Volume 5, Issue 3, September 2020, Page: 135-151
Staphylococcal Pore-forming Leukotoxins: Opening of Ca2+-activated K+ Channels and Specificity of Membrane Pores in Human Neutrophils
Leila Staali, Department of Biotechnology, Natural and Life Sciences Faculty, Ahmed Ben Bella Oran1-University, Oran, Algeria; Bacteriology Institute of Medical Faculty, Louis Pasteur University, Strasbourg, France
Didier Andre Colin, Bacteriology Institute of Medical Faculty, Louis Pasteur University, Strasbourg, France
Received: Jul. 14, 2020;       Accepted: Jul. 27, 2020;       Published: Aug. 20, 2020
DOI: 10.11648/j.ijmb.20200503.19      View  180      Downloads  65
Abstract
Pore-forming toxins are key virulence determinants produced by human bacterial pathogens Staphylococcus aureus, inducing two independent cellular events in neutrophils. Upon a specific binding to membrane receptors, both Panton and Valentin Leukocidin and γ-hemolysin induced an increase of Na+ and K+ fluxes, likely associated to the activation of preexisting ionic channels or to the membrane pores formation. This was investigated by using, spectrofluorometry techniques and, specific molecular probes in human neutrophils. Interestingly, we found that, in the absence of extracellular Ca2+, leukotoxins did form membrane pores, which were large enough to allow a massive entry of ethidium into neutrophils. Simultaneously, sustained Na+ influx and K+ efflux were observed. Another set of experiments carried out in the presence of extracellular Ca2+ did show that, the percentage of pores formed by leukotoxins was significantly, reduced due to the Ca2+ effect to eventually protect cells from lysis. The simultaneous recording of Na+ and K+ movements showed a significant increase of the K+ efflux although, the Na+ influx was reduced. By using potassium channels blockers, we found that, the potassium efflux enhanced by the presence of extracellular Ca2+, was markedly, inhibited in apamin-, charybdotoxin-, tetrodotoxin-, and quinine-pretreatment neutrophils. We also found that, the increase of the K+ efflux was reduced by either, thapsigargin or TMB8, potent blockers of the internal Ca2+ stores depletion. Consequently, we proposed that, the activation of another potassium pathway by leukotoxins, known as Ca2+-activated K+ channels following the Ca2+ stores depletion. Furthermore, potassium channels blockers did not affect ethidium, Na+ and K+ movements, in the absence of extracellular Ca2+. Moreover, in this condition, no monovalent ions movement was recorded, when the pores formation was altered by tetra-ethyl-ammonium. In the present study, we further highlighted the specificity of membrane pores to Na+ and K+ ions when, the pores formation was completely blocked by divalent ions blockers (Ca2+ and Zn2+). Under these conditions, no monovalent ions movement, was recorded although, a significant influx of Ca2+ and Zn2+ was observed after the leukotoxins application. In conclusion, our data provided an evidence that, staphylococcal leukotoxins induced in human neutrophils: 1) the opening of Ca2+-activated K+ channels, only in the presence of 1 mM extracellular Ca2+; 2) the formation of membrane pores, which exhibited a high specificity to monovalent cations and, 3) an influx of sodium, through a tetrodotoxin not-sensitive pathway ruling out the hypothesis that, Na+ channels could be activated by leukotoxins.
Keywords
Staphylococcal Pore-forming Leukotoxins: Opening of Ca2+-activated K+ Channels and Specificity of Membrane Pores in Human Neutrophils
To cite this article
Leila Staali, Didier Andre Colin, Staphylococcal Pore-forming Leukotoxins: Opening of Ca2+-activated K+ Channels and Specificity of Membrane Pores in Human Neutrophils, International Journal of Microbiology and Biotechnology. Vol. 5, No. 3, 2020, pp. 135-151. doi: 10.11648/j.ijmb.20200503.19
Copyright
Copyright © 2020 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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