Publication Database

The type-2 Streptococcus canis M protein SCM-2 binds fibrinogen and facilitates antiphagocytic properties (2023)

Art

Zeitschriftenartikel / wissenschaftlicher Beitrag

Autoren

Lapschies, Antje-Maria (WE 7)

Aubry, Etienne (WE 7)

Kohler, Thomas P.

Goldmann, Oliver

Hammerschmidt, Sven

Nerlich, Andreas (Tiermedizinisches Zentrum für Resistenzforschung)

Eichhorn, Inga (WE 7)

van Vorst, Kira (WE 7)

Fulde, Marcus (WE 7)

Quelle

Frontiers in microbiology

Bandzählung: 14

Seiten: Artikel 1228472

ISSN: 1664-302x

Sprache

Englisch

Verweise

URL (Volltext): https://pubmed.ncbi.nlm.nih.gov/37965557/

DOI: 10.3389/fmicb.2023.1228472

Pubmed: 37965557

Kontakt

Institut für Mikrobiologie und Tierseuchen

Robert-von-Ostertag-Str. 7-13
14163 Berlin
+49 30 838 51843 / 66949
mikrobiologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

Streptococcus canis is a zoonotic agent that causes severe invasive diseases in domestic animals and humans, but little is known about its pathogenesis and virulence mechanisms so far. SCM, the M-like protein expressed by S. canis, is considered one of the major virulence determinants. Here, we report on the two distinct groups of SCM. SCM-1 proteins were already described to interact with its ligands IgG and plasminogen as well as with itself and confer antiphagocytic capability of SCM-1 expressing bacterial isolates. In contrast, the function of SCM-2 type remained unclear to date. Using whole-genome sequencing and subsequent bioinformatics, FACS analysis, fluorescence microscopy and surface plasmon resonance spectrometry, we demonstrate that, although different in amino acid sequence, a selection of diverse SCM-2-type S. canis isolates, phylogenetically representing the full breadth of SCM-2 sequences, were able to bind fibrinogen. Using targeted mutagenesis of an SCM-2 isolate, we further demonstrated that this strain was significantly less able to survive in canine blood. With respect to similar studies showing a correlation between fibrinogen binding and survival in whole blood, we hypothesize that SCM-2 has an important contribution to the pathogenesis of S. canis in the host.