ライフサイエンスコーパス: S. aureus

1 S. aureus agr mutant HU-14 (IS256 insertion in agrC) fro

2 S. aureus expresses a variety of virulence factors that

3 S. aureus produce membrane-bound, spherical, nano-sized,

4 S. aureus produces an array of bicomponent pore-forming

5 S. aureus USA300 isolates utilize the copBL and copAZ ge

6 S. aureus was the most common pathogen identified in pre

7 S. aureus, like all organisms, requires essential biosyn

8 In this study, we screened 75 S. aureus strains for their ability to induce type I and

9 We estimated 55,764 S. aureus post-surgical infections occurred annually in

10 MRSA (97%), followed by P. aeruginosa (81%), S. aureus (79%) and Candida spp (72%), with lower reduct

11 ase the efficacy of vancomycin in clearing a S. aureus infection.

12 adhesion to each host ligand, we generated a S. aureus Genetic Adhesion Network, which identified a c

13 the same concentration of CD11b blocking Ab, S. aureus killing by female BMN was greatly reduced comp

14 equencing of 16S ribosomal RNA, and absolute S. aureus abundance was measured by quantitative PCR.

15 PP alone, including 22/92 (23.9%) additional S. aureus isolates and 25/92 (27.2%) H. influenzae isola

16 Additionally, S. aureus did not develop resistance to auranofin after

17 An increase in adherent S. aureus was observed after exposure to both IFN-alpha

18 he redox state of the disulfide bond affects S. aureus biofilm formation and toxic shock syndrome tox

19 miting NK cell production of IFN-gamma after S. aureus infection in a TLR4-dependent manner.

20 to 32-fold increase of the activity against S. aureus and 16- to 64-fold against E. coli and P. aeru

21 reened for quorum quenching activity against S. aureus, including direct protein output assessment (d

22 for more than 259 days and 147 days against S. aureus and P. aeruginosa, respectively, compared to 7

23 t factors important for host defense against S. aureus.

24 SFE extract exhibited effectiveness against S. aureus, E. coli, and S. typhimurium, with minimum inh

25 s with potent anti-virulence effects against S. aureus.

26 nduced inflammation and protect mice against S. aureus-induced sepsis and meningitis after DA treatme

27 emolysin-specific antibodies protect against S. aureus-induced dermonecrosis, a key feature of skin a

28 evasion can promote host protection against S. aureus bloodstream infection.

29 he T7SS gene cluster and is found across all S. aureus strains as well as in Listeria and Enterococci

30 orum sensing inhibition activity against all S. aureus accessory gene regulator (agr) alleles in abse

31 Each compound inhibits all S. aureus accessory gene regulator (agr) alleles (IC(50)

32 Although S. aureus is a leading cause of postsurgical infections,

33 An S. aureus bursa aurealis Tn library consisting of 1,952

34 We generated an S. aureus ddh/ldh1/ldh2 triple Tn mutant that cannot pro

35 demonstrate that exposing P. aeruginosa and S. aureus cells to sphingosine results in a very rapid,

36 in tuberculosis, leprosy, P. aeruginosa and S. aureus infections, where it develops via missense mut

37 Both P. aeruginosa and S. aureus require iron to infect the mammalian host.

38 acterial pathogens such as P. aeruginosa and S. aureus, cloaking the bacteria from neutrophils.

39 vant organisms: M. leprae, P. aeruginosa and S. aureus, despite weak sequence identity.

40 e report that histone H2A enters E. coli and S. aureus through membrane pores formed by the AMPs LL-3

41 chlorhexidine solutions against E. coli and S. aureus.

42 better understand both barrier function and S. aureus colonization in LE, two new potential therapeu

43 , blocking CD11b reduced both ROS levels and S. aureus killing by murine BMN from both sexes.

44 action between primary human neutrophils and S. aureus biofilms and provides insight into how S. aure

45 sable for survival during osteomyelitis, and S. aureus instead has a critical need for anaplerosis.

46 ion or pleural fluid, with S. pneumoniae and S. aureus the leading pathogens identified.

47 xin domain of TspA is highly polymorphic and S. aureus strains encode multiple tsaI homologs at the t

48 crobial discovery to fight Gram-positive and S. aureus infections.

49 Patients with septic shock and S. aureus bacteremia admitted directly from the emergenc

50 interplay between the host immune system and S. aureus that has evolved under the dual selective pres

51 ion in the development of host-directed anti-S. aureus treatments.

