SwePub - search: WFRF:(Kwiecinski Jakub 1985)

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1.	Kwiecinski, Jakub, 1985, et al. (author) Staphylokinase Promotes the Establishment of Staphylococcus aureus Skin Infections While Decreasing Disease Severity 2013 In: Journal of Infectious Diseases. - : Oxford University Press. - 0022-1899 .- 1537-6613. ; 208:6, s. 990-999 Journal article (peer-reviewed)abstract Skin infections are frequently caused by Staphylococcus aureus and can lead to a fatal sepsis. The microbial mechanisms controlling the initiation and progression from mild skin infection to a severe disseminated infection remain poorly understood. Using a combination of clinical data and in vitro and ex vivo assays, we show that staphylokinase, secreted by S. aureus, promoted the establishment of skin infections in humans and increased bacterial penetration through skin barriers by activating plasminogen. However, when infection was established, the interaction between staphylokinase and plasminogen did not promote systemic dissemination but induced the opening and draining of abscesses and decreased disease severity in neutropenic mice. Also, increased staphylokinase production was associated with noninvasive S. aureus infections in patients. Our results point out the dual roles of staphylokinase in S. aureus skin infections as promoting the establishment of infections while decreasing disease severity.
2.	Ali, Abukar, 1988, et al. (author) Antibiotic-killed Staphylococcus aureus induces destructive arthritis in mice. 2015 In: Arthritis & rheumatology (Hoboken, N.J.). - : Wiley. - 2326-5205 .- 2326-5191. ; 67:1, s. 107-116 Journal article (peer-reviewed)abstract Objective: Permanent reduction in joint function is a severe post-infectious complication in patients with Staphylococcus aureus septic arthritis. This reduction in joint function might be caused by persistent joint inflammation after the adequate eradication of bacteria by antibiotics. Methods: We studied whether antibiotic-killed S. aureus induced joint inflammation in mice and elucidated the molecular and cellular mechanism of this type of arthritis. Results: The intraarticular injection of antibiotic-killed S. aureus induced mild to moderate synovitis and bone erosions that lasted for a minimum of 14 days. The frequency and severity of synovitis were significantly reduced in tumor necrosis factor receptor 1 (TNFR1), receptor for Advanced Glycation End Products (RAGE), and toll like receptor 2 (TLR2) knockout mice compared with wild-type animals. The combined depletion of monocytes and neutrophils resulted in a significantly lower frequency of synovitis. Among bacterial factors, insoluble cell debris played a more important role than bacterial DNA or soluble components in inducing joint inflammation. Importantly, anti-TNF therapy abrogated the joint inflammation induced by antibiotic-killed S. aureus. Conclusion: Antibiotic-killed S. aureus induced and maintained the joint inflammation that is mediated through TLR2, TNFR1, and RAGE receptor. The cross-talk between neutrophils and monocytes is responsible for this type of arthritis. Anti-TNF therapy might be used as a novel therapeutic strategy, in combination with antibiotics, to treat staphylococcal septic arthritis. © 2014 American College of Rheumatology.
3.	Ali, Abukar, 1988, et al. (author) CTLA4-Ig but not anti-TNF therapy promotes staphylococcal septic arthritis in mice. 2015 In: The Journal of infectious diseases. - : Oxford University Press (OUP). - 1537-6613 .- 0022-1899. ; 212:8, s. 1308-1316 Journal article (peer-reviewed)abstract The development of biologics has greatly increased the quality of life as well as the life expectancy of many RA patients. However, a large number of these patients are at an increased risk of developing serious infections. The aim of this study was to examine differential effects of anti-TNF versus CTLA4-Ig treatment on both immunological response and host defense in a murine model of septic arthritis.
