Pneumococcal surface protein A (PspA) prevents killing of Streptococcus pneumoniae by indolicidin
(2024) In Scientific Reports 14(1).- Abstract
Pneumococcal surface protein A (PspA) is an important virulence factor in Streptococcus pneumoniae that binds to lactoferrin and protects the bacterium from the bactericidal action of lactoferricins—cationic peptides released upon lactoferrin proteolysis. The present study investigated if PspA can prevent killing by another cationic peptide, indolicidin. PspA-negative pneumococci were more sensitive to indolicidin-induced killing than bacteria expressing PspA, suggesting that PspA prevents the bactericidal action of indolicidin. Similarly, chemical removal of choline-binding proteins increased sensitivity to indolicidin. The absence of capsule and PspA had an additive effect on pneumococcal killing by the AMP. Furthermore, anti-PspA... (More)
Pneumococcal surface protein A (PspA) is an important virulence factor in Streptococcus pneumoniae that binds to lactoferrin and protects the bacterium from the bactericidal action of lactoferricins—cationic peptides released upon lactoferrin proteolysis. The present study investigated if PspA can prevent killing by another cationic peptide, indolicidin. PspA-negative pneumococci were more sensitive to indolicidin-induced killing than bacteria expressing PspA, suggesting that PspA prevents the bactericidal action of indolicidin. Similarly, chemical removal of choline-binding proteins increased sensitivity to indolicidin. The absence of capsule and PspA had an additive effect on pneumococcal killing by the AMP. Furthermore, anti-PspA antibodies enhanced the bactericidal effect of indolicidin on pneumococci, while addition of soluble PspA fragments competitively inhibited indolicidin action. Previous in silico analysis suggests a possible interaction between PspA and indolicidin. Thus, we hypothesize that PspA acts by sequestering indolicidin and preventing it from reaching the bacterial membrane. A specific interaction between PspA and indolicidin was demonstrated by mass spectrometry, confirming that PspA can actively bind to the AMP. These results reinforce the vaccine potential of PspA and suggest a possible mechanism of innate immune evasion employed by pneumococci, which involves binding to cationic peptides and hindering their ability to damage the bacterial membranes.
(Less)
- author
- Waz, Natalha T.
; Milani, Barbara
; Assoni, Lucas
; Coelho, Guilherme Rabelo
; Sciani, Juliana M.
; Parisotto, Thaís
; Ferraz, Lucio F.C.
; Hakansson, Anders P.
LU
; Converso, Thiago R. and Darrieux, Michelle LU
- organization
- publishing date
- 2024-12
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Cationic peptide, Immune evasion, Indolicidin, Pneumococcal surface protein A, Streptococcus pneumoniae
- in
- Scientific Reports
- volume
- 14
- issue
- 1
- article number
- 23517
- publisher
- Nature Publishing Group
- external identifiers
-
- scopus:85205984587
- pmid:39384882
- ISSN
- 2045-2322
- DOI
- 10.1038/s41598-024-73564-9
- language
- English
- LU publication?
- yes
- additional info
- Publisher Copyright: © The Author(s) 2024.
- id
- 7ebd2fd7-7a6d-433f-8364-10f69833b96f
- date added to LUP
- 2024-11-27 14:33:58
- date last changed
- 2025-07-10 09:17:28
@article{7ebd2fd7-7a6d-433f-8364-10f69833b96f, abstract = {{<p>Pneumococcal surface protein A (PspA) is an important virulence factor in Streptococcus pneumoniae that binds to lactoferrin and protects the bacterium from the bactericidal action of lactoferricins—cationic peptides released upon lactoferrin proteolysis. The present study investigated if PspA can prevent killing by another cationic peptide, indolicidin. PspA-negative pneumococci were more sensitive to indolicidin-induced killing than bacteria expressing PspA, suggesting that PspA prevents the bactericidal action of indolicidin. Similarly, chemical removal of choline-binding proteins increased sensitivity to indolicidin. The absence of capsule and PspA had an additive effect on pneumococcal killing by the AMP. Furthermore, anti-PspA antibodies enhanced the bactericidal effect of indolicidin on pneumococci, while addition of soluble PspA fragments competitively inhibited indolicidin action. Previous in silico analysis suggests a possible interaction between PspA and indolicidin. Thus, we hypothesize that PspA acts by sequestering indolicidin and preventing it from reaching the bacterial membrane. A specific interaction between PspA and indolicidin was demonstrated by mass spectrometry, confirming that PspA can actively bind to the AMP. These results reinforce the vaccine potential of PspA and suggest a possible mechanism of innate immune evasion employed by pneumococci, which involves binding to cationic peptides and hindering their ability to damage the bacterial membranes.</p>}}, author = {{Waz, Natalha T. and Milani, Barbara and Assoni, Lucas and Coelho, Guilherme Rabelo and Sciani, Juliana M. and Parisotto, Thaís and Ferraz, Lucio F.C. and Hakansson, Anders P. and Converso, Thiago R. and Darrieux, Michelle}}, issn = {{2045-2322}}, keywords = {{Cationic peptide; Immune evasion; Indolicidin; Pneumococcal surface protein A; Streptococcus pneumoniae}}, language = {{eng}}, number = {{1}}, publisher = {{Nature Publishing Group}}, series = {{Scientific Reports}}, title = {{Pneumococcal surface protein A (PspA) prevents killing of Streptococcus pneumoniae by indolicidin}}, url = {{http://dx.doi.org/10.1038/s41598-024-73564-9}}, doi = {{10.1038/s41598-024-73564-9}}, volume = {{14}}, year = {{2024}}, }