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1 ic interactions between P. aeruginosa and S. aureus.
2 ns like methicillin-resistant Staphylococcus aureus.
3  the corneal ulcers are P. aeruginosa and S. aureus.
4 robial, broadly applicable to Staphylococcus aureus.
5 ions of neutrophils during infection with S. aureus.
6 in the biofilms of both S. pneumoniae and S. aureus.
7 cium and meticillin-resistant Staphylococcus aureus.
8 ases and NF-kappaB pathway in response to S. aureus.
9 he pathophysiology of DFUs colonized with S. aureus.
10 uirements for protective immunity against S. aureus.
11 gSAP1 has anti-biofilm properties against S. aureus.
12  the greatest induction after exposure to S. aureus.
13 m Acinetobacter baumannii and Staphylococcus aureus.
14  aeruginosa and ten honey samples against S. aureus.
15 us spp. and 120CFU/ml in pure culture for S. aureus.
16 te of the host and increased virulence of S. aureus.
17 fectively killed two different strains of S. aureus.
18 and persistently colonised by Staphylococcus aureus.
19 e identified core FtsH target proteins in S. aureus.
20 isms such as enteric rods and Staphylococcus aureus.
21 e for degradation of unfolded proteins in S. aureus.
22                               Staphylococcus aureus (12.9%) and Pseudomonas aeruginosa (11.5%) were t
23 l of 658 Staphylococcus species isolates (S. aureus, 211 isolates; S. lugdunensis, 3 isolates; and St
24 systemic infections caused by Staphylococcus aureus, a leading cause of bacterial endocarditis.
25                               Staphylococcus aureus, a metabolically flexible gram-positive pathogen,
26 lavone rich extract "430D-F5" against all S. aureus accessory gene regulator (agr) alleles in the abs
27 emonstrate a key contribution of saNOS to S. aureus aerobic respiratory metabolism.
28 cytokines, which dominated the response to S aureus alpha-hemolysin, were of low concentration or abs
29 formation and the presence of Staphylococcus aureus, an organism frequently colonizing the upper airw
30 sets were more efficient at internalizing S. aureus and B. anthracis compared with E. coli Alveolar m
31                                           S. aureus and E. coli antigens were detected in immune-blot
32 icroarrayed HDM allergen molecules and to S. aureus and E. coli by IgE immunoblotting.
33 losis; mannitol, with selective uptake in S. aureus and E. coli; and sorbitol, accumulating only in E
34  S. aureus both through direct killing of S. aureus and enhancing the antimicrobial function of macro
35 d against two gram positive (Staphyllococcus aureus and Enterococcus) and two gram negative pathogens
36 red infections: gram-positive Staphylococcus aureus and gram-negative Pseudomonas aeruginosa (99.3 +/
37 rived protein SplD is a potent allergen of S aureus and induces a TH2-biased inflammatory response in
38 mative density cutoffs were not found for S. aureus and M. catarrhalis, and a lack of confirmed case
39         The dominant bacteria species was S. aureus and MRSA infection is increasingly prevalent.
40 tain immune equilibrium and decrease PGN, S. aureus and MRSA-triggered inflammatory response.
41 tween cardiovascular infections caused by S. aureus and nonsynonymous SNPs in FnBPA.
42 dentify a functional adenylate cyclase in S. aureus and only detected 2',3'-cAMP but not 3',5'-cAMP i
43 are likely to be specifically recruited to S aureus and possibly other microorganisms and form EETs a
44 typically polymicrobial, with Staphylococcus aureus and Pseudomonas aeruginosa being the two most com
45 lus cereus, Escherichia coli, Staphylococcus aureus and Pseudomonas aeruginosa) and in vitro anti-pro
46  of bioluminescent strains of Staphylococcus aureus and Pseudomonas aeruginosa.
47                       The "Big Papi" (paired aureus and pyogenes for interactions) approach described
48 coli, Listeria monocytogenes, Staphylococcus aureus and Salmonella enteritidis.
