کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10967686 | 1102842 | 2013 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
fH-dependent complement evasion by disease-causing meningococcal strains with absent fHbp genes or frameshift mutations
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: fH-dependent complement evasion by disease-causing meningococcal strains with absent fHbp genes or frameshift mutations fH-dependent complement evasion by disease-causing meningococcal strains with absent fHbp genes or frameshift mutations](/preview/png/10967686.png)
چکیده انگلیسی
Meningococci bind human fH to down-regulate complement, which enhances survival of the bacteria in serum. A major fH ligand is the vaccine candidate, factor H-binding protein (fHbp). Although fHbp has been considered an essential meningococcal virulence factor, rarely, invasive isolates with absent fHbp genes or frameshift mutations have been identified. In previous studies fH binding to these isolates was not detected. The aim of the present study was to investigate fH binding and complement evasion by invasive meningococcal serogroup B clinical isolates with absent fHbp genes or frameshift mutations. Four of the seven isolates tested bound human fH by flow cytometry and survived in IgG-depleted human serum. In all four, fH binding was decreased after inactivating the gene encoding NspA. Binding of fH to fHbp and NspA is specific for human fH. To investigate fH-dependent evasion of host defenses, human fH transgenic infant rats, or control littermates negative for human fH, were challenged IP with 103-104Â CFU of two of the isolates with no detectable fH binding by flow cytometry. At 6Â h, bacteremia caused by both strains was higher in human fH transgenic rats than in control rats (PÂ <Â 0.002). In conclusion, six of the seven isolates had evidence of fH binding and/or human fH-dependent complement evasion in transgenic rats. In four, NspA was as an alternative fH ligand. fHbp vaccination may select for mutants that do not require fHbp for complement evasion. Inclusion of additional target antigens in vaccines containing fHbp may delay emergence of these mutants.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Vaccine - Volume 31, Issue 38, 28 August 2013, Pages 4192-4199
Journal: Vaccine - Volume 31, Issue 38, 28 August 2013, Pages 4192-4199
نویسندگان
Serena Giuntini, David M. Vu, Dan M. Granoff,