4.	Eick, Sigrun, et al. (author) Honey - a potential agent against Porphyromonas gingivalis: an in vitro study 2014 In: BMC Oral Health. - : Springer Science and Business Media LLC. - 1472-6831. ; 14:1 Journal article (peer-reviewed)abstract Abstract Background Honey has been discussed as a therapeutic option in wound healing since ancient time. It might be also an alternative to the commonly used antimicrobials in periodontitis treatment. The in-vitro study was aimed to determine the antimicrobial efficacy against Porphyromonas gingivalis as a major periodontopathogen. Methods One Manuka and one domestic beekeeper honey have been selected for the study. As a screening, MICs of the honeys against 20 P. gingivalis strains were determined. Contents of methylglyoxal and hydrogen peroxide as the potential antimicrobial compounds were determined. These components (up to 100 mg/l), propolis (up to 200 mg/l) as well as the two honeys (up to 10% w/v) were tested against four P. gingivalis strains in planktonic growth and in a single-species biofilm. Results 2% of Manuka honey inhibited the growth of 50% of the planktonic P. gingivalis, the respective MIC50 of the German beekeeper honey was 5%. Manuka honey contained 1.87 mg/kg hydrogen peroxide and the domestic honey 3.74 mg/kg. The amount of methylglyoxal was found to be 2 mg/kg in the domestic honey and 982 mg/kg in the Manuka honey. MICs for hydrogen peroxide were 10 mg/l - 100 mg/l, for methylglyoxal 5 – 20 mg/l, and for propolis 20 mg/l – 200 mg/l. 10% of both types of honey inhibited the formation of P. gingivalis biofilms and reduced the numbers of viable bacteria within 42 h-old biofilms. Neither a total prevention of biofilm formation nor a complete eradication of a 42 h-old biofilm by any of the tested compounds and the honeys were found. Conclusions Honey acts antibacterial against P. gingivalis. The observed pronounced effects of Manuka honey against planktonic bacteria but not within biofilm can be attributed to methylglyoxal as the characteristic antimicrobial component.
5.	Elmwall, Jonas, et al. (author) Galectin-3 Is a Target for Proteases Involved in the Virulence of Staphylococcus aureus 2017 In: Infection and Immunity. - : American Society for Microbiology. - 0019-9567 .- 1098-5522. ; 85:7 Journal article (peer-reviewed)abstract Staphylococcus aureus is a major cause of skin and soft tissue infection. The bacterium expresses four major proteases that are emerging as virulence factors: aureolysin (Aur), V8 protease (SspA), staphopain A (ScpA), and staphopain B (SspB). We hypothesized that human galectin-3, a beta-galactoside-binding lectin involved in immune regulation and antimicrobial defense, is a target for these proteases and that proteolysis of galectin-3 is a novel immune evasion mechanism. Indeed, supernatants from laboratory strains and clinical isolates of S. aureus caused galectin-3 degradation. Similar proteolytic capacities were found in Staphylococcus epidermidis isolates but not in Staphylococcus saprophyticus. Galectin-3-induced activation of the neutrophil NADPH oxidase was abrogated by bacterium-derived proteolysis of galectin-3, and SspB was identified as the major protease responsible. The impact of galectin-3 and protease expression on S. aureus virulence was studied in a murine skin infection model. In galectin-3 (+)/(+) mice, SspB-expressing S. aureus caused larger lesions and resulted in higher bacterial loads than protease-lacking bacteria. No such difference in bacterial load or lesion size was detected in galectin-3 (+)/(+) mice, which overall showed smaller lesion sizes than the galectin-3 (+)/(+) animals. In conclusion, the staphylococcal protease SspB inactivates galectin-3, abrogating its stimulation of oxygen radical production in human neutrophils and increasing tissue damage during skin infection.
