ライフサイエンスコーパス: S. aureus

1 S. aureus and E. coli antigens were detected in immune-b

2 S. aureus bacteremia is often associated with an adverse

3 S. aureus biofilms showed less susceptibility to killing

4 S. aureus colonizes the skin of the majority of children

5 S. aureus increases biofilm formation in response to hyp

6 S. aureus infection in the intensive care unit (ICU) mos

7 S. aureus is internalized by Cftr-deficient macrophages

8 S. aureus nasal carriage prevalence was higher among IHO

9 S. aureus strains from clonal complexes 1 and 8 were mor

10 S. aureus toxins and virulence proteases often circulate

11 S. aureus uses secreted cyclic autoinducing peptides (AI

12 S. aureus was isolated from 527 participants (67.0%), an

13 Furthermore, 182 S. aureus genes are uniquely essential during co-infecti

14 A total of 311 S. aureus isolates were collected from respiratory cultu

15 l cells, abundance changes for more than 400 S. aureus proteins were quantified, revealing, e.g., the

16 From approximately 2.15 x 10(5) S. aureus cells, 578 proteins were identified.

17 pid (<1h) detection of P. aeruginosa (6294), S. aureus(LAC), through on-chip electrical sensing of ba

18 The extent of ABR S. aureus exposure in IHO workers and children living in

19 nce and potential sources of exposure to ABR S. aureus among children living with IHO workers.

20 or influence on disease outcome during acute S. aureus infection.

21 Specifically, aerobic S. aureus nos mutant cultures presented with elevated en

22 loss of a single transporter did not affect S. aureus However, disruption of any two systems signifi

23 ed as catheter lock solutions (CLSs) against S. aureus biofilm infections.

24 latelets participate in host defense against S. aureus both through direct killing of S. aureus and e

25 elets to participate in host defense against S. aureus infection was determined by assessing two poss

26 rgets to promote host innate defense against S. aureus skin infection.

27 requirements for protective immunity against S. aureus.

28 t MgSAP1 has anti-biofilm properties against S. aureus.

29 mily is indispensable for protection against S. aureus infection and its clearance at wound sites.

30 unction of macrophages in protection against S. aureus infection.

31 P. aeruginosa and ten honey samples against S. aureus.

32 blish long-term protective Ab titers against S. aureus was not a consequence of diminished formation

33 a flavone rich extract "430D-F5" against all S. aureus accessory gene regulator (agr) alleles in the

34 nds to the capacity of each isolate to alter S. aureus antibiotic susceptibility.

35 We characterized an S. aureus strain that contained a transposon inserted in

36 ulate interactions between P. aeruginosa and S. aureus We demonstrate that P. aeruginosa quorum sensi

37 istic interactions between P. aeruginosa and S. aureus.

38 use the corneal ulcers are P. aeruginosa and S. aureus.

39 to differentiate S. hyicus, S. agnetis, and S. aureus was developed.

40 d selectively differentiate both E. coli and S. aureus infections from sterile inflammation in vivo.

41 imilarity of S. aureus colonizing humans and S. aureus in meat from the stores in which those individ

42 es in the biofilms of both S. pneumoniae and S. aureus.

43 Enhancement of macrophage anti-S. aureus activities is independent of contact with plat

44 Livestock-associated S. aureus nasal carriage predominated among IHO workers.

45 mice exhibited abnormal abscess formation at S. aureus-infected skin wound sites and were also more s

46 ted cefoxitin disk diffusion for 37 atypical S. aureus isolates (156 readings) with MHA supplemented

47 (HDM) has shown that Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) species are ab

48 -inflammatory role in Staphylococcus aureus (S. aureus) and methicillin-resistant S. aureus (MRSA) in

49 Staphylococcus aureus (S. aureus) carriage and sensitization to S. aureus enter

50 Staphylococcus aureus (S. aureus) infections are among the most common and seve

51 zation of the skin by Staphylococcus aureus (S. aureus) is increased in atopic dermatitis and can res

52 Staphylococcus aureus (S. aureus) is one of the most common etiological agents

53 Correspondingly, Staphylococcus aureus (S. aureus) isolates from lesional skin of patients with

54 geted small interfering RNA silencing before S. aureus exposure blocked the increase in protease acti

55 have previously shown an association between S. aureus carriage and severe allergic disease and aller

56 ded to live rats with an induced bloodstream S. aureus infection.

57 urther, Il17a(-/-)f(-/-) mice showed blunted S. aureus-induced inflammation.