52 eukocidins to impair the development of anti-S. aureus adaptive immunity and facilitate reinfection i

53 n mutant results in increased levels of anti-S. aureus antibodies compared with mice infected with th

54 ins negatively impact the generation of anti-S. aureus antibodies in vivo.

55 Staphylococcus aureus (S. aureus) is a common colonizer of healthy skin and muc

56 gene for detection of Staphylococcus aureus (S. aureus) or Streptococcus pneumoniae (S. pneumoniae),

57 ia coli (E. coli) and Staphylococcus aureus (S. aureus), which decreased first and then increased in

58 get bacteria E. coli and non-target bacteria S. aureus, K. pneumonia and P. aeruginosa.

59 at EPS protects hosts from acute bloodstream S. aureus infection not only by inducing macrophages tha

60 to describe the genetic variation of bovine S. aureus in Europa.

61 tosus lesions are highly colonized (~50%) by S. aureus.

62 sue, which inhibits aspartate acquisition by S. aureus Together, these data elucidate the metabolic p

63 Bacillus subtilis, and inhibited biofilms by S. aureus to a lesser extent.

64 ponse to physiological stress experienced by S. aureus in diverse environments.

65 m bacteria trapped in NETs is facilitated by S. aureus nuclease (Nuc)-mediated degradation of NET DNA

66 Streptococcus pneumoniae (33%), followed by S. aureus (22%).

67 trates the heterogeneity of IFN induction by S. aureus and uncovered an interesting property of a VIS

68 r result in overaccumulation of phosphate by S. aureus However, it does reduce the ability of S. aure

69 About 30% of individuals carry S. aureus asymptomatically in their nares, a risk factor

70 ogue selenocystine to initially characterize S. aureus homologues of the Bacillus subtilis cystine tr

71 e transporter MntC) for detection of chronic S. aureus infection.

72 study provides maiden evidence that chronic S. aureus biofilm infection in wounds results in impaire

73 Wild-type (WT) (Fib+) mice rapidly cleared S. aureus following intraperitoneal infection with elimi

74 ivatable P2&3TT probe distinguishes clinical S. aureus-positive blood cultures from non-S. aureus-pos

75 Here, we discovered that clinical S. aureus isolates activate human monocytes, leading to

76 hest antimicrobial activity against E. coli, S. aureus, and S. typhi in in vitro antimicrobial tests,

77 f major spoilage pathogens, such as E. coli, S. aureus, Salmonella sp., Listeria sp., yeast and mould

78 cordant when detected at low concentrations (S. aureus, P < 0.001; H. influenzae, P < 0.0001) and in

79 In conclusion, S. aureus organisms that escape the infected bone may re

80 In contrast, S. aureus resistance to mupirocin emerged rapidly.

81 novel, ecological therapies for controlling S. aureus carriage.

82 atient elective surgical discharges, 180-day S. aureus incidence was 1.19% (0.25% BSI, 0.75% SSI no B

83 atient elective surgical discharges, 180-day S. aureus infection incidence was 1.35% (0.30% BSI, 0.74

84 Over these same decades S. aureus has perfected resistance mechanisms against th

85 Decreased S. aureus abundance during dupilumab treatment correlate

86 to adhesion, we profiled a sequence-defined S. aureus transposon mutant library, identifying mutants

87 sits in participants' homes, swabs to detect S. aureus were collected from participants, environmenta

88 T7SS mutants generated in different S. aureus strain backgrounds also displayed an increased

89 barriers, as an alternative target to disarm S. aureus.

90 an episode of bacteremia, especially during S. aureus bacteremia.

91 l regulatory element of SrrB function during S. aureus infection.

92 Mice failed to eliminate S. aureus deficient in vWbp, but clearance of these same

93 The Isd components enable S. aureus to extract heme from hemoglobin (Hb), transpor

94 LukED enables S. aureus to acquire iron by lysing erythrocytes, which

95 he feasibility that stable, non-encapsulated S. aureus mutants can regain expression of key virulence

96 of host cell death that failed to eradicate S. aureus and instead promoted DeltahemB SCV pathogenici

97 ial and endothelial cells by IsdB-expressing S. aureus cells was promoted by Vn, and an alpha(v)beta(

98 Using a chicken egg OVA-expressing S. aureus strain to analyze OVA-specific T cell response

99 pathogen, of which 287/332 (86.4%) featured S. aureus as the sole isolated organism.

