Surface antigens contribute differently to the pathophysiological features in serotype K1 and K2 Klebsiella pneumoniae strains isolated from liver abscesses

Abstract

BackgroundThe virulence role of surface antigens in a single serotype of Klebsiella pneumoniae strain have been studied, but little is known about whether their contribution will vary with serotype.MethodTo investigate the role of K and O antigen in hyper-virulent strains, we constructed O and K antigen deficient mutants from serotype K1 STL43 and K2 TSGH strains from patients with liver abscess, and characterized their virulence in according to the abscess formation and resistance to neutrophil phagocytosis, serum, and bacterial clearance in liver.ResultsBoth of K1 and K2-antigen mutants lost their wildtype resistance to neutrophil phagocytosis and hepatic clearance, and failed to cause abscess formation. K2-antigen mutant became serum susceptible while K1-antigen mutant maintained its resistance to serum killing. The amount of glucuronic acid, indicating the amount of capsular polysaccharide (CPS, K antigen), was inversed proportional to the rate of phagocytosis. O-antigen mutant of serotype K1 strains had significantly more amount of CPS, and more resistant to neutrophil phagocytosis than its wildtype counterpart. O-antigen mutants of serotype K1 and K2 strains lost their wildtype serum resistance, and kept resistant to neutrophil phagocytosis. While both mutants lacked the same O1 antigen, O-antigen mutant of serotype K1 became susceptible to liver clearance and cause mild abscess formation, but its serotype K2 counterpart maintained these wildtype virulence.ConclusionWe conclude that the contribution of surface antigens to virulence of K. pneumoniae strains varies with serotypes.

Survival of Carbapenem-Resistant Klebsiella pneumoniae Sequence Type 258 in Human Blood

“…The finding that some of the isolates tested were readily killed in human blood or serum was surprising to us, since bacteremia is relatively common (among individuals with infections caused by carbapenem-resistant K. pneumoniae isolates) and ST258 isolates whose genomes encode the same capsule polysaccharide subtype (e.g., cps-2) are genetically very similar (30,39). Previous studies have shown that the Klebsiella lipopolysaccharide (LPS) O antigen and/or the capsule polysaccharide contributes to resistance to the bactericidal activity of human serum (40)(41)(42)(43)(44)(45). Merino et al proposed that the deposition of complement C3b occurs too far from the membrane of serumresistant strains of K. pneumoniae, and thus, the C5b-C9 MAC fails to form (43).…”

Cell envelope defects of different capsule‐null mutants in K1 hypervirulentKlebsiella pneumoniaecan affect bacterial pathogenesis

“…The capsule is a key virulence factor of hvKP and is important for resistance to complement (Alvarez, Merino, Tomas, Benedi, & Alberti, ; Cortés et al, ; Tan, Gamage, & Gan, ), dissemination to the liver (Fang, Chuang, Shun, Chang, & Wang, ) and during systemic infection (Cheng et al ; Ho et al ; Palacios et al ; Yeh et al , ). The bacterial capsule could potentially protect hvKP from the assault of the antimicrobial peptides such as cathelicidins, defensins and bile salts present in colonic mucus (Antoni et al, ; Campos et al, ).…”

Effect in virulence of switching conserved homologous capsular polysaccharide genes fromKlebsiella pneumoniaeserotype K1 into K20

“…Bacterial cell surface polysaccharides, including both capsular-(K antigen) and lipo-polysaccharides, have been well documented as important virulent factors in the establishment of infection. 3,4 Capsular polysaccharides (CPS) are a major barrier to macrophage or neutrophil phagocytosis. More than 77 serotypes of K. pneumoniae have been distinguished, and strains that produce CPS are generally more virulent than non-capsulated strains.…”