6.	Fei, Ying, et al. (author) The combination of a tumor necrosis factor inhibitor and antibiotic alleviates staphylococcal arthritis and sepsis in mice. 2011 In: The Journal of infectious diseases. - : Oxford University Press (OUP). - 1537-6613 .- 0022-1899. ; 204:3, s. 348-57 Journal article (peer-reviewed)abstract (See the editorial commentary by Chow, on pages 332-4) Background.Despite advances in medical practices, in recent decades permanent reductions in joint function have not been achieved, and the high mortality rate of patients with staphylococcal septic arthritis has not substantially improved. Methods.We evaluated the effects of a combined tumor necrosis factor (TNF) inhibitor and antibiotic therapy on the course of Staphylococcus aureus arthritis and sepsis in mice. Results.Treatment with the combination of a TNF inhibitor and an antibiotic resulted in a quicker relief of clinical arthritis in mice with septic arthritis, compared with an antibiotic monotherapy. Both histopathologically verified synovitis and the extent of joint destruction were reduced by this combined treatment. Importantly, anti-TNF treatment significantly improved the survival rate of mice with S. aureus sepsis and staphylococcal enterotoxin shock syndrome; this effect might be the result of a partial restoration of the hemostatic balance between coagulation and fibrinolysis. Finally, we demonstrated that anti-TNF treatment downregulates high-mobility group protein B1 in staphylococcal enterotoxin shock syndrome. Conclusions.Thus, simultaneous systemic TNF inhibition and antibiotic therapy has beneficial effects on the outcome of S. aureus arthritis and sepsis in a mouse model, suggesting that the combination of a TNF inhibitor and antibiotics represents a novel therapeutic strategy for the treatment of staphylococcal infections.
7.	Kwiecinski, Jakub, 1985, et al. (author) Activation of plasminogen by staphylokinase reduces the severity of Staphylococcus aureus systemic infection. 2010 In: The Journal of infectious diseases. - : Oxford University Press (OUP). - 1537-6613 .- 0022-1899. ; 202:7, s. 1041-9 Journal article (peer-reviewed)abstract BACKGROUND: Staphylokinase (SAK) is produced by the majority of Staphylococcus aureus strains. It is an extracellular protein that activates the conversion of human plasminogen (plg) to plasmin. The role played by SAK in staphylococcal infection is unclear. METHODS: Wild-type S. aureus strain LS-1, which lacks the ability to produce SAK, was modified by an insertion of the sak gene into its chromosome. The sak gene was integrated in 2 forms--(1) linked to its own promoter and (2) fused to the promoter of the protein A gene--which resulted in the overexpression of SAK. SAK is highly specific for human plg and exhibits almost no activity toward murine plg. To investigate the role played by SAK in a murine infection model, human plg transgenic mice and their wild-type counterparts were inoculated intravenously with congenic S. aureus strains differing in SAK production. RESULTS: Human plg transgenic mice inoculated with SAK-expressing strains displayed significantly reduced mortality, less weight loss, and lower bacterial loads in kidneys than did the wild-type mice. No difference in the severity of sepsis was observed between transgenic and wild-type mice infected with a SAK-deficient strain. CONCLUSIONS: The results suggest that expression of SAK followed by activation of plg alleviates the course of S. aureus sepsis.
8.	Kwiecinski, Jakub, 1985 (author) Biofilm formation by pathogenic Prototheca algae 2015 In: Letters in Applied Microbiology. - : Oxford University Press (OUP). - 0266-8254 .- 1472-765X. ; 61:6, s. 511-517 Journal article (peer-reviewed)abstract Prototheca microalgae are the only plants known to cause infections in humans and animals. The mechanisms of Prototheca infections are poorly understood, and no good treatments are available. Biofilms-surface-attached, three-dimensional microbial communities contributing to chronic infections-are formed by many pathogenic bacteria and fungi, but it is not known if Prototheca algae also have this ability. This study shows that various Prototheca species form biofilms composed of surface-attached cells in all growth phases, linked together by matrix containing DNA and polysaccharides. Biofilm formation was modulated by the presence of host plasma or milk. Compared to planktonic cells, Prototheca biofilms caused decreased release of IL-6 by mononuclear immune cells and responded differently to treatment with antimicrobials. Prototheca biofilms possibly contribute to chronic and hard-to-treat character of those algal infections.
