ライフサイエンスコーパス: staphylococcal

1 al survival and the long-term persistence of staphylococcal abscess communities.

2 The staphylococcal accessory regulator A locus (sarA) is a m

3 us grown with HQNO and significantly reduced staphylococcal adhesion to fibronectin.

4 nding the role of homophilic interactions in staphylococcal adhesion, and for the design of new molec

5 ), and show that aggA and aggC contribute to staphylococcal agglutination with fibrin fibrils in huma

6 residues in length, making them the largest staphylococcal AIPs identified to date.

7 man keratinocytes from the lethal effects of staphylococcal alpha toxin through apolipoprotein L1-ind

8 man keratinocytes from cell death induced by staphylococcal alpha toxin.

9 We examined mutants of the staphylococcal alpha-hemolysin pore so severely truncate

10 Two heptameric staphylococcal alpha-hemolysin pores were covalently lin

11 c assembly shares structural homology to the staphylococcal alpha-hemolysin.

12 on with Th1, Th2, Th17 and Th22 cytokines or staphylococcal alpha-toxin, respectively, at the mRNA an

13 Streptococcus pyogenes and protected against staphylococcal alpha-toxin-induced keratinocyte cell dea

14 ession protect against cell death induced by staphylococcal alpha-toxin.

15 microdilution (BMD) reference method for 134 staphylococcal and 84 enterococcal clinical isolates.

16 were culture-positive, the most common being Staphylococcal and Streptococcal species.

17 Toxic shock syndrome (TSS) is caused by staphylococcal and streptococcal superantigens (SAgs) th

18 s ferric hydroxamate uptake D2 and conserved staphylococcal antigen 1A.

19 ly of structurally related proteins mediates staphylococcal attachment to host tissues, contributing

20 Staphylococcal aureus can be a cause of severe pneumonia

21 tein by mass spectrometry revealed the major staphylococcal autolysin Atl as a bacterial binding prot

22 conjugate vaccine showed rapid clearance of staphylococcal bacteremia in vivo relative to mice simil

23 ther nafcillin, oxacillin, or cefazolin) for staphylococcal bacteremia may improve infection-related

24 tion strategy could help treat patients with Staphylococcal bacteremia without a need for novel antib

25 last resort treatment for streptococcal and staphylococcal bacteria including methicillin-resistant

26 Staphylococcal bacteria, including Staphylococcus epider

27 ncated bacteriophage endolysin CHAPK and the staphylococcal bacteriocin lysostaphin have been co-admi

28 CRISPR-Cas9 system after infection with the staphylococcal bacteriophage varphi12.

29 However, it has yet to be determined if all staphylococcal bicomponent leukotoxin family members exh

30 The staphylococcal bicomponent pore-forming toxins Panton-Va

31 tanding the regulatory program that controls staphylococcal biofilm development, as well as the envir

32 ies SdrC as a novel molecular determinant in staphylococcal biofilm formation and describes the mecha

33 ar biomass formation, biofilm formation, and staphylococcal biofilm in skin tissues.

34 tic intervention, we sought to identify anti-staphylococcal biofilm targets for the development of a

35 or the interaction of human neutrophils with staphylococcal biofilms and demonstrated that PhnD-speci

36 nt anti-biofilm activity against established staphylococcal biofilms and demonstrates the ability to

37 Staphylococcal biofilms are the most common cause of cen

38 Association of staphylococcal biofilms with AD pathogenesis.

39 active and significantly reduced established staphylococcal biofilms.

40 Osteomyelitis is a mostly posttraumatic, Staphylococcal bone infection.

41 clinical data supporting the elimination of staphylococcal breakpoints for other beta-lactam agents.

42 ated methicillin-resistant S. aureus (MRSA), staphylococcal BSI in cancer patients is associated with

43 Here, we modeled staphylococcal BSI in leukopenic CD-1 mice that had been

44 onses that protected leukopenic mice against staphylococcal BSI.

45 otic therapy for MRSA-BSI; (4) management of staphylococcal BSIs in neonatal intensive care units; an

46 Loss of MntABC and MntH results in reduced staphylococcal burdens in the livers of wild-type but no

47 flanking conjugative transposon ICE6013, the staphylococcal cassette chromosome (SCC) and genomic isl

48 ased on complex multiplex PCRs targeting the staphylococcal cassette chromosome mec (SCCmec) DNA junc

49 ylococcus aureus (MRSA) with an unrecognized staphylococcal cassette chromosome mec (SCCmec) right-ex

50 Staphylococcal cassette chromosome mec (SCCmec) types II

51 MRSA isolates also underwent staphylococcal cassette chromosome mec (SCCmec) typing a

52 n a large (20 kb to > 60 kb) genomic island, staphylococcal cassette chromosome mec (SCCmec), that ex

53 emerged via acquisition of a mobile element, staphylococcal cassette chromosome mec (SCCmec).