49 bacteria in the upper airway (Staphylococcus aureus and Staphylococcus epidermidis) and intestinal mi
50 oli, Mycobacterium smegmatis, Staphylococcus aureus and Staphylococcus simulans.
51     Regarding microorganisms, Staphylococcus aureus and streptococci slightly declined, whereas coagu
52  solute-binding proteins that Staphylococcus aureus and Streptococcus pneumoniae, Gram-positive bacte
53  bactericidal effects against Staphylococcus aureus and Streptococcus pyogenes and protected against
54 growth of both gram-positive (Staphylococcus aureus and Streptococcus pyogenes) and gram-negative bac
55  orthogonal Cas9 enzymes from Staphylococcus aureus and Streptococcus pyogenes.
56  potent exotoxins secreted by Staphylococcus aureus and Streptococcus pyogenes.
57 nts (approximately 38%) colonized only by S. aureus and treated with appropriate antibiotic for at le
58  in sepsis caused by G(+) bacteria (e.g., S. aureus) and antibiotic-resistant bacteria (e.g., MRSA).
59 DM) has shown that Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) species are abund
60 eptibility to both bacterial (Staphylococcus aureus) and viral (murine CMV) infection in vivo.
61 rum beta-lactamase, methicillin-resistant S. aureus, and carbapenem-resistant strains was also observ
62 niae, Pseudomonas aeruginosa, Staphylococcus aureus, and coagulase-negative staphylococci strains.
63 iently by IFN-beta than was the wild-type S. aureus, and immunoblotting showed that IFN-beta interact
64 ulations of Escherichia coli, Staphylococcus aureus, and Mycobacterium smegmatis to quinolone antibio
65 Colonization densities of M. catarrhalis, S. aureus, and P. jirovecii are unlikely to be of diagnosti
66 enzae, Moraxella catarrhalis, Staphylococcus aureus, and Pneumocystis jirovecii.
67 the impact of interspecies interaction on S. aureus antibiotic susceptibility remains poorly understo
68  to the capacity of each isolate to alter S. aureus antibiotic susceptibility.
69  and staphyloferrin B (SB) of Staphylococcus aureus are essential for iron acquisition in the iron-re
70 of nafithromycin were tested: Staphylococcus aureus ATCC 25923 (disk only), S. aureus ATCC 29213 (bro
71 ges were determined to be 25 to 31 mm for S. aureus ATCC 25923, 25 to 31 mm for S. pneumoniae ATCC 49
72 hylococcus aureus ATCC 25923 (disk only), S. aureus ATCC 29213 (broth only), Enterococcus faecalis AT
73  determined to be 0.06 to 0.25 mug/ml for S. aureus ATCC 29213, 0.016 to 0.12 mug/ml for E. faecalis
74                               Staphylococcus aureus bacteraemia is a common cause of severe community
75 ontrolled trial, adults (>/=18 years) with S aureus bacteraemia who had received </=96 h of active an
76 standard antibiotic therapy in adults with S aureus bacteraemia.
77 ukin 10 (IL-10) production in Staphylococcus aureus bacteremia (SaB) animal models, but clinical data
78 IL-10 production and its association with S. aureus bacteremia (SaB) mortality.
79  to improve the management of Staphylococcus aureus bacteremia (SAB).
80  an important complication of Staphylococcus aureus bacteremia (SAB).
81                                           S. aureus bacteremia is often associated with an adverse ou
82 ram-negative (E. coli) and Gram-positive (S. aureus) bacteria to a great extent.
83 a, Moraxella catarrhalis, and Staphylococcus aureus, bacteria that occasionally colonize and infect t
84 ring S. aureus, demonstrated sex-specific S. aureus bactericidal capacity ex vivo.
85 ld infants with AD were not colonized with S aureus before having AD.
