Streptococcus suis Serotype 2 Biofilms Inhibit the Formation of Neutrophil Extracellular Traps

Abstract

Invasive infections caused by Streptococcus suis serotype 2 (SS2) has emerged as a clinical problem in recent years. Neutrophil extracellular traps (NETs) are an important mechanism for the trapping and killing of pathogens that are resistant to phagocytosis. Biofilm formation can protect bacteria from being killed by phagocytes. Until now, there have only been a few studies that focused on the interactions between bacterial biofilms and NETs. SS2 in both a biofilm state and a planktonic cell state were incubated with phagocytes and NETs, and bacterial survival was assessed. DNase I and cytochalasin B were used to degrade NET DNA or suppress phagocytosis, respectively. Extracellular DNA was stained with impermeable fluorescent dye to quantify NET formation. Biofilm formation increased up to 6-fold in the presence of neutrophils, and biofilms were identified in murine tissue. Both planktonic and biofilm cells induced neutrophils chemotaxis to the infection site, with neutrophils increasing by 85.1 and 73.8%, respectively. The bacteria in biofilms were not phagocytized. The bactericidal efficacy of NETs on the biofilms and planktonic cells were equal; however, the biofilm extracellular matrix can inhibit NET release. Although biofilms inhibit NETs release, NETs appear to be an important mechanism to eliminate SS2 biofilms. This knowledge advances the understanding of biofilms and may aid in the development of treatments for persistent infections with a biofilm component.

2018 international consensus meeting on musculoskeletal infection: Summary from the biofilm workgroup and consensus on biofilm related musculoskeletal infections

“…https://www.ors.org/wp-content/uploads/2018/11/Biofilm-Question-3.pdf addresses biofilm susceptibility to host phagocytosis. While neutrophils and macrophages (10–20 μm) have the ability to access the surface and enter the channels of a mature biofilm (100 μm), they are not able to access biofilm encased microorganisms . When a fragment of biofilm is small enough, phagocytes can engulf it, but they are not able to destroy the bacteria .…”

Streptococcus suis: a re-emerging pathogen associated with occupational exposure to pigs or pork products. Part II – Pathogenesis

“…Interesting results were obtained recently by Ma et al [94] who demonstrated experimentally that S. suis type 2 can form biofilms in vivo in some murine tissues, such as the liver, spleen and kidney. The bacteria in the biofilms were not phagocytized.…”

“…Biofilm formation increased up to 6-fold in the presence of neutrophils and the biofilm extracellular matrix can inhibit release of the neutrophil extracellular traps (NETs) and increase the survival of bacteria in the blood. Nevertheless, the protection is not complete and according to the authors NETs appear to be an important mechanism to eliminate S. suis biofilms [94].…”

Characterization of Filifactor alocis and its immune evasion strategies employed against human neutrophils.

“…Periodontal disease caused by polymicrobial synergy among periodontal bacteria in subgingival biofilms may be successful in their colonization of the region through their NET degradation capacities (367). It has been reported in a few studies that biofilm formation can inhibit NETs and this can be attributed to the extracellular matrix structure, as detached planktonic bacteria can induce NETs (398). NET formation is an effective mechanism employed by neutrophils to respond to infection, therefore, lack of NET formation has disease promoting implications.…”