9.	Kwiecinski, Jakub, 1985, et al. (author) Biofilm formation by Staphylococcus aureus clinical isolates correlates with the infection type. 2019 In: Infectious diseases. - : Informa UK Limited. - 2374-4243 .- 2374-4235. ; 51:6, s. 446-451 Journal article (peer-reviewed)abstract Biofilms are involved in many Staphylococcus aureus infections, but relation of biofilm formation and the infection types or the clinical outcomes remain unclear.We measured biofilm formation, with a microtiter plate assay, of a collection of methicillin-sensitive clinical isolates from 159 invasive S. aureus infections, encompassing all cases occurring within a hospital catchment area during two years, and from additional 49 non-invasive skin infections from the same region. Results were related to available clinical and microbiological documentation.Isolates from medical device infections (intravenous line-associated and prosthetic joint infections), as well as isolates from superficial skin infections, were particularly proficient in forming biofilms. No increased biofilm-forming capacity was seen in isolates from endocarditis, osteomyelitis, or other infections. There was also a correlation of biofilm formation with the agr type of the isolates. Thicker biofilms were more resistant to antibiotic treatment in vitro. No correlation between biofilm formation and clinical outcomes was noted.S. aureus isolates from 'classical' biofilm-related infections, but also from superficial skin infections, are especially proficient in forming biofilms. There is, however, no obvious relation of biofilm-forming capacity of isolates and the clinical outcome of the infection, and more studies on this issue are needed.
10.	Kwiecinski, Jakub, 1985, et al. (author) Biofilm Formation by Staphylococcus aureus Isolates from Skin and Soft Tissue Infections. 2015 In: Current microbiology. - : Springer Science and Business Media LLC. - 1432-0991 .- 0343-8651. ; 70:5, s. 698-703 Journal article (peer-reviewed)abstract Many diseases caused by Staphylococcus aureus are associated with biofilm formation. However, the ability of S. aureus isolates from skin and soft tissue infections to form biofilms has not yet been investigated. We tested 160 isolates from patients with various skin infections for biofilm-forming capacity in different growth media. All the isolates formed biofilms, the extent of which depended on the type of growth medium. The thickest biofilms were formed when both plasma and glucose were present in the broth; in this case, S. aureus incorporated host fibrin into the biofilm's matrix. There were no differences in the biofilm formation between isolates from different types of skin infections, except for a particularly good biofilm formation by isolates from diabetic wounds and a weaker biofilm formation by isolates from impetigo. In conclusion, biofilm formation is a universal behavior of S. aureus isolates from skin infections. In some cases, such as in diabetic wounds, a particularly strong biofilm formation most likely contributes to the chronic and recurrent character of the infection. Additionally, as S. aureus apparently uses host fibrin as part of the biofilm structure, we suggest that plasma should be included more frequently in in vitro biofilm studies.
11.	Kwiecinski, Jakub, 1985, et al. (author) Fibrinolysis is down-regulated in mouse collagen-induced arthritis, but its normalization does not alleviate the course of disease. 2011 In: Inflammation research : official journal of the European Histamine Research Society ... [et al.]. - : Springer Science and Business Media LLC. - 1420-908X. ; 60:11, s. 1021-1029 Journal article (peer-reviewed)abstract OBJECTIVE: Down-regulation of fibrinolysis and increased fibrin deposition in joints are hallmarks of rheumatoid arthritis (RA), and are believed to be involved in disease progression. The mouse model of collagen-induced arthritis (CIA) closely resembles RA and has been used to explore mechanism and treatments of RA, but neither the fibrinolytic system nor pro-fibrinolytic therapies were investigated in CIA. MATERIALS AND METHODS: Plasmin activity, levels of plasminogen activator inhibitor (PAI-1), D-dimer, and IL-6 were measured in plasma of CIA mice. Fibrin deposition and PAI-1 levels were also measured in inflamed joints. Mice were treated with plasminogen activators uPA (urokinase-type plasminogen activator) or tPA (tissue-type plasminogen activator). Effects of treatment on disease severity and fibrinolytic system were assessed. RESULTS: CIA caused decrease in plasmin activity, accompanied by increase in PAI-1 levels, in both blood and inflamed joints. This resulted in massive fibrin deposition in synovium. PAI-1 levels correlated negatively with plasmin activity and positively with IL-6. Treatments with uPA and tPA improved plasmin activity and removed fibrin deposits in inflamed joints. However, disease severity remained unchanged. CONCLUSIONS: Fibrinolytic changes in CIA parallel changes in RA, making CIA a suitable model to study fibrinolysis in RA. Normalization of plasmin activity in CIA after treatment with plasminogen activators had no effect on disease severity.