86 to summarize our current understanding of S. aureus biofilm development, focusing on the description
87 and the molecular mechanisms that control S. aureus biofilm formation and the basis for the recalcitr
88  was also highly effective in eradicating S. aureus biofilm infection when used in a CLS rat central
89 as catheter lock solutions (CLSs) against S. aureus biofilm infections.
90 vel information on staphopains present in S. aureus biofilms in vivo, and illustrate the complex inte
91 and rifampicin) in preventing Staphylococcus aureus biofilms was investigated using Microtiter Well P
92 y analysis showed that LL-37 binds to the S. aureus biofilms.
93 elets participate in host defense against S. aureus both through direct killing of S. aureus and enha
94 nge with Escherichia coli and Staphylococcus aureus, but had no significant effect after challenge wi
95 nvolved in internalization of Staphylococcus aureus by A549 lung epithelial cells.
96  investigated for the presence of EETs and S aureus by using immunofluorescent staining and the PNA-F
97 a LasA endopeptidase potentiates lysis of S. aureus by vancomycin, rhamnolipids facilitate proton-mot
98 quired, methicillin-resistant Staphylococcus aureus (CA-MRSA) with specific molecular characteristics
99 hy colonization of superantigen-producing S. aureus can induce, under some circumstances, mucosal typ
100                      However, the role of S. aureus carriage and SE sensitization on allergic multimo
101 e previously shown an association between S. aureus carriage and severe allergic disease and allergic
102                 SE sensitization, but not S. aureus carriage, was associated with poly-sensitization
103  In galectin-3(+/+) mice, SspB-expressing S. aureus caused larger lesions and resulted in higher bact
104                           The Staphylococcus aureus cell surface contains cell wall-anchored proteins
105 tracked spacer acquisition in Staphylococcus aureus cells harbouring a type II CRISPR-Cas9 system aft
106           From approximately 2.15 x 10(5) S. aureus cells, 578 proteins were identified.
107 ociated methicillin-resistant Staphylococcus aureus clonal complex 398 (LA-MRSA CC398) is causing an
108        As far as this review, Staphylococcus aureus, Coagulase negative Staphylococci, Streptococcus
109                  Current animal models of S. aureus colonisation are expensive and normally require a
110 tal model, impact of adaptive immunity on S. aureus colonisation could be assessed.
111                               Staphylococcus aureus colonization contributes to skin inflammation in
112 ar, vaccination, participants with AD with S aureus colonization experienced (1) lower seroprotection
113                               Staphylococcus aureus colonization levels inversely correlated with the
114 rospective clinical trial that shows that S. aureus colonization precedes onset of atopic dermatitis
115          To examine the microevolution of S. aureus colonization, we deep sequenced S. aureus populat
116                                           S. aureus colonizes the skin of the majority of children wi
117 his, the origins and genetic diversity of S. aureus colonizing individual patients during AE disease
118 el control approaches, we have identified S. aureus components that are required for growth in human
119 under conditions mimicking infection with S. aureus conferred responsiveness to IL-20 that manifested
120 anisms by which miR response to cutaneous S. aureus contributes to DFU pathophysiology are unknown.
121          The annual rates of infection by S. aureus declined from 2003 to 2014 by 4.2% (2.7% to 5.6%)
122 ally, neutrophils, essential for clearing S. aureus, demonstrated sex-specific S. aureus bactericidal
123                                        The S aureus-derived protein SplD is a potent allergen of S au
124 e observations indicate that Pi uptake by S. aureus differs from established models and that acquisit
125                 These data illustrate how S. aureus directly influences the skin barrier integrity by
126 termined the ability of platelets to kill S. aureus directly; and, second, we tested the possibility
127 nowledge of the molecular pathogenesis of S. aureus disease, we suggest that the application of molec
128    Altogether this further indicates that S. aureus does not produce 3',5'-cAMP, which would otherwis
129 diversity skin microbiota and Staphylococcus aureus dominance.
