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Microb Pathog. 2019 Nov;136:103653. doi: 10.1016/j.micpath.2019.103653. Epub 2019 Aug 6.

PspA facilitates evasion of pneumococci from bactericidal activity of neutrophil extracellular traps (NETs).

Author information

1
University of Texas School of Public Health, Division of Epidemiology, Brownsville Regional Campus, Brownsville, TX, USA.
2
Lahore University of Management Sciences Department of Biology, Pakistan.
3
University of Texas Health Science Center, School of Public Health, Division of Epidemiology, Human Genetics, and Environmental Science, Center for Infectious Diseases, Houston, TX, USA.
4
University of Texas at Brownsville, Texas South Most College, Department of Biology Brownsville, Texas, USA.
5
University of Alabama at Birmingham, Department of Microbiology and Pediatrics, Birmingham, AL, USA; Department of Biological Sciences, Sungkyunkwan University, Suwon, South Korea.
6
Forsyth Institute, Cambridge, MA, USA.
7
Lahore University of Management Sciences Department of Biology, Pakistan. Electronic address: shaper.mirza@lums.edu.pk.

Abstract

Pneumococcal strains are variably resistant to killing by neutrophil extracellular traps (NETs). We hypothesize that this variability in resistance is due to heterogeneity in pneumococcal surface protein A (PspA), a structurally diverse virulence factor of Streptococcus pneumoniae. Pneumococcal strains showed variability in induction of NETs and in susceptibility to killing by NETs. The variability in susceptibility to NETs-mediated killing of pneumococcal strains is attributed to PspA, as strains lacking the surface expression of PspA were significantly more sensitive to NETs-mediated killing compared to the wild-type strains. Using pspA switch mutants we were further able to demonstrate that NETs induction and killing by NETs is a function of PspA as mutants with switch PspA demonstrated donor phenotype. Antibody to PspA alone showed an increase in induction of NETs, and NETs thus generated were able to trap and kill pneumococci. Pneumococci opsonized with antibody to PspA showed increase adherence to NETs but a decrease susceptibility to killing by NETs. In conclusion we demonstrate a novel role for pneumococcal PspA in resisting NETs mediated killing and allowing the bacteria to escape containment by blocking binding of pneumococci to NETs.

KEYWORDS:

Microbial killing; NETs; PspA; S. pneumoniae

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