54 resistant Staphylococcus aureus strains were staphylococcal cassette chromosome mec IV.

55 rences also were seen between HAHO-MRSA (60% staphylococcal cassette chromosome mec type II [SCCmec I

56 However, the small size of staphylococcal cells has impaired analysis of changes in

57 e mechanistic basis for the agglomeration of staphylococcal cells in biofilms has been investigated i

58 -associated genetic lineage that carries the staphylococcal chromosomal cassette mec (SCCmec) type IV

59 sequence is maintained upon insertion of the staphylococcal chromosome cassette mec (SCCmec) genomic

60 from and inserts site-specifically into the staphylococcal chromosome.

61 FXIII activity in staphylococcal clots could be attributed to thrombin-dep

62 Two screening methods to detect staphylococcal colonization in humans were compared.

63 Staphylococcal complement inhibitors (SCINs) are one imp

64 Although the majority of staphylococcal complement inhibitors act on the alternat

65 rocin-resistant derivative of the pGO1/pSK41 staphylococcal conjugative plasmid lineage, and pGO400::

66 Fewer coagulase-negative staphylococcal (CoNS) contaminants grew in the FA Plus b

67 ng lipoproteins, the TLR2 agonists, from the staphylococcal cytoplasmic membrane.

68 ed on DL1a, a synthetic peptide derived from staphylococcal delta-lysin.

69 essential role for autophagy in tolerance to Staphylococcal disease and highlight how a single virule

70 Invasive community-onset staphylococcal disease has emerged worldwide associated

71 TIRAP and anti-LTA Ab deficiencies underlie staphylococcal disease in this patient.

72 Life-threatening staphylococcal disease occurred during childhood in the

73 few years to become the predominant cause of staphylococcal disease, but it also appears to have incr

74 f these mechanisms in the pathophysiology of staphylococcal diseases.

75 of post-influenza pneumonia, and increasing staphylococcal drug resistance makes the development of

76 rtant target for the development of new anti-staphylococcal drugs--as a model system to rationalize a

77 hways regulating retinal innate responses in staphylococcal endophthalmitis.

78 Labeled staphylococcal enterotoxin (SE) A, SED, and SEE were use

79 wide range of ~3 decades, while detection of staphylococcal enterotoxin A (SEA) and toxic shock syndr

80 monstrate that bacterial isolates containing staphylococcal enterotoxin A (SEA) from the affected ski

81 ogress towards reference materials (RMs) for Staphylococcal enterotoxin A (SEA) in cheese.

82 Ovalbumin (OVA)-specific, staphylococcal enterotoxin A (SEA)-nonreactive naive CD4

83 -dependent mouse model of SIRS that utilizes staphylococcal enterotoxin A specific for Vbeta3(+) T ce

84 on of three bacterial toxins: cholera toxin, staphylococcal enterotoxin A, and toxic shock syndrome t

85 rinsic defect lying downstream of the TCR in staphylococcal enterotoxin A-specific CD8(+) T cells.

86 -10 (Fo = 0.16% versus 0.007%; p = 0.04) and staphylococcal enterotoxin B (Fo = 0.49% versus 0.26%; p

87 Staphylococcal enterotoxin B (SEB) causes food poisoning

88 s article, we present the x-ray structure of staphylococcal enterotoxin B (SEB) in complex with its r

89 Staphylococcal enterotoxin B (SEB) is a bacterial supera

90 Staphylococcal enterotoxin B (SEB) is a potent superanti

91 Staphylococcal enterotoxin B (SEB) is a superantigen tha

92 Systemic exposure to staphylococcal enterotoxin B (SEB) rapidly and selective

93 Staphylococcal enterotoxin B (SEB), a potential biologic

94 d immunoassays of a common food-borne toxin, Staphylococcal enterotoxin B (SEB).

95 ufficient counterparts for responsiveness to staphylococcal enterotoxin B (SEB).

96 lls are hyperresponsive to SAgs, typified by staphylococcal enterotoxin B (SEB); ii) the human MAIT c

97 In this study, we show that staphylococcal enterotoxin B activates a Galphaq and PLC

98 n of naive CD4(+) T lymphocytes with soluble staphylococcal enterotoxin B and anti-CD28.

99 pplications of a house dust mite extract and Staphylococcal enterotoxin B induced eczematous skin les

100 PBMC were cultured for 7 d with staphylococcal enterotoxin B or IL-7 in the absence or p

101 Choric exposure to staphylococcal enterotoxin B precipitated a lupus-like i

102 hanced activation-induced proliferation (via staphylococcal enterotoxin B stimulation) but inhibited

103 cytokine production by cells in response to staphylococcal enterotoxin B stimulation.

104 with CpG and stimulation of the TCR with the staphylococcal enterotoxin B superantigen.

105 T, mmCT, or dmLT plus a polyclonal stimulus (staphylococcal enterotoxin B) or specific bacterial Ags,

106 This phenotype was reproduced with staphylococcal enterotoxin B, a heterologous SAg that al

107 potential biological warfare agents, ricin, staphylococcal enterotoxin B, and epsilon toxin, in comp

108 y similar between human AD skin and allergen/staphylococcal enterotoxin B-induced mouse skin lesions,

109 nditions mimicking a robust immune response (staphylococcal enterotoxin B-induced T cell activation).

110 strated decreased pulmonary HIV-specific and staphylococcal enterotoxin B-reactive CD4(+) memory resp

111 uantified in either anti-CD3/28 antibody- or staphylococcal enterotoxin B-stimulated single-positive

112 induced by the atopic dermatitis-associated staphylococcal enterotoxin B.

113 cells of mice immunized with a superantigen, staphylococcal enterotoxin B.

114 g genes per isolate and a high prevalence of staphylococcal enterotoxin D and the enterotoxin gene cl

115 ion with a MRSA strain carrying the gene for staphylococcal enterotoxin P (sep).

116 Staphylococcal enterotoxin-like K (SEl-K) is a potent mi

117 DFU isolates also had a high prevalence of staphylococcal enterotoxin-like X.

118 ns produced by Staphylococcus aureus, called staphylococcal enterotoxins (abbreviated SEA to SEU).

119 that SA isolates from involved skin express staphylococcal enterotoxins (SEs) that induce crosstalk

120 a mouse model of asthma to determine whether staphylococcal enterotoxins promote TH2 differentiation

121 e association between asthma and exposure to staphylococcal enterotoxins.

122 he immunometabolic roles for a newly defined staphylococcal enzyme family.

123 tached peptidoglycan are the determinants of staphylococcal escape from adaptive immune responses.

124 emphasize the critical role of coagulase in staphylococcal escape from opsonophagocytic killing and

125 lococcus aureus (S. aureus) that produce the staphylococcal exotoxin alpha-toxin.

126 Human macrophages were prestimulated with staphylococcal exotoxins (SEB, alpha-toxin) to up-regula

127 However, the role of these staphylococcal exotoxins in disease pathogenesis remains

128 induces pro-inflammatory cytokines following staphylococcal exotoxins' stimulation in human macrophag

129 We measured humoral responses to 2 staphylococcal exotoxins, alpha-hemolysin (Hla) and Pant

130 ezolid inhibits in vivo production of potent staphylococcal exotoxins, including Panton-Valentine leu

131 s after up-regulation of IL-31 receptor with staphylococcal exotoxins.

132 llowing up-regulation of IL-31 receptor with staphylococcal exotoxins.

133 Staphylococcal food poisoning is caused by enterotoxins

134 -sequestering protein calprotectin surrounds staphylococcal heart abscesses, calprotectin is not rele

135 The current model for staphylococcal hemoglobin-iron acquisition proposes that

136 The four-domain staphylococcal immunoglobulin binding (Sbi) protein inte

137 itro and increased survival significantly in staphylococcal-induced bacteremia compared to treatment

138 ribe here a novel, spontaneous model of oral staphylococcal infection in double knockout mice, defici

139 thicillin-resistant S. aureus, many cases of staphylococcal infection in the ICU are now classified a

140 minase activity and heightened resistance to Staphylococcal infection in TOC keratinocytes.

141 inhibition by S. aureus in vitro and promote staphylococcal infection in vivo.