130                            Concomitantly, S. aureus elicits the production of proinflammatory cytokin
131 nes a previously unknown pathway by which S. aureus epicutaneous exposure promotes skin inflammation
132                                            S aureus epidemiology in the ICU and HDU is characterised
133 ke in vitro in live bacteria (Staphylococcus aureus, Escherichia coli, and Pseudomonas aeruginosa) re
134                         The extent of ABR S. aureus exposure in IHO workers and children living in th
135                      Herein, epicutaneous S. aureus exposure to mouse skin promoted MyD88-dependent s
136                               Staphylococcus aureus expresses a panel of cell wall-anchored adhesins,
137 sed, further linking fibrin deposition to S. aureus expression of clfA and infection severity.
138 uding MDROs such as methicillin-resistant S. aureus, extended-spectrum beta-lactamase-producing, and
139                                            S aureus extracellular proteins targeted by human serum Ig
140      Here, we identify a single strain of S. aureus found to be persistently colonising the gastroint
141                               Staphylococcus aureus from these 2 groups were introduced into whole bl
142 at IFN-beta can directly kill Staphylococcus aureus Further, a mutant S. aureus that is more sensitiv
143                          Furthermore, 182 S. aureus genes are uniquely essential during co-infection.
144          However, the driving allergens of S aureus have remained elusive.
145               The genetic adaptability of S. aureus, heterogeneity of disease presentation, clinical
146 ss of a single transporter did not affect S. aureus However, disruption of any two systems significan
147 s suggests that intracellular survival of S. aureus in macrophages may allow the pathogen to chronica
148  (SYK) activity and uptake of Staphylococcus aureus in microglial cell line BV-2 in a kinase-dependen
149 onsequently, excess Mn is bioavailable to S. aureus in the heart.
150 ic operon crtOPQMN, promoting survival of S. aureus in the presence of oxidants.
151                   Furthermore, fitness of S. aureus in these sites of replication is not compromised
152 phagocytosis and intracellular killing of S. aureus In this study we report evidence in support of bo
153 (in laboratory and AD clinical strains of S. aureus) inducing barrier integrity impairment and tight
154 al course, and outcome between individual S. aureus-infected ICU patients remains enigmatic, suggesti
155 e exhibited abnormal abscess formation at S. aureus-infected skin wound sites and were also more susc
156 ranulopoiesis and effective resolution of S. aureus-infected wounds, revealing a potential antibiotic
157 ells, expanded during chronic Staphylococcus aureus infection and promoted bacterial persistence by i
158 of molecular pathological epidemiology to S. aureus infection can usher in a new era of highly focuse
159 g vaccine recipients in whom postsurgical S. aureus infection developed, emphasizing the potential fo
160 e response to treat methicillin-resistant S. aureus infection in immunodeficient patients.
161 ffect was restricted to participants with S. aureus infection.
162 he human immune system in protection from S. aureus infection.
163 tion of macrophages in protection against S. aureus infection.
164 tribute to protection against Staphylococcus aureus infection.
165  to live rats with an induced bloodstream S. aureus infection.
166 thway, which may be targeted for treating S. aureus infection.
167  institutions in Boston, MA, a decline in S. aureus infections has been accompanied by a shift toward
168 lear whether this represents a decline in S. aureus infections overall.
169                    Staphylococcus aureus (S. aureus) infections are among the most common and severe
170                        Here, we show that S. aureus inhibits wound closure and induces miR-15b-5p in
171 sociation and phagocytosis of Staphylococcus aureus into macrophages.
172 e most patients with AD are colonized with S aureus, intramuscular influenza vaccination should be gi
173 tion with other AMPs, in the treatment of S. aureus intravenous catheter infections.