58 of S. aureus The downregulation of IP-10 by S. aureus was mediated by components of its cell wall, b

59 , these results demonstrate an adaptation by S. aureus to obesity/T2D with increased expression of cl

60 tment option to prevent lung edema caused by S. aureus alpha-toxin.

61 between cardiovascular infections caused by S. aureus and nonsynonymous SNPs in FnBPA.

62 tic of atopic eczema (AE) is colonization by S. aureus, with exacerbations associated with an increas

63 repressed IkappaBalpha activation induced by S. aureus via PKA-MKP-1 pathway.

64 The annual rates of infection by S. aureus declined from 2003 to 2014 by 4.2% (2.7% to 5.

65 e trends in the annual rates of infection by S. aureus subtypes and mean antibiotic resistance, we co

66 tients (approximately 38%) colonized only by S. aureus and treated with appropriate antibiotic for at

67 trate that lipoyl-E2-PDH is also released by S. aureus and moonlights as a macrophage immunosuppressa

68 hese observations indicate that Pi uptake by S. aureus differs from established models and that acqui

69 on of peptidoglycan, a mechanism utilized by S. aureus to block bacterial cell wall breakdown, limits

70 Bioavailable Mn is utilized by S. aureus to detoxify reactive oxygen species and protec

71 on-atopic children asymptomatically carrying S. aureus nasally.

72 Colonization densities of M. catarrhalis, S. aureus, and P. jirovecii are unlikely to be of diagno

73 ionally, neutrophils, essential for clearing S. aureus, demonstrated sex-specific S. aureus bacterici

74 Colonization by clonal S. aureus populations was observed in both AE patients a

75 and strategies are urgently needed to combat S. aureus associated infections.

76 the host senses virulent, but not commensal, S. aureus to trigger inflammation remain unclear.

77 Concomitantly, S. aureus elicits the production of proinflammatory cyto

78 rstand the molecular mechanisms that control S. aureus biofilm formation and the basis for the recalc

79 echanisms by which miR response to cutaneous S. aureus contributes to DFU pathophysiology are unknown

80 ounds infected with an isogenic AT-deficient S. aureus strain was unimpeded, exhibiting efficient bac

81 re challenged with an isogenic SpA-deficient S. aureus mutant, cells proliferated in the BM survival

82 e inoculated with wild-type or SpA-deficient S. aureus mutant.

83 experiments employing alpha-toxin-deficient S. aureus and the corresponding wild-type strain reveal

84 Mice were infected i.v. using 8 different S. aureus strains, and development of the infection was

85 Interestingly, without this enzyme S. aureus were repressed in their ability to secrete cyt

86 Herein, epicutaneous S. aureus exposure to mouse skin promoted MyD88-dependen

87 d skin inflammatory response to epicutaneous S. aureus infection.

88 and was also highly effective in eradicating S. aureus biofilm infection when used in a CLS rat centr

89 In galectin-3(+/+) mice, SspB-expressing S. aureus caused larger lesions and resulted in higher b

90 to bacterial virulence in vivo, since fewer S. aureus subsp. aureus NCTC8325-4 DeltasdrD bacteria th

91 th records revealed an odds ratio of 2.4 for S. aureus SSTI in males versus females.

92 provided a nasal swab which was analyzed for S. aureus, methicillin-resistant S. aureus (MRSA), multi

93 illus spp. and 120CFU/ml in pure culture for S. aureus.

94 formative density cutoffs were not found for S. aureus and M. catarrhalis, and a lack of confirmed ca

95 ere determined to be 0.06 to 0.25 mug/ml for S. aureus ATCC 29213, 0.016 to 0.12 mug/ml for E. faecal

96 on limits as low as 7, 40 and 100 CFU/mL for S. aureus in pure broth culture, and inoculated in food

97 ranges were determined to be 25 to 31 mm for S. aureus ATCC 25923, 25 to 31 mm for S. pneumoniae ATCC

98 es yielded statistically similar results for S. aureus typing.

99 roduction of methicillin, which selected for S. aureus strains carrying the mecA determinant.

100 f the human immune system in protection from S. aureus infection.

101 y structure of the native 100S ribosome from S. aureus, revealing the molecular mechanism of its form

102 Deletion of sdrD from S. aureus subsp. aureus strain NCTC8325-4 attenuated bac

103 MCL in sepsis caused by G(+) bacteria (e.g., S. aureus) and antibiotic-resistant bacteria (e.g., MRSA

104 These data illustrate how S. aureus directly influences the skin barrier integrity

105 ovide insight into the role of meat in human S. aureus colonization.

