Encapsulated Streptococcus suis impairs optimal neutrophil functions which are not rescued by priming with colony-stimulating factors.

Autor: Bleuzé M; Faculty of Veterinary Medicine, Research Group on Infectious Diseases in Production Animals (GREMIP) & Swine and Poultry Infectious Diseases Research Center (CRIPA), Université de Montréal, St-Hyacinthe, Quebec, Canada., Lavoie JP; Faculty of Veterinary Medicine, Department of Clinical Sciences, Université de Montréal, St-Hyacinthe, Quebec, Canada., Bédard C; Faculty of Veterinary Medicine, Department of Pathology and Microbiology, Université de Montréal, St-Hyacinthe, Quebec, Canada., Gottschalk M; Faculty of Veterinary Medicine, Research Group on Infectious Diseases in Production Animals (GREMIP) & Swine and Poultry Infectious Diseases Research Center (CRIPA), Université de Montréal, St-Hyacinthe, Quebec, Canada., Segura M; Faculty of Veterinary Medicine, Research Group on Infectious Diseases in Production Animals (GREMIP) & Swine and Poultry Infectious Diseases Research Center (CRIPA), Université de Montréal, St-Hyacinthe, Quebec, Canada.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2024 Jan 23; Vol. 19 (1), pp. e0296844. Date of Electronic Publication: 2024 Jan 23 (Print Publication: 2024).
DOI: 10.1371/journal.pone.0296844
Abstrakt: The porcine pathogen and zoonotic agent Streptococcus suis induces an exacerbated inflammation in the infected hosts that leads to sepsis, meningitis, and sudden death. Several virulence factors were described for S. suis of which the capsular polysaccharide (CPS) conceals it from the immune system, and the suilysin exhibits cytotoxic activity. Although neutrophils are recruited rapidly upon S. suis infection, their microbicidal functions appear to be poorly activated against the bacteria. However, during disease, the inflammatory environment could promote neutrophil activation as mediators such as the granulocyte colony-stimulating factor granulocyte (G-CSF) and the granulocyte-macrophages colony-stimulating factor (GM-CSF) prime neutrophils and enhance their responsiveness to bacterial detection. Thus, we hypothesized that CPS and suilysin prevent an efficient activation of neutrophils by S. suis, but that G-CSF and GM-CSF rescue neutrophil activation, leading to S. suis elimination. We evaluated the functions of porcine neutrophils in vitro in response to S. suis and investigated the role of the CPS and suilysin on cell activation using isogenic mutants of the bacteria. We also studied the influence of G-CSF and GM-CSF on neutrophil response to S. suis by priming the cells with recombinant proteins. Our study confirmed that CPS prevents S. suis-induced activation of most neutrophil functions but participates in the release of neutrophil-extracellular traps (NETs). Priming with G-CSF did not influence cell activation, but GM-CSF strongly promote IL-8 release, indicating its involvement in immunomodulation. However, priming did not enhance microbicidal functions. Studying the interaction between S. suis and neutrophils-first responders in host defense-remains fundamental to understand the immunopathogenesis of the infection and to develop therapeutical strategies related to neutrophils' defense against this bacterium.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2024 Bleuzé et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
Databáze: MEDLINE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje