ライフサイエンスコーパス: acnes

1 L-26 lacked antimicrobial potency against P. acnes.

2 , neck, chest, and back by Propionibacterium acnes.

3 to the commensal bacterium Propionibacterium acnes.

4 lated to, yet distinct (by sequence) from P. acnes.

5 to indolent agents of infection, such as P. acnes.

6 y augmented when S. aureus was grown with P. acnes.

7 vity against S. aureus and Propionibacterium acnes.

8 rol, the CD209(+) cells responded only to P. acnes.

9 cine provoked specific antibodies against P. acnes.

10 tly mediate the innate immune response to P. acnes.

11 ultiple factors, including Propionibacterium acnes.

12 rmation on the actions of Proprionibacterium acnes.

13 -regulated monocyte cytokine induction by P. acnes.

14 riostatic antibiotics in their control of P. acnes.

15 y proteases and more effective in killing P. acnes.

16 nes secreted molecules sufficient to kill P. acnes.

17 sts and osteoclasts were infected by live C. acnes.

18 gamma and prevent TLR4 desensitization by P. acnes.

19 for NF-kappa B activation in response to P. acnes.

20 ockout mice, produced IL-6 in response to P. acnes.

21 hich may be due to increased abundance of P. acnes.

22 most frequent isolate was Propionibacterium acnes (11/26) vs coagulase-negative Staphylococcus (57/9

23 The P. acnes 16S rRNA gene was detectable in 4 of 15 carotid ar

24 of glycerol with Propionibacterium acnes (P. acnes), a skin commensal bacterium, can function as a sk

25 level and genome level of Propionibacterium acnes, a dominant skin commensal, between 49 acne patien

26 h S. aureus may commandeer Propionibacterium acnes, a key member of the human skin microbiome, to spr

27 towska et al. confirm that Propionibacterium acnes activates inflammasomes leading to the production

28 ing mononuclear cell numbers 7 days after P. acnes administration was significantly reduced in B6 com

29 sequent inflammatory cytokine response to P. acnes after 1 week of therapy.

30 P. acnes also induced activation of IL-12 p40 promoter acti

31 nflammatory cytokines in response to both P. acnes and a TLR2 ligand control, the CD209(+) cells resp

32 fectively neutralized the cytotoxicity of P. acnes and attenuated the production of proinflammatory c

33 ers, and 1 isolate each of Propionibacterium acnes and coagulase-negative staphylococci) in FAN bottl

34 Propionibacterium acnes and coagulase-negative Staphylococcus species were

35 e direct antibacterial activities against P. acnes and enhance the skin's innate antibacterial defens

36 data demonstrate that IL-17 is induced by P. acnes and expressed in acne lesions and that both vitami

37 Although early colonisation with P acnes and family history might have important roles in t

38 This study explored the role of P. acnes and its ability to induce matrix metalloproteinase

39 strain-based resolution of Propionibacterium acnes and its association with the common teenage malady

40 he Gram-positive bacterium Propionibacterium acnes and its potential association with biofilm structu

41 In vivo Th1 response to Propionibacterium acnes and lipopolysaccharide in IFN-gamma production and

42 of ICE-/- mice exposed to Propionibacterium acnes and lipopolysaccharide.

43 formation of resistance in Propionibacterium acnes and other bacteria, with clinical consequences.

44 requiring helpers such as Propionibacterium acnes and Prevotella intermedia for stimulation, with be

45 PA6 infected only P. acnes and produced clear plaques with turbid centers, bu

46 the skin lesions caused by coinfection of P. acnes and S. aureus.

47 onstrated that human monocytes respond to P. acnes and secrete mature IL-1beta partially via the NLRP

48 attenuate inflammatory responses against P. acnes and the inhibition of bacterial growth may lead to

49 ited robust bactericidal activity against P. acnes, and complete breaches in the bacterial cell envel

50 irulence organisms such as Propionibacterium acnes are the most common culprit organisms, and treatme

51 The CC18 C. acnes ATCC6919 isolate could survive intracellularly for

52 We report a patient with Propionibacterium acnes bacteremia and late prosthetic valve endocarditis,

53 tilocus sequence typing scheme (MLST) for P. acnes based on seven housekeeping genes.

54 acnes with heat was employed to create a P. acnes-based vaccine.