106 enge model with a highly virulent agr type I S. aureus isolate, PP7-AIP1S vaccination reduced pathoge

107 novel control approaches, we have identified S. aureus components that are required for growth in hum

108 If S. aureus is present, then the subject tends to have mor

109 However, it is unclear if S. aureus is a cause of atopic dermatitis or a consequen

110 Recent evidence implicates S. aureus as an emerging cause of chorioamnionitis and p

111 taphylococcus aureus protein A, an important S. aureus virulence factor involved in immune evasion an

112 es were lowered in the presence of ajoene in S. aureus.

113 o identify a functional adenylate cyclase in S. aureus and only detected 2',3'-cAMP but not 3',5'-cAM

114 are institutions in Boston, MA, a decline in S. aureus infections has been accompanied by a shift tow

115 unclear whether this represents a decline in S. aureus infections overall.

116 ocesses involved in microcolony formation in S. aureus and suggests that these structures originate a

117 hat this assembly mode underlies function in S. aureus.

118 d a significant exacerbation of infection in S. aureus-infected mice.

119 e show here that WTA is directly involved in S. aureus strain-specific virulence and provide insight

120 identified a new subset of MDSC (Eo-MDSC) in S. aureus-infected mice that phenotypically resembles eo

121 a programmed cell lysis (PCL) phenomenon in S. aureus leading to the release of cellular polymers th

122 novel information on staphopains present in S. aureus biofilms in vivo, and illustrate the complex i

123 , we identified core FtsH target proteins in S. aureus.

124 able for degradation of unfolded proteins in S. aureus.

125 Resistance in S. aureus decreased from 2000 to 2014 by 0.8 antibiotics

126 mall dual-function regulatory RNA, RNAIII in S. aureus, that controls expression of key virulence fac

127 n, a previously undescribed role of saNOS in S. aureus aerobic physiology was reported.

128 ess the further function of SfaA and SbnD in S. aureus fitness, we tested its effect on murine absces

129 -oxide (HQNO) induces multidrug tolerance in S. aureus through respiratory inhibition and reduction o

130 rculosis; mannitol, with selective uptake in S. aureus and E. coli; and sorbitol, accumulating only i

131 nical course, and outcome between individual S. aureus-infected ICU patients remains enigmatic, sugge

132 Instead, S. aureus triggered activation of MAPKs p38 and ERK, as

133 subsets were more efficient at internalizing S. aureus and B. anthracis compared with E. coli Alveola

134 e current study, we used lethally irradiated S. aureus as a model multicomponent vaccine and showed t

135 otal of 658 Staphylococcus species isolates (S. aureus, 211 isolates; S. lugdunensis, 3 isolates; and

136 inosa to produce virulence factors that kill S. aureus These data could provide important clues regar

137 determined the ability of platelets to kill S. aureus directly; and, second, we tested the possibili

138 iffraction and that it is sufficient to kill S. aureus These results suggest that, in addition to its

139 al capacity play important roles in limiting S. aureus SSTI in females.

140 ntermittently exposed, some individuals lose S. aureus rapidly.

141 -deficient mice was sufficient for mediating S. aureus-induced skin inflammation.

142 kill Staphylococcus aureus Further, a mutant S. aureus that is more sensitive to antimicrobial peptid

143 To study associations of both nasal S. aureus carriage and SE sensitization to allergic dise

144 Participants were tested for nasal S. aureus carriage, serum total IgE and specific IgE to

145 It has been proposed that the native S. aureus PBPs can use cell wall precursors having diffe

146 compared the ability of PBP2a and two native S. aureus transpeptidases to cross-link peptidoglycan st

147 Even after uptake by neutrophils, S. aureus shows resistance to killing, which suggests th

148 SE sensitization, but not S. aureus carriage, was associated with poly-sensitizati

149 Here, we identify and characterise a novel S. aureus leukocidin; LukPQ.

150 or PitA significantly reduced the ability of S. aureus to cause infection.

151 siderophore SA contributes to the ability of S. aureus to replicate in abscesses and epithelial cells

152 We also assessed the ability of S. aureus to survive following alkalinization of the pha

153 The genetic adaptability of S. aureus, heterogeneity of disease presentation, clinic

154 investigate the time-resolved adaptation of S. aureus to the intracellular niche in human bronchial

155 Whether adaptation of S. aureus to the unique environment of the obese/T2D hos

156 irst time the in vivo proteome adaptation of S. aureus.

