MA 02114 USA
关键词
Streptococcus pneumoniae; Nontypeable; Conjunctivitis; Mucin; Neuraminidase;
D O I
10.1016/j.micpath.2007.08.016
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Conjunctivitis outbreaks have occurred in the US in which nontypeable (NT) Streptococcus pneumoniae (Pnc) strains have been identified as the etiologic agent; however, the pathogenesis of Pnc conjunctivitis has not been extensively evaluated. Here we assessed the adhesive and invasive properties of 13 NT US conjunctivitis outbreak strains (cPnc) using an immortalized human conjunctival epithelial cell (HQjE) line expressing high or low levels of mucin as a surrogate for in vivo ocular surface events. Studies reveal differential binding efficiencies (up to 18-fold) among cPnc strains to HQjE cells and reduced or little adherence efficiency to high mucin-expressing (HME-HCjE). Additionally, in the presence of exogenous mucin there is considerable inhibition (20% to similar to 100%) of bacterial binding to the HQjE cells. Invasion assays suggest that the cPnc are internalized in HCjE, and less in HME-HCjE cells. Microarray analysis of cPnc isolates revealed an up-regulation of Pnc neuraminidases, and treatment of HME-HCjE cells with exogenous neuraminidase resulted in a 2-13-fold enhancement in cPnc binding. The results indicate that mucin acts as a protective barrier in vitro and that neuraminidases, which can degrade mucin, may be contributing factors leading to bacterial adherence, a first step in the pathogenesis of this transmissible infection. Published by Elsevier Ltd.
引用
收藏
页码:175 / 185
页数:11
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