Enterococcus faecalis suppresses Staphylococcus aureus-induced NETosis and promotes bacterial survival in polymicrobial infections

Author:

Kao Patrick Hsien-Neng12,Ch'ng Jun-Hong3456,Chong Kelvin K L2,Stocks Claudia J2,Wong Siu Ling78,Kline Kimberly A129ORCID

Affiliation:

1. School of Biological Sciences, Nanyang Technological University , Singapore 637551

2. Singapore Centre for Environmental Life Sciences Engineering, Nanyang Technological University , Singapore 637551

3. Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore , Singapore 117545

4. Singapore Centre for Environmental Life Sciences Engineering, National University of Singapore , Singapore 117456

5. Department of Surgery Yong Loo Lin School of Medicine, National University of Singapore , Singapore 117597

6. Infectious Disease Translational Research Program, National University Health System , Singapore 117545

7. Lee Kong Chian School of Medicine, Nanyang Technological University , Singapore 636921

8. Tan Tock Seng Hospital , National Healthcare Group , Singapore 308433

9. Department of Microbiology and Molecular Medicine, Faculty of Medicine, University of Geneva , Geneva , Switzerland 1211

Abstract

Abstract Enterococcus faecalis is an opportunistic pathogen that is frequently co-isolated with other microbes in wound infections. While E. faecalis can subvert the host immune response and promote the survival of other microbes via interbacterial synergy, little is known about the impact of E. faecalis-mediated immune suppression on co-infecting microbes. We hypothesized that E. faecalis can attenuate neutrophil-mediated responses in mixed-species infection to promote survival of the co-infecting species. We found that neutrophils control E. faecalis infection via phagocytosis, ROS production, and degranulation of azurophilic granules, but it does not trigger neutrophil extracellular trap formation (NETosis). However, E. faecalis attenuates Staphylococcus aureus-induced NETosis in polymicrobial infection by interfering with citrullination of histone, suggesting E. faecalis can actively suppress NETosis in neutrophils. Residual S. aureus-induced NETs that remain during co-infection do not impact E. faecalis, further suggesting that E. faecalis possess mechanisms to evade or survive NET-associated killing mechanisms. E. faecalis-driven reduction of NETosis corresponds with higher S. aureus survival, indicating that this immunomodulating effect could be a risk factor in promoting the virulence polymicrobial infection. These findings highlight the complexity of the immune response to polymicrobial infections and suggest that attenuated pathogen-specific immune responses contribute to pathogenesis in the mammalian host.

Funder

National Research Foundation Singapore

Ministry of Education

Nanyang Technological University

National University of Singapore

Ministry of Education - Singapore

Publisher

Oxford University Press (OUP)

Subject

General Earth and Planetary Sciences,General Engineering,General Environmental Science

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