157 erial proteins that promote the adherence of S. aureus to AD corneocytes.

158 Results of semiquantitative analyses of S. aureus burden in serial endotracheal-aspirate (ETA) s

159 ant difference in the genetic backgrounds of S. aureus colonizing AE cases versus controls (Fisher ex

160 they reduced the biofilm bacterial burden of S. aureus (CFU cm(-2)) by three logs with no statistical

161 gr-mediated quorum sensing by all classes of S. aureus.

162 the amount of a major cell wall component of S. aureus, termed wall teichoic acid (WTA).

163 Planktonic culture of S. aureus was exposed to antibiotics for one hour follow

164 ed cysteine proteases, and the dependence of S. aureus on L27 cleavage by Prp validates the enzyme as

165 form is a powerful tool for the detection of S. aureus as a potential point-of-care diagnostic platfo

166 e this, the origins and genetic diversity of S. aureus colonizing individual patients during AE disea

167 tus in mice challenged with a lethal dose of S. aureus.

168 Furthermore, fitness of S. aureus in these sites of replication is not compromis

169 inhibit heme transfer to IsdB and growth of S. aureus, and a ternary complex of IsdB.Hb.Hp was obser

170 receptor CD36 reduced the internalization of S. aureus RN6390 by A549 cells, but the dependence on CD

171 laboratory strains and clinical isolates of S. aureus caused galectin-3 degradation.

172 mous SNPs in fnbA among clinical isolates of S. aureus that cause endovascular infections.

173 nst S. aureus both through direct killing of S. aureus and enhancing the antimicrobial function of ma

174 ge phagocytosis and intracellular killing of S. aureus In this study we report evidence in support of

175 nosa LasA endopeptidase potentiates lysis of S. aureus by vancomycin, rhamnolipids facilitate proton-

176 To examine the microevolution of S. aureus colonization, we deep sequenced S. aureus popu

177 s between male and female mice in a model of S. aureus dermonecrosis.

178 art, liver, and kidneys in a murine model of S. aureus sepsis.

179 Current animal models of S. aureus colonisation are expensive and normally requir

180 omponent vaccines to target the multitude of S. aureus virulence factors.

181 g knowledge of the molecular pathogenesis of S. aureus disease, we suggest that the application of mo

182 as suppressed by the concomitant presence of S. aureus The downregulation of IP-10 by S. aureus was m

183 uggestive evidence of a higher prevalence of S. aureus, MRSA, and MDRSA among children living with an

184 phylogenomic structure of a diverse range of S. aureus, including both MRSA and MSSA.

185 l granulopoiesis and effective resolution of S. aureus-infected wounds, revealing a potential antibio

186 However, the role of S. aureus carriage and SE sensitization on allergic mult

187 Examining the similarity of S. aureus colonizing humans and S. aureus in meat from t

188 s suggest meat is not an important source of S. aureus colonization in shoppers.

189 Immuno-gold staining of S. aureus biofilm of AD skin detected the S. aureus deri

190 The golden pigment, staphyloxanthin, of S. aureus colonies distinguishes it from other staphyloc

191 Here, we identify a single strain of S. aureus found to be persistently colonising the gastro

192 or (in laboratory and AD clinical strains of S. aureus) inducing barrier integrity impairment and tig

193 effectively killed two different strains of S. aureus.

194 We argue that whole-genome surveillance of S. aureus populations could lead to better forecasting o

195 This suggests that intracellular survival of S. aureus in macrophages may allow the pathogen to chron

196 hetic operon crtOPQMN, promoting survival of S. aureus in the presence of oxidants.

197 y, no change in antibiotic susceptibility of S. aureus isolates was observed during treatment.

198 that alpha-toxin, one of the major toxins of S. aureus, induces activation of acid sphingomyelinase a

199 ination with other AMPs, in the treatment of S. aureus intravenous catheter infections.

200 is to summarize our current understanding of S. aureus biofilm development, focusing on the descripti

201 state of the host and increased virulence of S. aureus.

202 act of galectin-3 and protease expression on S. aureus virulence was studied in a murine skin infecti

203 mental model, impact of adaptive immunity on S. aureus colonisation could be assessed.

204 y, the impact of interspecies interaction on S. aureus antibiotic susceptibility remains poorly under

205 taphylococcus aureus ATCC 25923 (disk only), S. aureus ATCC 29213 (broth only), Enterococcus faecalis

206 y score, colonization by C. neonatale and/or S. aureus is significantly associated with NEC.