55 nasal immunization using heat-inactivated P. acnes-based vaccines provided a simple modality to devel

56 strated that laboratory-grown cultures of P. acnes biofilms were susceptible to induction of a biofil

57 microbial property of lauric acid against P. acnes both in vitro and in vivo.

58 onstrated potent and selective killing of P. acnes but not against human skin cells in vitro.

59 The host range of PA6 was restricted to P. acnes, but the phage was able to infect and lyse all P.

60 Studies suggest that responses to P. acnes by host immunity play important roles in its patho

61 mpared the antibiotic susceptibilities of P. acnes by using the National Committee for Clinical Labor

62 nce factors (S. aureus beta-hemolysin and P. acnes CAMP (Christie, Atkins, Munch-Peterson) factor) as

63 tion was significantly abrogated when the P. acnes CAMP factor was neutralized or beta-hemolysin of S

64 These results demonstrate that P. acnes can infect the carotid arteries of humans with ath

65 When monocytes were stimulated with live P. acnes, caspase-1 and caspase-5 gene expression was upreg

66 Propionibacterium acnes, causative agent of chronic prostatitis possibly c

67 ere found to induce the disruption of the P. acnes cell membrane, providing a mechanism for the bacte

68 tivity, as treatment with Pentobra killed P. acnes cells and caused leakage of intracellular contents

69 rated in vivo protective immunity against P. acnes challenge and facilitated the resolution of ear in

70 Recent work revealed that P. acnes clinical isolates can be classified into distinct

71 The clade of 11 C. acnes clinical isolates was determined by MLST.

72 y increasing resistance of Propionibacterium acnes clinical isolates.

73 tobramycin (by 5-7 logs) against multiple P. acnes clinical strains.

74 acid effectively decreased the number of P. acnes colonized with mouse ears, thereby relieving P. ac

75 d superior antimicrobial activity against P. acnes compared with BP alone while demonstrating less to

76 +) cells were more effective in uptake of P. acnes, compared with the CD1b(+) cells, and demonstrated

77 lack of sensitization to TLR2 ligands by P. acnes correlated with no increase in hepatic TLR1 or TLR

78 biofilm bacteria within all samples, with P. acnes detectable in 4 samples.

79 aerococcus, Peptoniphilus, Propionibacterium acnes, Dorea, and Ruminococcus and reduced proportions o

80 Neither resident- nor Proprionibacterium acnes-elicited peritoneal Mphi-induced PMN apoptosis.

81 egarding a multipronged approach by which P. acnes elicits inflammation in early versus late acne and

82 apenem and meropenem in a rabbit model of P. acnes endophthalmitis are warranted.

83 obial agents for use in a rabbit model of P. acnes endophthalmitis.

84 luding Bacillus anthracis, Propionibacterium acnes, Enterococcus faecalis, and both Methicillin-sensi

85 Furthermore, P. acnes exacerbated S. aureus-induced skin lesions in vivo

86 In contrast, P. acnes failed to sensitize to TLR2 ligands (peptidoglycan

87 new explanations about the development of C. acnes foreign-body infections.

88 Cutibacterium acnes (formerly Propionibacterium acnes) is recognized a

89 n period is necessary for the recovery of P. acnes from patients with PJI.

90 eported P. acnes strains and comparing 71 P. acnes genomes, we identified potential genetic determina

91 planted, and intravitreal cultures showed P. acnes growth after 5 days.

92 immune response targeting Propionibacterium acnes has a significant role in its pathogenesis.

93 Propionibacterium acnes has been identified as a significant agent of noso

94 e microaerophylic organism Propionibacterium acnes has shown consistent association with prostate can

95 Given at the moment of priming with P. acnes, IL-18BP-Fc decreases P. acnes-induced granuloma f

96 n advance with heat-killed Propionibacterium acnes, IL-18BP-Fc prevents LPS-induced liver damage and

97 ylococci in 6.0% (27/448), Propionibacterium acnes in 4.7% (21/448), and Pseudomonas aeruginosa in 3.

98 Moreover, peptide D-31-50v44w killed P. acnes in isolated human microcomedone preparations.

99 vation of peripheral blood monocytes with P. acnes in vitro induced their differentiation into two di

100 ossessing a helix-loop-helix motif killed P. acnes in vitro.

101 Furthermore, P. acnes induced expression of mRNA for the cytokines IL-15

102 Furthermore, P. acnes induced IL-12 and IL-8 protein production by prima

103 P. acnes induced key inflammasome genes including NLRP1 and

104 In vitro, we found that P. acnes induced MMP-9 and MMP-1 mRNA, and the expression o

105 Furthermore, P. acnes induced production of IFN-gamma in vivo as well as

106 P. acnes induced the mRNA expression of tissue inhibitors o

107 ts as demonstrated by suppression of some P. acnes-induced chemokines.

108 We investigated whether TLR2 mediates P. acnes-induced cytokine production in acne.

109 EA extract in mice effectively attenuated P. acnes-induced ear swelling and granulomatous inflammatio

110 onized with mouse ears, thereby relieving P. acnes-induced ear swelling and granulomatous inflammatio

111 iming with P. acnes, IL-18BP-Fc decreases P. acnes-induced granuloma formation, macrophage-inflammato

112 tralizing antibodies completely inhibited P. acnes-induced IL-17 production.

113 ssion by small interfering RNA attenuated P. acnes-induced IL-1beta secretion.

114 . var. abbreviata Ser.) on Propionibacterium acnes-induced inflammation and to identify the bioactive

115 uggest that NO-np can effectively prevent P. acnes-induced inflammation by both clearing the organism

116 inflammatory properties as they inhibited P. acnes-induced inflammatory cytokine production in human

117 Propionibacter acnes-induced intracutaneous inflammation showed no diff

118 n-expressing BM cells, we identified that P. acnes-induced liver inflammatory foci are of BM origin.

119 These data indicate that P. acnes-induced MMPs and TIMPs may be involved in acne pat

120 The mechanism of P. acnes-induced NLRP3 activation and subsequent IL-1beta s

121 that TLR9 and TLR2 mediate Propionibacterium acnes-induced sensitization to lipopolysaccharide-trigge

122 r vaccination against P. acnes suppressed P. acnes-induced skin inflammation.

123 in D (1,25-dihydroxyvitamin D3) inhibited P. acnes-induced Th17 differentiation.

124 Agak et al. report that Propionibacterium acnes induces IL-17 expression in peripheral blood monon

125 es; yet, the molecular mechanism by which P. acnes induces inflammation is not known.

126 Propionibacterium acnes induction of IL-1 cytokines through the NLRP3 (NLR

127 Propionibacterium acnes induction of inflammatory responses is a major eti

128 zed to endotoxin damage by Propionibacterium acnes infection.

129 , co-treatment of monocytes with ATRA and P. acnes inhibited MMP-9 and MMP-1 induction, while augment

130 fter heat-killed Propionibacterium acnes (P. acnes) injection into wild-type C57BL/6 (B6) mice or IFN

131 Propionibacterium acnes is a critical component in the pathogenesis of acn

132 Propionibacterium acnes is a key pathogen involved in the progression of i

133 Propionibacterium acnes is a key therapeutic target in acne, yet this bact

134 Propionibacterium acnes is a known cause of postneurosurgical meningitis;

135 Propionibacterium acnes is a major etiological factor of acne, triggering

136 he Gram-positive bacterium Propionibacterium acnes is a member of the normal human skin microbiota an

137 In this study, we have demonstrated that P. acnes is a potent inducer of T helper 17 (Th17) and Th1,

138 Propionibacterium acnes is a skin commensal bacterium that contributes to

139 Propionibacterium acnes is a well-known cause of delayed endophthalmitis f

140 Propionibacterium acnes is also associated with inflammatory acne vulgaris

141 portunistic human pathogen Propionibacterium acnes is composed of a number of distinct phylogroups, d

142 ACNES is hardly ever considered in the differential diag

143 Propionibacterium acnes is increasingly recognized as an important agent o

144 , and S. epidermidis growth indicate that P. acnes is the most sensitive to lauric acid among these b

145 ibacterium acnes (formerly Propionibacterium acnes) is recognized as a pathogen in foreign-body infec

146 The clinical P. acnes isolates also displayed high-level susceptibility

147 overy of nondiagnostic isolates: 21.7% of P. acnes isolates believed to be clinically unimportant wer

148 When applied to 312 P. acnes isolates previously characterized by MLST and repr

149 t detailed population genetic analysis of P. acnes isolates recovered from paired lesional and non-le

150 the phage was able to infect and lyse all P. acnes isolates tested.