142 Staphylococcal infection of bone marrow-derived osteocla

143 ocytes (PMN) are the first responders during staphylococcal infection, but 15-50% of the initial inge

144 El-K is commonly expressed in the setting of staphylococcal infection, in significant amounts.

145 Thus, using in vitro models of intracellular staphylococcal infection, we demonstrate that EsxA inter

146 and IL-22 protects against severe pulmonary staphylococcal infection.

147 andidiasis predisposes the host to secondary staphylococcal infection.

148 bers of neutrophils, the key defense against staphylococcal infection.

149 t antimicrobial strategies, leading to fatal staphylococcal infection.

150 Staphylococcal infections are a major source of global m

151 s from patients with invasive or superficial staphylococcal infections for use in the Tigecycline Eva

152 ing truncated AIPs as a means of attenuating staphylococcal infections in species beyond Staphylococc

153 Persistent staphylococcal infections often involve surface-associat

154 unities are often associated with persistent staphylococcal infections that place a tremendous burden

155 groups, the mortality rate in patients with staphylococcal infections was significantly higher among

156 The worse outcome of staphylococcal infections with a higher vancomycin MIC c

157 c target of the humoral immune system during staphylococcal infections, we developed a synthetic meth

158 for attenuating current multidrug resistant staphylococcal infections.

159 potential treatment for multidrug-resistant staphylococcal infections.

160 nly 1 initiated CAS; 67% (8/12) of these had staphylococcal infections.

161 he development of novel targets for treating staphylococcal infections.

162 ctams with approved clinical indications for staphylococcal infections.

163 a rise in enterococci and coagulase-negative staphylococcal infections.

164 ng into question the role of Agr in invasive staphylococcal infections.

165 rtality, and economic impact associated with staphylococcal infections.

166 omplement resistance and the pathogenesis of staphylococcal infections.

167 gnificant clinical implications for relapsed staphylococcal infections.

168 nd develop therapeutic approaches to control staphylococcal infections.

169 Finally, the effects of staphylococcal invasion on the integrity of different ce

170 a, providing broad-spectrum efficacy against staphylococcal invasive disease.

171 model involving Duts in the transfer of the staphylococcal islands (SaPIs) has been suggested, quest

172 Staphylococcal isolates from elderly patients were more

173 Methicillin resistance was prevalent among staphylococcal isolates from ocular infections, with man

174 All staphylococcal isolates were susceptible to vancomycin.

175 ith resistance trends reported for nonocular staphylococcal isolates.

176 e important insight into the pathogenesis of staphylococcal joint infection and the mechanisms underl

177 and chemokinesis were markedly impaired, but staphylococcal killing was normal, and neutrophil oxidat

178 spite decades since the first description of staphylococcal leukocidal activity, the host factors res

179 identifies HlgAB and HlgCB as major secreted staphylococcal leukocidins.

180 e whole-blood response to the TLR2/6 agonist staphylococcal lipoteichoic acid (LTA) was abolished onl

181 ti-LTA Abs rescue TLR2-dependent immunity to staphylococcal LTA in individuals with inherited TIRAP d

182 activity of Podoviridae, a unique family of staphylococcal lytic phages with short, non-contractile

183 three potential hydrolase motifs resembling staphylococcal LytM, soluble lytic transglycosylase (SLT

184 Here, we investigate the staphylococcal malate-quinone and l-lactate-quinone oxid

185 ary epithelial cells and in a mouse model of staphylococcal mastitis.

186 etter understand the roles that BSH plays in staphylococcal metabolism, we constructed and examined s

187 We recently described Tudor-staphylococcal/micrococcal-like nuclease (TSN)-mediated

188 pic analyses demonstrate that CP outcompetes staphylococcal MntC and streptococcal PsaA for Mn(II).

189 VH3 idiotype Ig; however, the mechanisms for staphylococcal modification of immune responses are not

190 f the biofilm repress the production of anti-staphylococcal molecules.

191 The staphylococcal multiresistance plasmids are key contribu

192 A mediates the specific replicon assembly of staphylococcal multiresistant plasmids.

193 This process is essential for staphylococcal nasal colonization and resistance to the

194 to examine in detail the folding reaction of staphylococcal nuclease (SNase) and of some of its cavit

195 (CPHMD(MSlambdaD)) framework to a series of staphylococcal nuclease (SNase) mutants with buried ioni

196 aised against a peptide (SNpep) derived from staphylococcal nuclease (SNase) with both eliciting pept

197 ic volumetric properties of various forms of staphylococcal nuclease (SNase), including three variant

198 Tudor Staphylococcal Nuclease (TSN or Tudor-SN; also known as

199 ivated point mutants of two target proteins (staphylococcal nuclease and ribose binding protein).

200 Staphylococcal nuclease and tudor domain containing 1 (S

201 nditions by interacting with and stabilizing Staphylococcal nuclease domain-containing 1 (SND1).

202 harge pair buried in the hydrophobic core of staphylococcal nuclease was engineered by making the V23

203 ormed a 1.1-mus MD simulation of crystalline staphylococcal nuclease, providing 100-fold more samplin

204 ogen prevalence, in particular a more common staphylococcal origin, have affected outcomes, which hav

205 We conclude that Nfu is necessary for staphylococcal pathogenesis and establish Fe-S cluster m

206 amily of peptides with multiple functions in staphylococcal pathogenesis.

207 PSMs have multiple functions in staphylococcal pathogenesis; for example, they lyse red

208 Staphylococcal pathogenicity islands (SaPIs) are the pro

209 ling molecules that induce the cycle of some Staphylococcal pathogenicity islands (SaPIs) by binding

210 s), the gene-transfer agents (GTAs), and the staphylococcal pathogenicity islands (SaPIs), the primar

211 bited by the highly mobile phage satellites, staphylococcal pathogenicity islands (SaPIs), which carr

212 Here we report that the staphylococcal pathogenicity islands have a dual role in

213 vivo establishment of their contribution to staphylococcal pathophysiology.

214 to S. aureus infection, and adjuvancy with a staphylococcal peptidoglycan O-acetyltransferase mutant

215 nts maintain the structural integrity of the staphylococcal peptidoglycan.

216 We have named this protein "staphylococcal peroxidase inhibitor" (SPIN).

217 cteristic extra motif VI, present in all the staphylococcal phage coded trimeric Duts, as well as the

218 We have recently proposed that the trimeric staphylococcal phage encoded dUTPases (Duts) are signali

219 The trimeric staphylococcal phage-encoded dUTPases (Duts) are signall

220 Since lytic staphylococcal phages are considered as anti-S. aureus a

221 Unlike most staphylococcal phages, Podoviridae require a precise wal

222 ylation can prevent the infection by certain staphylococcal phages.

223 re essential for the life cycle of temperate staphylococcal phages.

224 We identified the staphylococcal phenol-soluble modulin (PSM) peptides as

225 deletion of the nfu gene negatively impacts staphylococcal physiology and pathogenicity.

226 , the collective role of the CidR regulon in staphylococcal physiology is not clearly understood.

227 target antibiotic resistance genes destroys staphylococcal plasmids that harbor antibiotic resistanc

228 the host can be protected against secondary staphylococcal pneumonia after sub-lethal influenza infe

229 dly reduces susceptibility to post-influenza staphylococcal pneumonia and that this may represent a n

230 quiring sfb influences the susceptibility to staphylococcal pneumonia via induction of type 17 immuni

231 tate-dependent potentiation of cell death in staphylococcal populations.

232 Several series predicting the prognosis of staphylococcal prosthetic joint infection (PJI) managed

233 er, our findings support a two-step model of staphylococcal prosthetic joint infection: As we previou

234 lso demonstrates a novel role for a secreted staphylococcal protease as a requirement for the develop

235 In conclusion, the staphylococcal protease SspB inactivates galectin-3, abr

236 Whether and which staphylococcal proteases account for Aap processing is y

237 The staphylococcal protein A (spa) gene was sequenced for al

238 Staphylococcal protein A (SpA) is an important virulence

239 Staphylococcal protein A (SpA) is anchored to the cell w

240 bility testing and characterization of their staphylococcal protein A (spa) type.

241 All S. aureus isolates were genotyped by staphylococcal protein A (spa) typing and with multilocu

242 ntibiotic susceptibility, biofilm formation, Staphylococcal protein A (spa) typing, SCCmec typing, an

243 Staphylococcal protein A (SPA) was used to modify the si

244 d antigen presentation to CD4(+) T cells and staphylococcal protein A (SpA), a cell wall-anchored sur

245 cluded multilocus sequence typing (MLST) and staphylococcal protein A gene (spa) typing results as we

246 In this study we show that staphylococcal protein A induces T cell-independent huma

247 ted-residue force field, for the B domain of staphylococcal protein A, we are able to (i) provide the

248 of the common model protein, the B domain of staphylococcal protein A.

249 lved in AD augment the toxicity of the lytic staphylococcal protein alpha toxin.

250 em) assays were used to detect genes for the staphylococcal protein SA0140 (SA) and the methicillin r

251 However, few staphylococcal proteins that mediate intracellular survi

252 reened a collection of recombinant, secreted staphylococcal proteins to determine whether S. aureus p

253 (Atl)-derived murein hydrolases and prevents staphylococcal release of DNA, which serves as extracell

254 alian New Zealand Cooperative on Outcomes in Staphylococcal Sepsis cohort for 1153 children with SAB

255 We identified staphylococcal serine protease-like proteins (Spls) as d

256 Here we identify Stk2, a staphylococcal serine/threonine kinase that provides eff

257 primary response gene 88 (MyD88) deficiency, staphylococcal skin and soft tissue infections are a lea

258 ML-mediated inflammation in a mouse model of staphylococcal skin infection.

259 tients with AD may enhance susceptibility to staphylococcal skin infection.

260 ; anti-interleukin (IL)-6 autoantibodies and staphylococcal skin infection; and anti-IL-17A, anti-IL-

261 of ebselen was evaluated in a mouse model of staphylococcal skin infections.

262 cal antimicrobial agent for the treatment of staphylococcal skin infections.

263 , as well as representative enterococcal and staphylococcal species (including MRSA and VISA).

264 ng bacteria, closely related less pathogenic staphylococcal species do not possess this importer.

265 ylococcus agnetis are two coagulase-variable staphylococcal species that can be isolated from bovine

266 andard biologic testing were used to confirm staphylococcal species.

267 faecalis isolates and other enterococcal and staphylococcal species.

268 binding specific positions on stem I and the Staphylococcal-specific stem Sa.

269 Staphylococcal SplB protease belongs to the chymotrypsin

270 Glycopeptides reduce the risk of resistant staphylococcal SSIs and enterococcal SSIs, but increase

271 glycopeptides reduced the risk of resistant staphylococcal SSIs by 48% (relative risk, 0.52; 95% con

272 superficial and deep chest SSIs, susceptible staphylococcal SSIs, and respiratory tract infections.

273 se to 100% protection against four different staphylococcal strains.

274 t other clinically relevant enterococcal and staphylococcal strains.

275 thology elicited by acute challenge with the staphylococcal superantigen enterotoxin B were comparabl

276 The staphylococcal superantigen SEE induced the production o

277 us aureus secretes a potent TLR2 antagonist, staphylococcal superantigen-like protein 3 (SSL3), which

278 Staphylococcal superantigens cause toxic shock syndrome,

279 ding an array of virulence factors including staphylococcal superantigens, proteases, and leukotoxins

280 matory patterns, including IgE antibodies to staphylococcal superantigens; several studies using biol

281 vaccines and antibody therapeutics targeting staphylococcal surface molecules have thus far failed to

282 tionship between mechanics and adhesion in a staphylococcal surface protein, which may represent a ge

283 A combination of separation of staphylococcal surface proteins by two-dimensional gel e

284 am infections by directing fibrinogen to the staphylococcal surface, generating a protective fibrin s

285 b enhances acquisition of FH from serum onto staphylococcal surfaces.

286 l sandwich-type immunoassay for detection of staphylococcal toxins in complex media of virtually any

287 a phosphocholine binding pocket found in the staphylococcal toxins.

288 ation predisposes to enhanced lethality from staphylococcal toxins.

289 dings can help inform future developments in staphylococcal vaccine development and studies into the

290 technology for creation of a multicomponent staphylococcal vaccine is described.

291 nt vaccine failures and the design of future staphylococcal vaccines.

292 The role of alpha-toxin in pediatric staphylococcal-viral coinfection is unclear.

293 Production of Hla and restoration of staphylococcal virulence can be achieved in the psm muta

294 l reagents that have the capacity to inhibit staphylococcal virulence expression.

295 assess the humoral response to extracellular staphylococcal virulence factors, including the bicompon

296 0-fold reduction in USA300 expression of the staphylococcal virulence regulator agr but had little ef

297 ome remodeling as a major determinant of the staphylococcal virulence repertoire.

298 The Esx proteins are required for staphylococcal virulence, but their functions during inf

299 loss of any one transporter did not decrease staphylococcal virulence.

300 Atl has also been identified previously as a staphylococcal vitronectin (Vn)-binding protein.