207 on of antibiotic-resistance genes from other S. aureus strains or even from other genera.

208 ted bacterial killing independently of other S. aureus proteins, since addition of recombinant SdrD p

209 In the strain Newman and some other S. aureus strains, the sensor histidine kinase SaeS has

210 aintain immune equilibrium and decrease PGN, S. aureus and MRSA-triggered inflammatory response.

211 Gram-positive S. aureus lacks an RMF homolog and the structural basis

212 ll-characterized collection of mecC-positive S. aureus isolates (n = 111) was used for evaluation.

213 l Gram-negative (E. coli) and Gram-positive (S. aureus) bacteria to a great extent.

214 throughout kidney tissue at early times post-S. aureus infection compared to antibiotic-treated but n

215 mong vaccine recipients in whom postsurgical S. aureus infection developed, emphasizing the potential

216 n why colonization of superantigen-producing S. aureus can induce, under some circumstances, mucosal

217 Pulmonary S. aureus infections in CF often occur very early and pr

218 o cystic fibrosis patients despite recurrent S. aureus infections.

219 ibiotic treatment is ineffective in reducing S. aureus colonization in the lower airways and preventi

220 . aureus (MSSA) and HO methicillin-resistant S. aureus (MRSA) BSIs for 2009-2013 at 2 hospitals and u

221 aureus (S. aureus) and methicillin-resistant S. aureus (MRSA) induced peritonitis.

222 The common USA300 methicillin-resistant S. aureus (MRSA) strains express a number of toxins, suc

223 o S. aureus, including methicillin-resistant S. aureus (MRSA) strains, despite high titers of specifi

224 nalyzed for S. aureus, methicillin-resistant S. aureus (MRSA), multidrug-resistant S. aureus (MDRSA),

225 tion of mecC-harboring methicillin-resistant S. aureus (MRSA), which failed to identify from 0 to 41%

226 e phagocytosis of both methicillin-resistant S. aureus and methicillin-sensitive S. aureus by >70%, a

227 mune response to treat methicillin-resistant S. aureus infection in immunodeficient patients.

228 ectrum beta-lactamase, methicillin-resistant S. aureus, and carbapenem-resistant strains was also obs

229 ncluding MDROs such as methicillin-resistant S. aureus, extended-spectrum beta-lactamase-producing, a

230 istant S. aureus (MRSA), multidrug-resistant S. aureus (MDRSA), absence of scn (putative marker of li

231 methicillin-susceptible penicillin-resistant S. aureus (MSSA) did not change.

232 e measured the survival of wild-type and SCV S. aureus in whole human blood, which contains high numb

233 functional electron transport chains in SCV S. aureus and wild-type E. faecalis results in reduced g

234 esistant S. aureus and methicillin-sensitive S. aureus by >70%, and restricted intracellular growth b

235 er sensitive isolates (methicillin-sensitive S. aureus: MSSA).

236 of S. aureus colonization, we deep sequenced S. aureus populations from nine children with moderate t

237 Adherence of single S. aureus bacteria to corneocytes from AD patients ex vi

238 learing S. aureus, demonstrated sex-specific S. aureus bactericidal capacity ex vivo.

239 riations showed that the ancestor of all ST8 S. aureus most likely emerged in Central Europe in the m

240 We evaluated HO methicillin-susceptible S. aureus (MSSA) and HO methicillin-resistant S. aureus

241 Large parts of ST8 methicillin-susceptible S. aureus (MSSA) isolated in Africa represent a symplesi

242 cC-harboring MRSA as methicillin-susceptible S. aureus This study underlines cefoxitin's status as th

243 Penicillin-susceptible S. aureus (PSSA) increased by 6.1% (4.2% to 8.1%) annual

244 dependent and T-cell-mediated mechanism than S. aureus strains with a WTA(low) phenotype.