174                               Staphylococcus aureus is a leading cause of both nosocomial and communi
175                               Staphylococcus aureus is a major cause of skin and soft tissue infectio
176                               Staphylococcus aureus is a medically important pathogen with an abundan
177                               Staphylococcus aureus is a serious human pathogen with remarkable adapt
178                               Staphylococcus aureus is an AD-associated pathogen producing virulence
179          Skin colonization by Staphylococcus aureus is associated with severity of atopic dermatitis
180 core, colonization by C. neonatale and/or S. aureus is significantly associated with NEC.
181                               Staphylococcus aureus is the leading cause of skin and skin structure i
182                               Staphylococcus aureus is the most common cause of skin and soft tissue
183                               Staphylococcus aureus is the most common infectious agent causing pyoge
184            We aimed to determine how often S aureus is transmitted from health-care workers or the en
185 ion of the skin by Staphylococcus aureus (S. aureus) is increased in atopic dermatitis and can result
186 d in 1998 at 7.7% and represented 18.4% of S aureus isolates in 2016.
187                            A total of 311 S. aureus isolates were collected from respiratory cultures
188 85% of all relaxases found in Staphylococcus aureus isolates.
189 gens: E nterococcus faecium, S taphylococcus aureus, K lebsiella pneumoniae, A cinetobacter baumannii
190 ted beta-lactam resistance in Staphylococcus aureus Kriegeskorte and colleagues report the performanc
191 ociated methicillin-resistant Staphylococcus aureus (LA-MRSA) is an emerging problem in many parts of
192 programmed cell lysis (PCL) phenomenon in S. aureus leading to the release of cellular polymers that
193 ere, we identify and characterise a novel S. aureus leukocidin; LukPQ.
194           These observations suggest that S. aureus may cause atopic dermatitis in some individuals.
195 s a previously unknown mechanism by which S. aureus may influence skin diseases.
196 l, our study suggests a mechanism whereby S. aureus modulates cytokines critical for induction of pro
197 tions showed that the ancestor of all ST8 S. aureus most likely emerged in Central Europe in the mid-
198 ces for methicillin-resistant Staphylococcus aureus (MRSA) and multidrug-resistant Acinetobacter baum
199         Methicillin-resistant Staphylococcus aureus (MRSA) caused 57% of the ISIs.
200  reduce methicillin-resistant Staphylococcus aureus (MRSA) growth.
201 tion by methicillin-resistant Staphylococcus aureus (MRSA) has declined over the past decade, but it
202 ence of methicillin-resistant Staphylococcus aureus (MRSA) infection was 24% and multidrug resistance
203         Methicillin-resistant Staphylococcus aureus (MRSA) is a bacterium that causes infections in d
204         Methicillin-resistant Staphylococcus aureus (MRSA) is the most common healthcare-associated m
205 ociated methicillin-resistant Staphylococcus aureus (MRSA) is unclear.
206 ages of methicillin-resistant Staphylococcus aureus (MRSA) over sensitive isolates (methicillin-sensi
207         Methicillin-resistant Staphylococcus aureus (MRSA) represents a major contributor to this tre
208         Methicillin-resistant Staphylococcus aureus (MRSA) was first observed in 1960, less than one
209          Meticillin-resistant Staphylococcus aureus (MRSA) was first reported in 1998 at 7.7% and rep
210 (MSSA), methicillin-resistant Staphylococcus aureus (MRSA), Listeria monocytogenes and Enterococcus f
211 n of mecC-harboring methicillin-resistant S. aureus (MRSA), which failed to identify from 0 to 41% of
212 ific to methicillin-resistant Staphylococcus aureus (MRSA).
213 against methicillin-resistant Staphylococcus aureus (MRSA).
214  with methicillin-susceptible Staphylococcus aureus (MSSA) infections, beta-lactams are recommended f
215 amely methicillin-susceptible Staphylococcus aureus (MSSA), methicillin-resistant Staphylococcus aure
216 sensitive isolates (methicillin-sensitive S. aureus: MSSA).
