Bacterial aggregate size determines phagocytosis efficiency of polymorphonuclear leukocytes
- PDF / 2,057,195 Bytes
- 12 Pages / 595.276 x 790.866 pts Page_size
- 1 Downloads / 180 Views
ORIGINAL INVESTIGATION
Bacterial aggregate size determines phagocytosis efficiency of polymorphonuclear leukocytes Maria Alhede1 · Melanie Lorenz1 · Blaine Gabriel Fritz1 · Peter Østrup Jensen1,2,3 · Hans Christian Ring4 · Lene Bay1 · Thomas Bjarnsholt1,2 Received: 1 March 2020 / Accepted: 19 August 2020 © The Author(s) 2020
Abstract The ability of bacteria to aggregate and form biofilms impairs phagocytosis by polymorphonuclear leukocytes (PMNs). The aim of this study was to examine if the size of aggregates is critical for successful phagocytosis and how bacterial biofilms evade phagocytosis. We investigated the live interaction between PMNs and Pseudomonas aeruginosa, Staphylococcus aureus, Escherichia coli and Staphylococcus epidermidis using confocal scanning laser microscopy. Aggregate size significantly affected phagocytosis outcome and larger aggregates were less likely to be phagocytized. Aggregates of S. epidermidis were also less likely to be phagocytized than equally-sized aggregates of the other three species. We found that only aggregates of approx. 5 μm diameter or smaller were consistently phagocytosed. We demonstrate that planktonic and aggregated cells of all four species significantly reduced the viability of PMNs after 4 h of incubation. Our results indicate that larger bacterial aggregates are less likely to be phagocytosed by PMNs and we propose that, if the aggregates become too large, circulating PMNs may not be able to phagocytose them quickly enough, which may lead to chronic infection. Keywords E. coli · P. aeruginosa · S. aureus · S. epidermidis · Chronic bacterial infection · Polymorphonuclear leukocytes (PMNs) · Phagocytosis
Introduction Polymorphonuclear leukocytes (PMNs) are part of the innate immune system and constitute the first line of host defense against infectious pathogens. PMNs are phagocytes and utilize phagocytosis to engulf and destroy microorganisms. Phagocytosis is an active, receptor-mediated process
by which bacteria are recognized, bound by the PMN’s cell membrane and internalized into a phagosome. Granules containing antimicrobial molecules then mobilize, fuse with the phagosome and kill the bacteria [1, 2]. PMNs can expand up to 300% during phagocytosis, allowing the uptake of large particles [3]. Failure of phagocytosis may result in the formation of neutrophil extracellular traps (NETs) with proinflammatory effect [4].
Edited by: Christian Bogdan. * Thomas Bjarnsholt [email protected] Melanie Lorenz [email protected] Blaine Gabriel Fritz [email protected] Peter Østrup Jensen [email protected] Hans Christian Ring [email protected] Lene Bay [email protected]
1
Costerton Biofilm Center, Department of Immunology and Microbiology, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen, Denmark
2
Department of Clinical Microbiology, Rigshospitalet, Afsnit 9301, Juliane Maries Vej 22, DK‑2100 Copenhagen Ø, Denmark
3
Institute for Inflammation Research, Center for Rheumatology and Spine Diseases, Rigshospitalet, 2100 Copen
Data Loading...