12.	Kwiecinski, Jakub, 1985 (author) First images of respiratory system in ancient Egypt: Trachea, bronchi and pulmonary lobes 2012 In: Canadian Respiratory Journal. - : Hindawi Limited. - 1916-7245 .- 1198-2241. ; 19:5 Journal article (peer-reviewed)abstract Examination of ancient Egyptians' depictions of the respiratory tract, dating back to the 30th century BC, reveals their awareness of the pulmonary anatomy: reinforced with cartilaginous rings, the trachea is split into two main bronchi, which then enter the lungs (lungs being divided into pulmonary lobes).
13.	Kwiecinski, Jakub, 1985 (author) Genetically modified abominations? Widespread opposition to GMOs might have deep-seated cultural causes. 2009 In: EMBO reports. - : EMBO. - 1469-3178 .- 1469-221X. ; 10:11, s. 1187-90 Journal article (peer-reviewed)abstract Opposition to genetically modified organisms (GMOs) is a widespread phenomenon, yet its basis is still not entirely clear. While it is usually attributed to irrational fears and political issues, it might have a deep-seated cultural causes. Exploration of the “anti – GMO” discourse reveals multiple similarities between the way genetic modifications are described by their opponents and the way impurity is depicted in ethnological theory of taboo. Those include “dirtiness”, “infectivity” and “trespassing boundaries”. Cultural identification of GMO with “impurity” and “taboo” partly explains the people’s hostility – and is an example of how new scientific achievements are assimilated by traditional cultural schemes.
14.	Kwiecinski, Jakub, 1985, et al. (author) No rheumatoid arthritis in ancient Egypt: a reappraisal 2016 In: Rheumatology International. - : Springer Science and Business Media LLC. - 0172-8172 .- 1437-160X. ; 36:6, s. 891-895 Journal article (peer-reviewed)abstract Antiquity of rheumatoid arthritis (RA) remains controversial, and its origins in Americas or in the Old World are disputed. Proponents of the latter frequently refer to RA in ancient Egypt, but validity of those claims has never been examined. Review of all reported RA cases from ancient Egypt revealed that none of them represent real RA, instead being either examples of changing naming conventions or of imprecise diagnostic criteria. Most cases represented osteoarthritis or spondyloarthropathies. Also review of preserved ancient Egyptian medical writings revealed many descriptions of musculoskeletal disorders, but none of them resembled RA. This suggests that RA was absent in ancient Egypt and supports the hypothesis of the New World origin of RA and its subsequent global spread in the last several centuries.
15.	Kwiecinski, Jakub, 1985 (author) Reactive arthritis in ancient Egypt: A possible description in medical papyri 2014 In: Journal of Rheumatology. - : The Journal of Rheumatology. - 0315-162X .- 1499-2752. ; 41:3, s. 556-557 Journal article (peer-reviewed)abstract Reactive arthritis (ReA) is a puzzling condition initiated by a genitourinary or gastrointestinal infection. Within 1–3 weeks after the triggering infection, the symptoms of ReA appear: joint inflammation, genitourinary symptoms (urethritis or cystitis), and eye inflammation, sometimes accompanied by enthesitis and sacroiliitis or dermatological changes1. This unusual constellation of symptoms was described in the 19th century by Alexandre-Urbain Yvan, Benjamin Brodie, and Astley Cooper, and recognized as a separate disease in the 20th century by researchers Adolf Vossius, Noël Fiessinger, Edgar Leroy, and the infamous Nazi physician Hans Reiter1,2,3,4. This late identification of ReA might suggest that it is a recent disease, caused by changed properties of microbes or newly developed immune responses. But this is probably not true. Cases resembling ReA appear in many texts starting from the 16th century, as well as in individual writings from ancient Rome and Greece3. And ReA is probably even older: I draw attention to an ancient Egyptian text describing symptoms strikingly resembling ReA — likely the very earliest description of this disease.