217 challenged with an isogenic SpA-deficient S. aureus mutant, cells proliferated in the BM survival nic
218                      Livestock-associated S. aureus nasal carriage predominated among IHO workers.
219 atopic children asymptomatically carrying S. aureus nasally.
220                     Specifically, aerobic S. aureus nos mutant cultures presented with elevated endog
221 s of ribosomal particles from Staphylococcus aureus obtained by X-ray crystallography have shed light
222 sociated infections caused by Staphylococcus aureus often lead to significant increases in morbidity
223 y Spls as triggering allergens released by S aureus, opening prospects for diagnosis and causal thera
224 to treat than most strains of Staphylococcus aureus or staph, because it is resistant to some commonl
225 gher in methicillin-resistant Staphylococcus aureus (OR, 2.80; 95% CI, 1.65-4.74) and in Escherichia
226 ells obtained from a 12-year-old boy with S. aureus osteomyelitis.
227 emiological investigations of Staphylococcus aureus outbreaks.
228 elationship between PBP 3 and Staphylococcus aureus PBP 2A, which is responsible for methicillin resi
229                               Staphylococcus aureus plays an important role in sepsis, pneumonia, wou
230 sociated with the clonal expansion of the S. aureus population, occurring over a period of weeks to m
231 S. aureus colonization, we deep sequenced S. aureus populations from nine children with moderate to s
232 ost-effectiveness of methicillin-resistant S aureus prevention strategies and recommends specific str
233 ortalized and primary keratinocytes, that S. aureus protease SspA/V8 is the dominant secreted factor
234 s protease rapidly hydrolyzes Staphylococcus aureus protein A, an important S. aureus virulence facto
235 ells, abundance changes for more than 400 S. aureus proteins were quantified, revealing, e.g., the pr
236 gh-accuracy quantification of Staphylococcus aureus proteins, we have developed a global ion library
237 rmittently exposed, some individuals lose S. aureus rapidly.
238 uch as the bacterial pathogen Staphylococcus aureus Recruitment and activation of neutrophils at site
239  including tandem repeats and Staphylococcus aureus repeat (STAR)-like elements.
240 tructure of the native 100S ribosome from S. aureus, revealing the molecular mechanism of its formati
241 st mites (HDM) has shown that Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) specie
242                               Staphylococcus aureus (S. aureus) infections are among the most common
243   Colonization of the skin by Staphylococcus aureus (S. aureus) is increased in atopic dermatitis and
244 ary outcome meta-analysis for Staphylococcus aureus skin or soft-tissue infections.
245 SSTIs), yet sex bias in susceptibility to S. aureus SSTI has not been described.
246 capacity play important roles in limiting S. aureus SSTI in females.
247 aneous identification (ID) of Staphylococcus aureus, Staphylococcus lugdunensis, and Staphylococcus s
248       Deletion of sdrD from S. aureus subsp. aureus strain NCTC8325-4 attenuated bacterial survival i
249                       We characterized an S. aureus strain that contained a transposon inserted in th
250 luding a multi-drug resistant Staphylococcus aureus strain Y5 and ampicillin resistant Pseudomonas ae
251 wever, superantigen-producing Staphylococcus aureus strains are often part of the human nasal microbi
252 of antibiotic-resistance genes from other S. aureus strains or even from other genera.
253 Mice were infected i.v. using 8 different S. aureus strains, and development of the infection was fol
254       In the strain Newman and some other S. aureus strains, the sensor histidine kinase SaeS has an
255 ix diverse bacterial species: Staphylococcus aureus, Streptococcus pneumoniae, Mycobacterium tubercul
256                     Deletion of sdrD from S. aureus subsp. aureus strain NCTC8325-4 attenuated bacter
257 uide activation of T cells by Staphylococcus aureus superantigen and, when preincubated with CMV anti
258 he ability of WLBU2 to remove Staphylococcus aureus surgical implant biofilms.
