The hypermucoviscosity of hypervirulent K. pneumoniae confers the ability to evade neutrophil-mediated phagocytosis

• Published in: Virulence Vol. 12; no. 1; pp. 2050 - 2059
• Main Authors: Xu, Qi, Yang, Xuemei, Chan, Edward Wai Chi, Chen, Sheng
• Format: Journal Article
• Language: English
• Published: United States Taylor & Francis 01-12-2021; Taylor & Francis Group
• Subjects: Animals; Bacterial Adhesion; Caco-2 Cells; capsule; Humans; hypermucoviscosity; Hypervirulent K. pneumoniae; Immune Evasion; Klebsiella Infections - immunology; Klebsiella pneumoniae - pathogenicity; neutrophil cells; Neutrophils - immunology; Phagocytosis; Research Paper; Virulence; phagocytosis; capsule; hypermucoviscosity; Hypervirulent K. pneumoniae; neutrophil cells
• ISSN: 2150-5594; 2150-5608
• DOI: 10.1080/21505594.2021.1960101

Hypervirulent Klebsiella pneumoniae (HvKP), which causes highly fatal infections, is a new threat to human health. In an attempt to investigate the underlying mechanisms of resistance to neutrophil-mediated killing and hence expression of high-level virulence by HvKP, we tested the binding affinity of HvKP strains to various types of human cells. Our data showed that HvKP exhibited weaker binding to both lung epithelial cells, intestinal Caco-2 cells and macrophages when compared to the classic, non-hypervirulent strains (cKP). Consistently, transconjugants that have acquired a rmpA or rmpA2-bearing plasmid were found to exhibit decreased adhesion to various types of human cells, and hence higher survival rate upon exposure to neutrophil cells. We further found that over production of hypermucoviscosity (HMV), but not capsular polysaccharide (CPS), contributed to the reduced binding and phagocytosis. The effect of hypermucoviscosity on enhancing HvKP virulence was further shown in human serum survival assays and animal experiments. Findings in this study therefore confirmed that rmpA/A2-mediated hypermucoviscosity in HvKP plays a key role in the pathogenesis of this organism through conferring the ability to evade neutrophil binding and phagocytosis.