16.	Kwiecinski, Jakub, 1985, et al. (author) Relationship between elevated cerebrospinal fluid levels of plasminogen activator inhibitor 1 and neuronal destruction in patients with neuropsychiatric systemic lupus erythematosus. 2009 In: Arthritis and rheumatism. - : Wiley. - 0004-3591 .- 1529-0131. ; 60:7, s. 2094-101 Journal article (peer-reviewed)abstract OBJECTIVE: A homeostatic imbalance between coagulation and fibrinolysis might occur intrathecally in neuropsychiatric systemic lupus erythematosus (NPSLE). However, there are no published data on levels of fibrinolytic factors in the cerebrospinal fluid (CSF) of patients with NPSLE. The present study was undertaken to assess CSF levels of fibrinolytic molecules, including urokinase plasminogen activator (uPA), tissue plasminogen activator (tPA), D-dimer, and plasminogen activator inhibitor 1 (PAI-1), in SLE patients with clinically verified neuropsychiatric involvement and to compare these levels with those in SLE patients without neuropsychiatric involvement and in healthy subjects. METHODS: Levels of uPA, tPA, and PAI-1 were assessed in CSF from 94 patients with SLE (33 who had NPSLE, 56 who did not have NPSLE, and 5 who were positive for antiphospholipid antibody [not included in the NPSLE or non-NPSLE group]) and from 53 age-matched controls. Patients were evaluated clinically, with magnetic resonance imaging of the brain, analyses of neuronal/glial degradation products in CSF, and neuropsychiatric testing. RESULTS: In the group of patients with NPSLE, intrathecal PAI-1 levels were significantly elevated compared with levels in SLE patients without overt neuropsychiatric involvement (P < 0.05) and in healthy controls (P < 0.001). In contrast, intrathecal levels of uPA did not differ significantly. Intrathecal levels of PAI-1 correlated significantly with CSF levels of interleukin-6 (IL-6) (r = 0.34, P < 0.001) and IL-8 (r = 0.33, P < 0.001). Importantly, increased PAI-1 and D-dimer levels were observed in SLE patients who had pathologically elevated levels of glial fibrillary acidic protein, neurofilament triplet protein, and tau protein in CSF. CONCLUSION: Intrathecal release of PAI-1 is increased in patients with NPSLE. This results in impaired fibrinolysis, which might contribute to neuronal and astrocytic damage in NPSLE.
17.	Kwiecinski, Jakub, 1985, et al. (author) Reply to Bouchiat et al. 2014 In: The Journal of infectious diseases. - : Oxford University Press (OUP). - 1537-6613 .- 0022-1899. ; 210:8, s. 1343-1344 Journal article (other academic/artistic)abstract Comment on: Buchiat Bouchiat C, Mehenni C, Meugnier H, Bes M, Tristan A, Vandenesch F. Limitations of staphylokinase as a marker for Staplylococcus aureus invasive infections in humans. J Infect Dis 2014;210:1341-3
18.	Kwiecinski, Jakub, 1985, et al. (author) Staphylokinase controls Staphylococcus aureus biofilm formation and detachment through host plasminogen activation. 2016 In: The Journal of infectious diseases. - : Oxford University Press (OUP). - 0022-1899 .- 1537-6613. ; 213:1, s. 139-148 Journal article (peer-reviewed)abstract Staphylococcus aureus biofilms, a leading cause of persistent infections, are highly resistant to immune defenses and antimicrobial therapies. In this study, we investigated the contribution of fibrin and staphylokinase to biofilm formation. Both in clinical S. aureus isolates and in laboratory strains, high staphylokinase-producing strains formed less biofilm than strains that lacked staphylokinase, suggesting that staphylokinase prevents biofilm formation. Additionally, staphylokinase induced detachment of mature biofilms. This effect depended on plasminogen activation by staphylokinase. Host-derived fibrin, the main substrate cleaved by staphylokinase-activated plasminogen, was a major component of biofilm matrix and dissolution of this fibrin scaffold greatly increased susceptibility of biofilms to antibiotics and neutrophil phagocytosis. Staphylokinase also attenuated biofilm-associated catheter infections in mouse models. In conclusion, our results reveal a novel role for staphylokinase-induced plasminogen activation that prevents S. aureus biofilm formation and induces detachment of existing biofilms through proteolytic cleavage of biofilm matrix components.