151 Propionibacterium acnes isolates usually have relatively low virulence and

152 ogenic versus truly commensal lineages of P. acnes may exist.

153 nto CD209(+) macrophages and enhanced the P. acnes-mediated differentiation of the CD209(+) subset.

154 rium species (n = 15), and Propionibacterium acnes (n = 19) isolates; all of these isolates were reco

155 To date, the direct impact of C. acnes on bone cells has never been explored.

156 We showed a direct impact of C. acnes on bone cells, providing new explanations about th

157 tro susceptibilities of 23 Propionibacterium acnes ophthalmic isolates to ertapenem, meropenem, and c

158 uction was not detected in Propionibacterium acnes or in representative species of the Listeria, Stap

159 ient BM showed no inflammatory foci after P. acnes or TLR2+TLR9 challenge, suggesting that recruitmen

160 ) 7 days after heat-killed Propionibacterium acnes (P. acnes) injection into wild-type C57BL/6 (B6) m

161 mentation of glycerol with Propionibacterium acnes (P. acnes), a skin commensal bacterium, can functi

162 natural antibiotic against Propionibacterium acnes (P. acnes), which promotes follicular inflammation

163 roles of TLR2 and TLR4 in Propionibacterium acnes (P. acnes)-primed, LPS-induced liver damage using

164 ith AgP, Actinomyces oris, Propionibacterium acnes, P. aeruginosa, Staphylococcus aureus, and Strepto

165 along with the bacterium Proprionebacterium acnes, Pa, and transferred into wild-type mice.

166 in agreement with our conclusion that the P. acnes pan-genome is closed.

167 ive surgical procedure for pain reduction in ACNES patients who failed to respond to a conservative r

168 es of propionibacteria and Propionibacterium acnes phage in healthy skin.

169 Escherichia coli phage T3, Propionibacterium acnes phage PA6, and Streptococcus mitis phage SM1.

170 On the other hand, P. acnes phylotypes associated with healthy skin induced 2-

171 We found that acne-associated P. acnes phylotypes induced 2- to 3-fold higher levels of I

172 ur data provide insight into how specific P. acnes phylotypes influence immune responses and the path

173 Comparative proteomic analysis of P. acnes phylotypes revealed a differential expression of s

174 Importantly, a diagnosis of P. acnes PJI would have been missed in 29.4% of patients ha

175 Although specimens from P. acnes PJIs were more commonly associated with the presen

176 In vitro, P. acnes pretreatment desensitized RAW macrophages to a sec

177 TLR2 and TLR4 in Propionibacterium acnes (P. acnes)-primed, LPS-induced liver damage using selective

178 ter low-dose (20 microg) LPS challenge in P. acnes-primed B6 mice was 100%, but 0% in GKO mice.

179 In vitro, P. acnes-primed Hepa 1-6 hepatocytes but not RAW macrophage

180 hese data suggest that IFN-gamma mediates P. acnes-primed low-dose LPS injury through the hepatic inf

181 In mice, P. acnes priming resulted in increased liver messenger RNA

182 In conclusion, P. acnes priming to selective TLR4-mediated liver injury is

183 In the liver, P. acnes-priming was associated with up-regulation of TLR4

184 te comparative genetic analyses in future P. acnes research.

185 ood acne, the emergence of Propionibacterium acnes resistance, and the rare but serious side effects

186 concentration (EC(50)) of lauric acid on P. acnes, S. aureus, and S. epidermidis growth indicate tha

187 e Th1 response inducing Ag Propionebacterium acnes, SEA-exposed DC exhibit a phenotype that is most s

188 C. acnes significantly decreased the resorption ability of

189 Incubation of the skin bacteria P. acnes, Staphylococcus aureus (S. aureus), and Staphyloco

190 s or phylotypes, including Propionibacterium acnes, Staphylococcus spp., and the opportunistic pathog

191 P. acnes stimulated expression of key Th17-related genes, i

192 ffects, as demonstrated by suppression of P. acnes-stimulated cytokine release.