100 likelihood of the occurrence of CM following S. aureus IMI and highlights the potential benefit of di

101 ureus Given that neutrophils are crucial for S. aureus clearance, understanding the mechanism(s) driv

102 a positive signal was clearly detectable for S. aureus-positive blood cultures with bacterial loads a

103 ty must be precisely controlled in order for S. aureus and other pathogens to cause infection.

104 s may serve as a novel secretory pathway for S. aureus to transport protected cargo in a concentrated

105 t leukocyte IL-10 production is required for S. aureus biofilm persistence in PJI.

106 is required for EPS-mediated protection from S. aureus infection in vivo We conclude that EPS protect

107 Heterologous expression of TspA from S. aureus strain RN6390 indicates its C-terminal domain

108 emic medical center in New York City who had S. aureus bloodstream infections between 1 January 2007

109 current MK (12/68, 17.6%) were found to have S. aureus isolated from both their conjunctiva and nose

110 es barrier disruption that allows for higher S. aureus colonization in SLE skin.

111 outcomes with non-inoculated and historical S. aureus-inoculated controls.

112 ureus biofilms and provides insight into how S. aureus evades the neutrophil response to cause persis

113 Knowledge of how S. aureus manipulates protective immunity has been hampe

114 iotics through a better understanding of how S. aureus protects the enzyme targets of the beta-lactam

115 ial benefit of diagnostics tools to identify S. aureus CC during bovine mastitis.

116 ication model that would be able to identify S. aureus independent of the culture growth stage and th

117 reconstruction of transcriptional modules in S. aureus, and a platform enabling its full elucidation.

118 role that this toxin-receptor pair plays in S. aureus pathophysiology.

119 n shown to affect many cellular processes in S. aureus, including autolysis, biofilm formation, capsu

120 s complement, as well as their receptors, in S. aureus recognition and clearance, we investigated the

121 stigate mechanisms of acquired resistance in S. aureus and identify key residues in FabI that stabili

122 n three orthogonal planes is not the rule in S. aureus.

123 trogen metabolism and c-di-AMP signalling in S. aureus.

124 Despite the critical role of SrrAB in S. aureus pathogenicity, the mechanism by which the SrrA

125 with the TRIM effect via in vivo studies in S. aureus infected mice demonstrates a promising strateg

126 tally validate sulfur acquisition systems in S. aureus and establish their importance during pathogen

127 dense circumferential orientation, while in S. aureus and division septa for both species, peptidogl

128 n, and SLE keratinocytes exhibited increased S. aureus-binding integrins.

129 gene content-based strain profiling, infant S. aureus strains are more similar to maternal strains.

130 l or infant nasal microbiomes that influence S. aureus acquisition and retention in early life.

131 teria monocytogenes, Haemophilus influenzae, S. aureus, Klebsiella spp. and non-typhoidal Salmonella

132 this isolate to be a vancomycin-intermediate S. aureus (VISA) strain, and reduced Ifnb was observed w

133 Introducing these mutations into S. aureus alters the ability of the bacterium to resist

134 for the coordinated defense against invading S. aureus, yet they have a limited life span with replac

135 esis of essential precursors during invasive S. aureus infection.

136 tions Program surveillance data for invasive S. aureus (SA) infections (isolated from a normally ster

137 ne, one of the most common sites of invasive S. aureus infection and a unique environment characteriz

138 female mice have an enhanced ability to kill S. aureus ex vivo compared with those of male mice.

139 urrently poorly understood whether localized S. aureus skin infections persistently alter the residen

140 : 32 mug/mL) and Harungana madagascariensis (S. aureus: MIC: 32 mug/mL; E. faecium: MIC: 32 mug/mL) s

141 indicate that T7SS contribute to maintaining S. aureus membrane integrity and homeostasis when bacter

142 nuating the polymerase activity of the major S. aureus peptidoglycan synthase.

143 Moreover, S. aureus-induced ULBP2 expression was linked to altered

144 Most S. aureus were resistant to penicillin.

145 to identify novel epitopes for a much-needed S. aureus-protective subunit vaccine.

146 l S. aureus-positive blood cultures from non-S. aureus-positive blood cultures and culture-negative b

147 levels over background for cultures with non-S. aureus Gram-positive bacteria.

148 Moreover, incubation of the probe with non-S. aureus-positive blood cultures yielded essentially ba

149 gies that converge to promote the ability of S. aureus biofilms to evade killing by neutrophils.