19.	Kwiecinski, Jakub, 1985, et al. (author) Sulfatide attenuates experimental Staphylococcal aureus sepsis through a CD1d-dependent pathway. 2013 In: Infection and immunity. - 1098-5522. ; 81:4, s. 1114-1120 Journal article (peer-reviewed)abstract Natural killer T (NKT) lymphocytes are implicated in the early response to microbial infection. Further, sulfatide, a myelin self-glycosphingolipid, activates a type II NKT cell subset, and can modulate disease in murine models. We examined the role of NKT cells and the effect of sulfatide treatment in a murine model of Staphylococcus aureus sepsis. Lack of CD1d-restricted NKT cells did not alter survival after a lethal inoculum of S. aureus. In contrast, sulfatide treatment significantly improved the survival rate of mice with S. aureus sepsis, accompanied by decreased levels of TNF-α and IL-6 in the blood. The protective effect of sulfatide treatment depended on CD1d, but not on type I NKT cells, suggesting that activation of type II NKT cells by sulfatide has beneficial effects on the outcome of S. aureus sepsis in this model.
20.	Kwiecinski, Jakub, 1985, et al. (author) Surface proteins of Staphylococcus aureus play an important role in experimental skin infection. 2014 In: APMIS : acta pathologica, microbiologica, et immunologica Scandinavica. - : Wiley. - 1600-0463. ; 122:12, s. 1240-1250 Journal article (peer-reviewed)abstract Staphylococcus aureus is the most common cause of skin infections that range from mild diseases up to life-threatening conditions. Mechanisms of S. aureus virulence in those infections remain poorly studied. To investigate the impact of S. aureus surface proteins on skin infection, we used mouse models of skin abscess formation and skin necrosis, induced by a subcutaneous injection of bacteria. In the skin abscess model, a sortase-deficient S. aureus strain lacking all of its cell-wall anchored proteins was less virulent than its wild-type strain. Also, strains specifically lacking protein A, fibronecting binding proteins, clumping factor A or surface protein SasF were impaired in their virulence. When a model of dermonecrosis was studied, the S. aureus surface proteins could not be shown to be involved. In summary, surface proteins play an important role in virulence of S. aureus skin abscess infections, but not in formation of skin necrosis.
21.	Kwiecinski, Jakub, 1985 (author) The dawn of medicine: ancient egypt and athotis, the king-physician. 2013 In: Perspectives in biology and medicine. - : Project Muse. - 0031-5982 .- 1529-8795. ; 56:1, s. 99-104 Journal article (peer-reviewed)abstract The earliest physician recorded in history is Athotis (Aha), one of the first rulers of ancient Egypt. While it is debatable whether the story of a king-physician is a fact or just a legend, it is clear that ancient Egyptian medicine developed around the time of his reign. The fortunate combination of earlier medical observations, the development of script, and favorable social conditions made the dawn of ancient Egypt also the dawn of medicine.
