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• W2087177871 abstract "The complement system, which functions by lysing pathogens directly or by promoting their uptake by phagocytes, is critical for controlling many microbial infections. Here, we show that in Streptococcus pneumoniae, increasing bacterial chain length sensitizes this pathogen to complement deposition and subsequent uptake by human neutrophils. Consistent with this, we show that minimizing chain length provides wild-type bacteria with a competitive advantage in vivo in a model of systemic infection. Investigating how the host overcomes this virulence strategy, we find that antibody promotes complement-dependent opsonophagocytic killing of Streptococcus pneumoniae and lysis of Haemophilus influenzae independent of Fc-mediated effector functions. Consistent with the agglutinating effect of antibody, F(ab')(2) but not Fab could promote this effect. Therefore, increasing pathogen size, whether by natural changes in cellular morphology or via antibody-mediated agglutination, promotes complement-dependent killing. These observations have broad implications for how cell size and morphology can affect virulence among pathogenic microbes." @default.
• W2087177871 created "2016-06-24" @default.
• W2087177871 creator A5041680234 @default.
• W2087177871 creator A5066405485 @default.
• W2087177871 date "2011-11-01" @default.
• W2087177871 modified "2023-10-13" @default.
• W2087177871 title "Minimization of Bacterial Size Allows for Complement Evasion and Is Overcome by the Agglutinating Effect of Antibody" @default.
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• W2087177871 doi "https://doi.org/10.1016/j.chom.2011.09.009" @default.
• W2087177871 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3222866" @default.
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