JBJI Journal of Bone and Joint Infection JBJI J. Bone Joint Infect. 2206-3552 Ivyspring Göttingen, Germany 10.7150/jbji.21567 Lower activation of caspase-1 by <em>Staphylococcus epidermidis</em> isolated from prosthetic joint infections compared to commensals Månsson Emeli 1 2 3 Sahdo Berolla 2 Nilsdotter-Augustinsson Åsa 4 Särndahl Eva 1 2 Söderquist Bo 1 5 School of Medical Sciences, iRiSC - Inflammatory Response and Infection Susceptibility Centre, Region Västmanland - Uppsala University, Centre for Clinical Research, Hospital of Västmanland Västerås, SE-721 89 Västerås, Sweden; Department of Infectious Diseases, and Department of Clinical and Experimental Medicine, Linköping University, SE-60182 Norrköping, Sweden. Department of Laboratory Medicine, Clinical Microbiology, Faculty of Medicine and Health, Örebro University, SE-701 82 Örebro, Sweden; 13 01 2018 3 1 10 14 Copyright: © 2018 Emeli Månsson et al. 2018 This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this licence, visit https://creativecommons.org/licenses/by/4.0/ This article is available from https://jbji.copernicus.org/articles/3/10/2018/jbji-3-10-2018.html The full text article is available as a PDF file from https://jbji.copernicus.org/articles/3/10/2018/jbji-3-10-2018.pdf

<p class="p p-first-last" id="__p2">Nosocomial sequence types of <em>Staphylococcus epidermidis</em> dominate in prosthetic joint infections. We examined caspase-1 activation in human neutrophils after incubation with <em>Staphylococcus epidermidis</em> isolated from prosthetic joint infections and normal skin flora. Active caspase-1 was lower after incubation with isolates from prosthetic joint infections than after incubation with commensal isolates. Both host and isolate dependent differences in active caspase-1 were noted. Our results indicate that there might be a host-dependent incapacity to elicit a strong caspase-1 response towards certain strains of <em>S. epidermidis.</em> Further experiments with a larger number of individuals are warranted.</p>

 References Kurtz SM, Lau E, Watson H, Schmier JK, Parvizi J. Economic Burden of Periprosthetic Joint Infection in the United States. The Journal of arthroplasty. 2012;27:61–5.e1. Tande AJ, Patel R. Prosthetic Joint Infection. Clinical Microbiology Reviews. 2014;27:302–45. [PMC free article] Gallo RL, Nakatsuji T. Microbial symbiosis with the innate immune defense system of the skin. J Invest Dermatol. 2011;131:1974–80. [PMC free article] Widmer AF, Frei R, Rajacic Z, Zimmerli W. Correlation between In Vivo and In Vitro Efficacy of Antimicrobial Agents against Foreign Body Infections. Journal of Infectious Diseases. 1990;162:96–102. Jonsson EÖ, Johannesdottir H, Robertsson O, Mogensen B. Bacterial contamination of the wound during primary total hip and knee replacement. Acta orthopaedica. 2014;85:159–64. [PMC free article] Hellmark B, Söderquist B, Unemo M, Nilsdotter-Augustinsson Å. Comparison of Staphylococcus epidermidis isolated from prosthetic joint infections and commensal isolates in regard to antibiotic susceptibility, agr type, biofilm production, and epidemiology. International Journal of Medical Microbiology. 2013;303:32–9. Bernthal NM, Pribaz JR, Stavrakis AI, Billi F, Cho JS, Ramos RI. et al. Protective role of IL-1beta against post-arthroplasty Staphylococcus aureus infection. J Orthop Res. 2011;29:1621–6. [PMC free article] Stuyt RJ, Kim SH, Reznikov LL, Fantuzzi G, Novick D, Rubinstein M. et al. Regulation of Staphylococcus epidermidis-induced IFN-gamma in whole human blood: the role of endogenous IL-18, IL-12, IL-1, and TNF. Cytokine. 2003;21:65–73. Mankan AK, Dau T, Jenne D, Hornung V. The NLRP3/ASC/Caspase-1 axis regulates IL-1beta processing in neutrophils. Eur J Immunol. 2012;42:710–5. Karmakar M, Katsnelson M, Malak HA, Greene NG, Howell SJ, Hise AG. et al. Neutrophil IL-1beta processing induced by pneumolysin is mediated by the NLRP3/ASC inflammasome and caspase-1 activation and is dependent on K+ efflux. Journal of immunology. 2015;194:1763–75. [PMC free article] Fatykhova D, Rabes A, Machnik C, Guruprasad K, Pache F, Berg J. et al. Serotype 1 and 8 Pneumococci Evade Sensing by Inflammasomes in Human Lung Tissue. PloS one. 2015;10:e0137108. [PMC free article] Sahdo B, Särndahl E, Elgh F, Söderquist B. Propionibacterium acnes activates caspase-1 in human neutrophils. APMIS: acta pathologica, microbiologica, et immunologica Scandinavica. 2013;121:652–63. Sahdo B, Fransén K, Asfaw Idosa B, Eriksson P, Söderquist B, Kelly A. et al. Cytokine profile in a cohort of healthy blood donors carrying polymorphisms in genes encoding the NLRP3 inflammasome. PloS one. 2013;8:e75457. [PMC free article] Paramel GV, Sirsjo A, Fransen K. Role of genetic alterations in the NLRP3 and CARD8 genes in health and disease. Mediators Inflamm. 2015;2015:846782. [PMC free article] Gattorno M, Tassi S, Carta S, Delfino L, Ferlito F, Pelagatti MA. et al. Pattern of interleukin-1beta secretion in response to lipopolysaccharide and ATP before and after interleukin-1 blockade in patients with CIAS1 mutations. Arthritis Rheum. 2007;56:3138–48. Karmakar M, Katsnelson MA, Dubyak GR, Pearlman E. Neutrophil P2X7 receptors mediate NLRP3 inflammasome-dependent IL-1beta secretion in response to ATP. Nat Commun. 2016;7:10555. [PMC free article] Miller CM, Boulter NR, Fuller SJ, Zakrzewski AM, Lees MP, Saunders BM. et al. The role of the P2X(7) receptor in infectious diseases. PLoS Pathog. 2011;7:e1002212. [PMC free article] Man SM, Karki R, Kanneganti TD. Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases. Immunol Rev. 2017;277:61–75. [PMC free article]