22.	Kwiecinski, Jakub, 1985, et al. (author) Tissue Plasminogen Activator Coating on Implant Surfaces Reduces Staphylococcus aureus Biofilm Formation 2016 In: Applied and Environmental Microbiology. - : American Society for Microbiology. - 0099-2240 .- 1098-5336. ; 82:1, s. 394-401 Journal article (peer-reviewed)abstract Staphylococcus aureus biofilm infections of indwelling medical devices are a major medical challenge because of their high prevalence and antibiotic resistance. As fibrin plays an important role in S. aureus biofilm formation, we hypothesize that coating of the implant surface with fibrinolytic agents can be used as a new method of antibiofilm prophylaxis. The effect of tissue plasminogen activator (tPA) coating on S. aureus biofilm formation was tested with in vitro microplate biofilm assays and an in vivo mouse model of biofilm infection. tPA coating efficiently inhibited biofilm formation by various S. aureus strains. The effect was dependent on plasminogen activation by tPA, leading to subsequent local fibrin cleavage. A tPA coating on implant surfaces prevented both early adhesion and later biomass accumulation. Furthermore, tPA coating increased the susceptibility of biofilm infections to antibiotics. In vivo, significantly fewer bacteria were detected on the surfaces of implants coated with tPA than on control implants from mice treated with cloxacillin. Fibrinolytic coatings (e.g., with tPA) reduce S. aureus biofilm formation both in vitro and in vivo, suggesting a novel way to prevent bacterial biofilm infections of indwelling medical devices.
23.	Peetermans, Marijke, et al. (author) Plasminogen activation by staphylokinase enhances local spreading of S. aureus in skin infections. 2014 In: BMC microbiology. - : Springer Science and Business Media LLC. - 1471-2180. ; 14:1 Journal article (peer-reviewed)abstract Background Staphylococcus aureus (S. aureus) is a frequent cause of skin and soft tissue infections. A unique feature of S. aureus is the combined presence of coagulases that trigger fibrin formation and of the plasminogen activator staphylokinase (SAK). Whereas the importance of fibrin generation for S. aureus virulence has been established, the role of SAK remains unclear.We studied the role of plasminogen activation by SAK in a skin infection model in mice and evaluated the impact of alpha-2-antiplasmin (¿2AP) deficiency on the spreading and proteolytic activity of S. aureus skin infections. The species-selectivity of SAK was overcome by adenoviral expression of human plasminogen. Bacterial spread and density was assessed non-invasively by imaging the bioluminescence of S. aureus Xen36.ResultsSAK-mediated plasmin activity increased the local invasiveness of S. aureus, leading to larger lesions with skin disruption as well as decreased bacterial clearance by the host. Even though fibrin and bacterial surfaces protected SAK-mediated plasmin activity from inhibition by ¿2AP, the deficiency of ¿2AP resulted in increased bacterial spreading. SAK-mediated plasmin also induced secondary activation of gelatinases, shown both in vitro and in lesions from the in vivo model.ConclusionSAK contributes to the phenotype of S. aureus skin infections by enhancing bacterial spreading as a result of fibrinolytic and proteolytic activation.
24.	Szweda, P., et al. (author) Chitosan-protein scaffolds loaded with lysostaphin as potential antistaphylococcal wound dressing materials 2014 In: Journal of Applied Microbiology. - : Oxford University Press (OUP). - 1364-5072. ; 117:3, s. 634-642 Journal article (peer-reviewed)abstract Aims: The development of technology for preparing chitosan-protein scaffolds loaded with lysostaphin, which potentially could be used as dressing for wound treatment and soft tissue infections caused by Staphylococcus aureus. Methods and Results: The unique technology of chitosan solubilization using gaseous CO2 instead of organic or inorganic acids was used for the incorporation of lysostaphin, the enzyme that exhibits bactericidal activity against staphylococci, within the structure of chitosan-protein sponges. The developed chitosan-protein scaffolds loaded with lysostaphin revealed high antistaphylococcal activity, which has been confirmed with a large (n = 143) collection of clinical (skin and wound infections) and animal (bovine mastitis) isolates of these bacteria, including MRSA. No change of bactericidal activity of the lyophilized materials has been observed during half-year storage at 4 degrees C. Conclusions: The developed materials are potential candidates for preparing biologically active, antistaphylococcal wound dressing materials. Significance and Impact of the Study: Staphylococci belong to the most popular and most burdensome aetiological factors of wound and soft tissues infections. The developed chitosan-protein scaffolds loaded with lysostaphin could be a possible solution to problems associated with treatment of these infections.

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