245 Taken together, our results demonstrate that S. aureus secretes a unique proteinaceous MPO inhibitor

246 high-fat-diet obese/T2D mice and found that S. aureus infection was more severe, including increases

247 We demonstrate here that S. aureus infects and forms biofilms on the choriodecidu

248 Altogether this further indicates that S. aureus does not produce 3',5'-cAMP, which would other

249 immortalized and primary keratinocytes, that S. aureus protease SspA/V8 is the dominant secreted fact

250 We propose that S. aureus infection in the ICU now presents a unique opp

251 Here, we show that S. aureus inhibits wound closure and induces miR-15b-5p

252 In this study, we show that S. aureus stimulates human keratinocytes to increase the

253 a prospective clinical trial that shows that S. aureus colonization precedes onset of atopic dermatit

254 These observations suggest that S. aureus may cause atopic dermatitis in some individual

255 ) importers, genomic analysis suggested that S. aureus possesses three distinct Pi transporters: PstS

256 of S. aureus biofilm of AD skin detected the S. aureus derived protease staphopain adjacent to the ba

257 X) as a bona fide dissociation factor of the S. aureus 100S ribosome.

258 associated with the clonal expansion of the S. aureus population, occurring over a period of weeks t

259 We have previously reported that the S. aureus cell wall downregulates the human T cell respo

260 copy analysis showed that LL-37 binds to the S. aureus biofilms.

261 s mediated by a sex-specific response to the S. aureus-secreted virulence factor alpha-hemolysin (Hla

262 f microarrayed HDM allergen molecules and to S. aureus and E. coli by IgE immunoblotting.

263 Consequently, excess Mn is bioavailable to S. aureus in the heart.

264 action between Tet38 and CD36 contributed to S. aureus internalization.

265 y of SdrD as an important key contributor to S. aureus survival and the ability to escape the innate

266 reased, further linking fibrin deposition to S. aureus expression of clfA and infection severity.

267 The high frequency of recurring SSSI due to S. aureus, including methicillin-resistant S. aureus (MR

268 on of molecular pathological epidemiology to S. aureus infection can usher in a new era of highly foc

269 Keratinocytes exposed to S. aureus showed enhanced degradation of desmoglein-1 an

270 ing the greatest induction after exposure to S. aureus.

271 ency in mice restores protective immunity to S. aureus infection, and adjuvancy with a staphylococcal

272 vated to expand PMN numbers in proportion to S. aureus abundance in a manner regulated by TLR2 and IL

273 keratinocyte Myd88 signaling in response to S. aureus PSMalpha drives an IL-17-mediated skin inflamm

274 10 in a TLR2-dependent manner in response to S. aureus, and adoptive transfer of B1a cells was protec

275 kinases and NF-kappaB pathway in response to S. aureus.

276 s demonstrate a key contribution of saNOS to S. aureus aerobic respiratory metabolism.

277 us (S. aureus) carriage and sensitization to S. aureus enterotoxins (SEs) have been associated with a

278 s (SSTIs), yet sex bias in susceptibility to S. aureus SSTI has not been described.

279 ave potential as therapeutic agents to treat S. aureus infections, and purification of the transmembr

280 WLBU2 effectively treated S. aureus biofilms formed by a variety of clinical MSSA

281 pathway, which may be targeted for treating S. aureus infection.

282 oresis (PFGE) for typing S. aureus Forty-two S. aureus isolates from three outbreaks and 12 reference

283 Infection with wild-type S. aureus suppressed inflammatory cytokine production in

284 ficiently by IFN-beta than was the wild-type S. aureus, and immunoblotting showed that IFN-beta inter

285 -field gel electrophoresis (PFGE) for typing S. aureus Forty-two S. aureus isolates from three outbre

286 nversion of approximately 25% of the in vivo S. aureus mono-culture essential genes to non-essential.

287 The dominant bacteria species was S. aureus and MRSA infection is increasingly prevalent.

288 rall, our study suggests a mechanism whereby S. aureus modulates cytokines critical for induction of

289 efines a previously unknown pathway by which S. aureus epicutaneous exposure promotes skin inflammati

290 ines a previously unknown mechanism by which S. aureus may influence skin diseases.

291 ns, thus expanding the environments in which S. aureus can successfully obtain Pi Consistent with thi

292 on IL-10 production and its association with S. aureus bacteremia (SaB) mortality.

293 B cells obtained from a 12-year-old boy with S. aureus osteomyelitis.

294 n the pathophysiology of DFUs colonized with S. aureus.

295 odeficient MyD88-knockout mice infected with S. aureus experienced lethal sepsis that was reversed by

296 ls under conditions mimicking infection with S. aureus conferred responsiveness to IL-20 that manifes

297 nctions of neutrophils during infection with S. aureus.

298 hly susceptible to pulmonary infections with S. aureus and fail to clear the pathogen during infectio

299 Boston, MA, of 31,753 adult inpatients with S. aureus isolated from clinical specimens.

300 l effect was restricted to participants with S. aureus infection.