150 in significant impairment in the ability of S. aureus to cause infection in both a subcutaneous and

151 ureus However, it does reduce the ability of S. aureus to grow in phosphate-replete defined medium.

152 ation of PhoPR would diminish the ability of S. aureus to resist nutritional immunity and cause infec

153 rotein results in the loss of the ability of S. aureus to secrete cytolytic toxins, protect itself fr

154 ial diversity increased and the abundance of S. aureus decreased.

155 al diversity and higher overall abundance of S. aureus than nonlesional skin.

156 microbial diversity and reduced abundance of S. aureus.

157 idates targeting defined surface antigens of S. aureus have failed to meet clinical endpoints.

158 The high burden of S. aureus infections after both inpatient and outpatient

159 ecurrent MK have higher rates of carriage of S. aureus suggesting endogenous site colonisation as a p

160 study demonstrates that characterization of S. aureus CC and virulence genes helps to predict the li

161 ty and 100% specificity for the diagnosis of S. aureus infection by ELISA.

162 for the sensitive and specific diagnosis of S. aureus prosthetic joint infection.

163 host range and greater genetic diversity of S. aureus than is already known, and understanding S. au

164 characterization of the C-terminal domain of S. aureus OatA.

165 The pathogenicity and establishment of S. aureus infections are tightly linked to its ability t

166 ellonella infection model, where exposure of S. aureus to LL-37 abolished the antimicrobial effect of

167 bsequently, MIPs were used for extraction of S. aureus from milk and rice.

168 a (IgG) interaction with virulence factor of S. aureus, staphylococcal protein A (SpA) in the presenc

169 ine, but not glutamate promote the growth of S. aureus.

170 te the drug response following incubation of S. aureus with oxacillin.

171 Incubation of S. aureus-positive blood culture samples with the P2&3TT

172 cid (LA) elicited an increased inhibition of S. aureus mutants lacking T7SS effectors EsxC, EsxA and

173 as IFN-gamma appeared to inhibit invasion of S. aureus.

174 Although bacterial isolates of S. aureus differ in their virulence potential it is larg

175 novel method was developed, for isolation of S. aureus from complex (food) samples using molecular im

176 he minimum inhibitory concentration (MIC) of S. aureus towards vancomycin by 75%, and resulted in sho

177 is known about ClpXP in the pathogenesis of S. aureus to include the respiratory tract.

178 Infants display distinctive patterns of S. aureus carriage, positively associated with Acinetoba

179 mmune cells, the invasion and persistence of S. aureus in submicron channels of cortical bone, and th

180 assay to enable the large-scale profiling of S. aureus adhesion to host ligands.

181 quisition strategy supports proliferation of S. aureus in these organs.

182 de (p < 0.01) and a higher isolation rate of S. aureus from their conjunctiva compared to control par

183 recurrent MK had a higher isolation rate of S. aureus from their cornea than those with a single epi

184 ponent system (TCS) is a global regulator of S. aureus virulence and critical for survival under envi

185 s have been shown to be a major reservoir of S. aureus in vivo(3), but the role of macrophages in the

186 ns (PSM) comprise the structural scaffold of S. aureus biofilms through self-assembly into functional

187 Thus, isogenic mutant stains of S. aureus with varying degree of biofilm formation abili

188 nofin's in vitro activity against strains of S. aureus (including MRSA) was not affected in the prese

189 nsitive and methicillin-resistant strains of S. aureus FmhC is encoded by a gene immediately adjacent

190 fect (PAE) in vitro against three strains of S. aureus tested.

191 Isogenic mutant strains of S. aureus with varying degree (DeltarexB > USA300 > Delt

192 y, we present the first crystal structure of S. aureus LcpA with bound substrate at 1.9 angstrom reso

193 SS substrate protein, encoded in a subset of S. aureus genomes, has been functionally characterized.

194 el of osteomyelitis, we examined survival of S. aureus mutants deficient in central metabolic pathway

195 tic-resistant strains is making all types of S. aureus infections more challenging to treat.

196 This improved understanding of S. aureus colonization is an important first step toward

197 6 and the lymph node homing molecule CCR7 on S. aureus-infected DCs.

198 ed the effects of type I and type II IFNs on S. aureus adherence and invasion.