259 f SdrD as an important key contributor to S. aureus survival and the ability to escape the innate imm
260  amount of a major cell wall component of S. aureus, termed wall teichoic acid (WTA).
261 s SNPs in fnbA among clinical isolates of S. aureus that cause endovascular infections.
262 ace of the bacterial pathogen Staphylococcus aureus that extracts heme from hemoglobin (Hb) to enable
263 l Staphylococcus aureus Further, a mutant S. aureus that is more sensitive to antimicrobial peptides
264 suppressed by the concomitant presence of S. aureus The downregulation of IP-10 by S. aureus was medi
265 sa to produce virulence factors that kill S. aureus These data could provide important clues regardin
266 raction and that it is sufficient to kill S. aureus These results suggest that, in addition to its we
267  later by an i.v. exposure to Staphylococcus aureus This procedure resulted in a marked propensity fo
268 ide (HQNO) induces multidrug tolerance in S. aureus through respiratory inhibition and reduction of c
269 al proteins that promote the adherence of S. aureus to AD corneocytes.
270 of peptidoglycan, a mechanism utilized by S. aureus to block bacterial cell wall breakdown, limits th
271            Bioavailable Mn is utilized by S. aureus to detoxify reactive oxygen species and protect a
272 hese results demonstrate an adaptation by S. aureus to obesity/T2D with increased expression of clfA
273           We also assessed the ability of S. aureus to survive following alkalinization of the phagol
274 vestigate the time-resolved adaptation of S. aureus to the intracellular niche in human bronchial epi
275                     Whether adaptation of S. aureus to the unique environment of the obese/T2D host a
276                                           S. aureus toxins and virulence proteases often circulate in
277  and identified the essential Staphylococcus aureus tRNA m(1)G37 methyltransferase enzyme TrmD, which
278 all-colony variants (SCVs) of Staphylococcus aureus typically lack a functional electron transport ch
279 yielded statistically similar results for S. aureus typing.
280 w that the bacterial pathogen Staphylococcus aureus unexpectedly secretes and repurposes the lipoylat
281    The Gram-positive pathogen Staphylococcus aureus uses one primary resistance mechanism.
282  The bacterial human pathogen Staphylococcus aureus uses oxygen as a terminal electron acceptor durin
283                                           S. aureus uses secreted cyclic autoinducing peptides (AIPs)
284 n due to meticillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, C difficile, a
285 hylococcus aureus protein A, an important S. aureus virulence factor involved in immune evasion and b
286 onent vaccines to target the multitude of S. aureus virulence factors.
287  of galectin-3 and protease expression on S. aureus virulence was studied in a murine skin infection
288 st Pseudomonas aeruginosa and Staphylococcus aureus was assessed by microdilution assay.
289  differentiate S. hyicus, S. agnetis, and S. aureus was developed.
290                                            S aureus was identified in 8-50% of environmental samples.
291  S. aureus The downregulation of IP-10 by S. aureus was mediated by components of its cell wall, but
292 sh long-term protective Ab titers against S. aureus was not a consequence of diminished formation of
293 te interactions between P. aeruginosa and S. aureus We demonstrate that P. aeruginosa quorum sensing
294 ichia coli, Enterococcus, and Staphylococcus aureus we observed that cocolonization with specific pai
295 clinically relevant bacterium Staphylococcus aureus, we demonstrate for the first time that these enz
296 secreted virulence factors of Staphylococcus aureus, we determine that the bacterial lipoic acid synt
297        Interestingly, without this enzyme S. aureus were repressed in their ability to secrete cytoly
298  opportunistic human pathogen Staphylococcus aureus, which generates the phenotypic bifurcation of th
299 st Pseudomonas aeruginosa and Staphylococcus aureus, with a particular focus on two major bee-derived
300  of atopic eczema (AE) is colonization by S. aureus, with exacerbations associated with an increased

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