Science and Technology Production
Congress
Authorship
Castro, Joselyn E.
;
Birnberg Weiss, Federico
;
Faccone Diego
;
Gomez, Sonia A.
;
Landoni, Verónica I
;
Fernández Gabriela C
Date
2024
Publishing House and Editing Place
ALACI
Summary
Information provided by the agent in
SIGEVA
Antimicrobial resistance is a major problem for the treatment of infectious diseases worldwide. Providencia stuartii (Ps) and Providencia rettgeri (Pr) are multidrug-resistant strains associated with nosocomial infections. The immune response against these pathogens had not been described previously. Our first study evaluated whether Ps and Pr triggered the bactericidal response in neutrophils (PMN). We reported that Ps and Pr were phagocytosed and induced some degree of respiratory burst. Howe...
Antimicrobial resistance is a major problem for the treatment of infectious diseases worldwide. Providencia stuartii (Ps) and Providencia rettgeri (Pr) are multidrug-resistant strains associated with nosocomial infections. The immune response against these pathogens had not been described previously. Our first study evaluated whether Ps and Pr triggered the bactericidal response in neutrophils (PMN). We reported that Ps and Pr were phagocytosed and induced some degree of respiratory burst. However, neither Ps nor Pr induced neutrophil extracellular traps (NETs) release. This lack of NETs formation may reflect an active strategy of immune evasion. Therefore, here our aim was to investigate the mechanisms behind the lack of NETs formation in the presence of Ps or Pr. We assessed whether Ps and Pr directly affect NET formation triggered by positive stimuli such as PMA and E. coli (Eco). Purified human PMN (n=6) were incubated with Eco (MOI 1) or PMA (40 nM) and Ps or Pr (MOI 10) for 3 h. We determined NETs by double-stranded DNA release and confocal microscopy. We found that NETs formation by Eco and PMA was inhibited by Ps or Pr (p<0.05). To determine whether this inhibition depends on bacterial viability or a soluble factor released from bacteria, we treated Ps and Pr with PFA (4%, 30 min) or added the supernatant of Ps or Pr cultures instead of bacteria to PMN and triggered NETs by PMA. The fixated bacteria or the supernatants were not able to inhibit PMA-induced NETs. Our results confirm that Ps and Pr are not only poor inducers of NET release, but that they inhibit NET induction triggered by positive stimuli. This inhibition is mediated by bacterial viability and soluble factors released by the bacteria. In conclusion, Ps and Pr show active strategies to subvert PMN-mediated NET formation.
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Key Words
EVASION INMUNEBACTERIAMULTIRRESISTENCIANEUTROFILOS