199 To define the impact of IFNs on S. aureus colonization, we examined the effects of type

200 rsus male BMN in response to serum-opsonized S. aureus Furthermore, blocking CD11b reduced both ROS l

201 m of ribosome shutdown in the human pathogen S. aureus and might deliver a novel target for pharmacol

202 nd our study to a second bacterial pathogen, S. aureus, and demonstrate that CP also inhibits iron up

203 t only fail to efficiently kill phagocytosed S. aureus, but also induce tolerance to multiple antibio

204 We classified positive S. aureus cultures using a hierarchy (bloodstream [BSI],

205 e the ability to inhibit both gram-positive (S. aureus) and gram-negative (E. coli) bacteria on solid

206 udy assessed cumulative 180-day postsurgical S. aureus incidence in real-world hospital settings.

207 A-DRD5-ARRB2-PP2A signaling axis can prevent S. aureus-induced inflammation and protect mice against

208 uted to the leukocidin LukAB, which promotes S. aureus survival during phagocytosis.

209 to P. aeruginosa, we show that heme protects S. aureus from CP-mediated inhibition of iron uptake and

210 o the cellular redox environment to regulate S. aureus survival and pathogenesis.

211 ane protein complex that spatially regulates S. aureus peptidoglycan synthesis.

212 i-induced myositis and a clinically relevant S. aureus wound infection murine model.

213 tricted to clinical settings, drug resistant S. aureus is now one of the key causative agents of comm

214 h S. aureus, including methicillin resistant S. aureus (MRSA).

215 e community-associated methicillin-resistant S. aureus (CA-MRSA) strain FPR3757 (USA300).

216 A) and 875 episodes of methicillin-resistant S. aureus (MRSA) bacteremia, with a rising proportion du

217 ccus aureus, including methicillin-resistant S. aureus (MRSA), has become a worldwide, major health c

218 SIs), particularly for methicillin-resistant S. aureus (MRSA).

219 patients with SaB (47 methicillin-resistant S. aureus [MRSA], 12 methicillin-sensitive S. aureus [MS

220 hose participants with methicillin-resistant S. aureus and methicillin-sensitive S. aureus bacteremia

221 ior to ventilation and methicillin-resistant S. aureus challenge showed a higher survival rate compar

222 prophylaxis had fewer methicillin-resistant S. aureus in the lungs compared with untreated control a

223 d improved survival of methicillin-resistant S. aureus infected rats, underscoring its potential in t

224 hey were infected with methicillin-resistant S. aureus strain AW7 via the endotracheal tube, extubate

225 ble tool for detecting methicillin-resistant S. aureus strains that express efflux transporters such

226 es had infections with methicillin-resistant S. aureus, fungal infections, Pseudomonas infections, an

227 Methicillin-resistant S. aureus, P. aeruginosa, C. difficile, and fungal infec

228 elevant activity against multidrug-resistant S. aureus.

229 multidrug-resistant and vancomycin-resistant S. aureus strain that is representative of the resistant

230 t only by inducing macrophages that restrict S. aureus growth and inhibit superantigen-activated T ce

231 in part, to hybrid macrophages that restrict S. aureus growth through reactive oxygen species and to

232 Cleavage of this probe by the secreted S. aureus enzyme micrococcal nuclease results in emissio

233 t S. aureus [MRSA], 12 methicillin-sensitive S. aureus [MSSA]) from 2015-2017.

234 esistant S. aureus and methicillin-sensitive S. aureus bacteremia.

235 VER as a promising candidate for sensitizing S. aureus that could be helpful to combat persistent or

236 e, P < 0.0001) and in sputum-type specimens (S. aureus, P < 0.05).

237 As such, S. aureus efficiently pillages vital nutrients from the

238 ere 1264 episodes of methicillin-susceptible S. aureus (MSSA) and 875 episodes of methicillin-resista

239 health importance of methicillin-susceptible S. aureus (MSSA) in selected communities.

240 Specific qPCR tests targeting S. aureus and S. pneumoniae did not provide additional d

241 The qPCR tests targeting S. aureus and S. pneumoniae gave earlier results than cu

242 mpt consideration that vaccination targeting S. aureus may be most effective if delivered prior to in

243 demand of skeletal cells, we discovered that S. aureus requires glycolysis for survival in bone.