193 Supernatants from P. acnes-stimulated PBMCs were sufficient to promote the di

194 atrix metalloproteinase (MMP)-9 levels in P. acnes-stimulated THP-1 cells.

195 r induction of TLR-2 expression following P. acnes stimulation.

196 e composition at the species level and at P. acnes strain level was more diverse than in healthy indi

197 ine of an early-colonizing Propionibacterium acnes strain similar to SK137 and the proliferation of n

198 blasts and osteoclasts than CC18 and CC28 C. acnes strains (p </= 0.05).

199 By sequencing 66 previously unreported P. acnes strains and comparing 71 P. acnes genomes, we iden

200 thy (PH) versus acne (PA) skin-associated P. acnes strains are currently unknown.

201 ting that more than 50% of Propionibacterium acnes strains are resistant to topical macrolides, makin

202 Almost all the P. acnes strains demonstrated E-test MICs within 2 dilution

203 potential genetic determinants of various P. acnes strains in association with acne or health.

204 strain-specific Th17 clones and show that P. acnes strains induce Th17 cells of varied phenotype and

205 in microbiome suggest that Propionibacterium acnes strains may contribute differently to skin health

206 Overall, our data suggest that P. acnes strains may differentially modulate the CD4(+) T-c

207 CC36 C. acnes strains were significantly less internalized by os

208 es in determining virulence properties of P. acnes strains, and some could be future targets for ther

209 ce of antibiotic-resistant Propionibacterium acnes strains.

210 Staphylococcus aureus, and Propionibacterium acnes strains.

211 We examined whether vaccination against P. acnes suppressed P. acnes-induced skin inflammation.

212 The catalogued data and the public P. acnes Sybil database provide a solid foundation for gene

213 proach for developing antibiotics against P. acnes that are effective in cutaneous environments.

214 analysis of 90 genomes of Propionibacterium acnes that represent the known diversity of the species.

215 activity in vitro against Propionibacterium acnes, the bacterium linked to the pathogenesis of acne.

216 in part to the ability of Propionibacterium acnes to activate TLR2.

217 Bacteriophage PA6 is the first phage of P. acnes to be sequenced and demonstrates a high degree of

218 C57BL/6 mice treated with Propionibacterium acnes to elicit high levels of macrophage-derived NO hav

219 Data concerning susceptibility of P. acnes to newer beta-lactam antibiotics and fluoroquinolo

220 t links the skin bacterium Propionibacterium acnes to the condition.

221 time course of P. chabaudi parasitemia as P. acnes-treated NOS20/0 mice, which do not produce NO; thi

222 Taken together, our results indicate that P. acnes triggers a key inflammatory mediator, IL-1beta, vi

223 These data suggest that P. acnes triggers inflammatory cytokine responses in acne b

224 lus species (type IV), and Propionibacterium acnes (type V).

225 ed biofilms, and these dispersion-induced P. acnes VP1 biofilms showed increased expression of mRNAs

226 P. acnes was found to be highly sensitive to all concentrat

227 supernatant of a strain of Propionibacterium acnes was investigated for its phospholipase (PL) activi

228 All subjects from whom P. acnes was isolated from sonicate fluid were male.

229 of 15 carotid artery samples, and viable P. acnes was one among 10 different bacterial species recov

230 Propionibacterium acnes was the commonest species detected among culture-p

231 tiple clinical isolates of Propionibacterium acnes, we have produced a draft genome sequence of a nov

232 ents older than 18 years with a diagnosis of ACNES were randomized to undergo a neurectomy or a sham

233 and proteolytic extracellular enzymes by P. acnes were shown to increase in iron-induced dispersed b

234 that although the relative abundances of P. acnes were similar, the strain population structures wer

235 hylococcus epidermidis and Propionibacterium acnes, were identified in bacteriologically investigated

236 microbial activity against Propionibacterium acnes, whereas the enhanced antimicrobial activity of hu

237 tibiotic against Propionibacterium acnes (P. acnes), which promotes follicular inflammation (inflamma

238 Inactivation of P. acnes with heat was employed to create a P. acnes-based

239 ld male with de novo meningitis caused by P. acnes with metastatic melanoma as the only identified ri

240 ization, and the action of Propionibacterium acnes within the follicle.

241 he pathogenesis of acne is Propionibacterium acnes; yet, the molecular mechanism by which P. acnes in