244 We discovered that S. aureus uses a rapid, superantigen-independent mechani

245 We therefore hypothesized that S. aureus acquires host-derived cysteine and cystine as

246 Here we report that S. aureus lacking T7SS components are more susceptible t

247 Together, these findings show that S. aureus FnBPA plays an important role in physical biof

248 enomic and epidemiological studies show that S. aureus has jumped between host species many times ove

249 Here we show that S. aureus secretes RNA and DNA molecules that are mostly

250 Additionally, we show that S. aureus SF8300, a clinically relevant strain from the

251 e we show, for three different strains, that S. aureus cells do not regularly divide in three alterna

252 and 4-allyl-2,6-dimethoxyphenol against the S. aureus NorA efflux pump (EP) in association with norf

253 Among the S. aureus isolates that exhibited antibiotic susceptibil

254 ICA decomposed the S. aureus transcriptome into 29 independently modulated

255 ake in rich medium rescues the growth of the S. aureus dacA mutant.

256 nce was observed in approximately 45% of the S. aureus infections.

257 in, which is encoded adjacent to tspA on the S. aureus chromosome.

258 We found that the S. aureus fibronectin binding protein A (FnBPA) is requi

259 >20-fold in a CodY-deficient strain in three S. aureus clinical isolates and in S. epidermidis.

260 At the same time, S. aureus is the most frequent cause of skin and soft ti

261 sociated with a loss of DCs, attributable to S. aureus alpha-toxin (Hla) expression.

262 keratinocytes exhibited increased binding to S. aureus.

263 y, we show that while neutrophils exposed to S. aureus biofilms produce extracellular traps (NETs) an

264 Human macrophages responded to S. aureus EVs by TLR2 signaling and activation of NLRP3

265 al key players in the early host response to S. aureus during bloodstream infection, promoting enhanc

266 nnate sex bias in the neutrophil response to S. aureus Given that neutrophils are crucial for S. aure

267 T cells for rapid activation in response to S. aureus In coculture with S. aureus-infected monocyte-

268 e critical for the innate immune response to S. aureus infection.

269 madelta T cells in human immune responses to S. aureus is almost entirely unknown.

270 RNA-sequencing expression profiles from two S. aureus clinical strains (TCH1516 and LAC).

271 We found that both wild-type S. aureus and a DeltahemB SCV prototype potently activat

272 gnificantly attenuated compared to wild-type S. aureus This defect is partially reversed in a calprot

273 tantially less IL-10 compared with wild-type S. aureus, which was also observed in a mouse model of P

274 eus than is already known, and understanding S. aureus host specificity in these hosts will mitigate

275 ys were differentially stimulated by various S. aureus strains independently of their isolation sites

276 ase, the most common identified pathogen was S. aureus in previously healthy and chronically ill chil

277 ely, our study describes mechanisms by which S. aureus EVs induce inflammasome activation and reveals

278 phils is the primary mechanism through which S. aureus infection is controlled by the immune system(2

279 cting quickly to administer antibiotics with S. aureus coverage to any patient suspected of having se

280 Pore-forming toxins associated with S. aureus EVs were critical for NLRP3-dependent caspase-

281 ided endocarditis infections associated with S. aureus, including methicillin resistant S. aureus (MR

282 'missed' PJI at the time of bacteremia with S. aureus (1.1%).

283 In cocultures of CD4(+) T cells with S. aureus-infected DCs, the addition of gammadelta T cel

284 n in response to S. aureus In coculture with S. aureus-infected monocyte-derived dendritic cells (DCs

285 , that is significantly anti-correlated with S. aureus in infants and mothers.

286 reduced bacterial count in milk of cows with S. aureus clinical mastitis compared to untreated cows.

287 We provide evidence that co-culturing with S. aureus induces a decrease in the activity of ClpXP in

288 infected mice compared to mice infected with S. aureus alone.

289 infected mice compared to mice infected with S. aureus alone.

290 at mice, which were previously infected with S. aureus, showed faster monocyte recruitment, increased

291 tment for mild-to-moderate PUs infected with S. aureus.

292 ococcus aureus Chronic tissue infection with S. aureus was associated with BPI antibody autoreactivit

293 Holstein Friesian cows were inoculated with S. aureus and treated intramammarily with vehicle (NEG;

294 ds of mice challenged intraperitoneally with S. aureus EVs.

295 septic shock (cohort 1) and 88 patients with S. aureus bacteremia (cohort 2).

296 A total of 506 patients with S. aureus bacteremia and septic shock were included in t

297 tudy, we randomly assigned 121 patients with S. aureus BSI/endocarditis to receive a single dose of e

298 ing sera from naive rabbits and rabbits with S. aureus-mediated osteomyelitis, and then we validated

299 in TNFR2pos Treg after culture in vitro with S. aureus.

300 s and is ubiquitous in representation within S. aureus clinical isolates.