ライフサイエンスコーパス: acnes

1 fection, notably Propionibacterium acnes (P. acnes).

2 nterior cutaneous nerve entrapment syndrome (ACNES).

3 ain fatty acids known to be produced from C. acnes.

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

5 to the commensal bacterium Propionibacterium acnes.

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

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

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

9 vity against S. aureus and Propionibacterium acnes.

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

11 cine provoked specific antibodies against P. acnes.

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

13 ultiple factors, including Propionibacterium acnes.

14 rmation on the actions of Proprionibacterium acnes.

15 -regulated monocyte cytokine induction by P. acnes.

16 riostatic antibiotics in their control of P. acnes.

17 y proteases and more effective in killing P. 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 acne and mouse skin lesions infected with C. acnes.

22 ams per milliliter against Propionibacterium acnes.

23 sociation with human commensal Cutibacterium acnes.

24 a coli., and 12 mm against Propionibacterium acnes.

25 e development of new treatments targeting C. acnes.

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

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

28 nes secreted molecules sufficient to kill P. acnes.

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

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

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

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

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

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

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

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

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

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

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

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

41 validated that AMTH17-mediated killing of C. acnes and bacterial pathogens was dependent on the secre

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

43 Propionibacterium acnes and coagulase-negative Staphylococcus species were

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

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

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

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

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

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

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

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

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

53 Culture supernatants from C. acnes and other species of Cutibacteria inhibited S. epi

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

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

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

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

58 the natural skin flora (e.g., Cutibacterium acnes and Staphylococcus epidermidis).

59 he species level, dominated by Cutibacterium acnes and Staphylococcus epidermidis, yet each person ha

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

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

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

63 acne lesions to rein in the overgrowth of C. acnes at the onset of acne vulgaris.

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

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

66 We hypothesized that the C. acnes bacteria recovered at the time of revision shoulde

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

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

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

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

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

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

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

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

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

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

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

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

79 dant skin-resident microbe Propionibacterium acnes can influence cytokine expression from human seboc

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

81 Propionibacterium acnes, causative agent of chronic prostatitis possibly c

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

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

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

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

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

87 y increasing resistance of Propionibacterium acnes clinical isolates.

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

89 C acnes colonization of human skin requires the protein Ro

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

91 6 S. epidermidis-colonized screws; n = 26 C. acnes-colonized screws (covering all three main subspeci

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

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

94 a of 1116 patients suspected and treated for ACNES consistently showed the presence of the following

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

96 Both short chain fatty acids and C. acnes culture supernatant also increased sensitivity of

97 crobial richness, depletion of Cutibacterium acnes, Dermacoccus and Methylobacterium species, individ

98 crobial richness, depletion of Cutibacterium acnes, Dermacoccus and Methylobacterium species, individ

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

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

101 secutive patients who received the diagnosis ACNES during evaluation at the SolviMax Center of Excell

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

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

104 Diagnosing C acnes endocarditis is difficult due to its atypical pres

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

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

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

108 e airborne microorganisms, Propionibacterium acnes, Escherichia coli, Acinetobacter lwoffii, Lactobac

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

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

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

112 Cutibacterium acnes (formerly Propionibacterium acnes) is recognized a

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

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

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

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

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

118 Sequencing of C. acnes has been proposed as a potential rapid diagnostic

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

120 affect the growth of its parent bacteria C. acnes, hence is a potent fermentation metabolite that do

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

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

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

124 hese observations suggest the presence of C. acnes in a diverse microbial community with S. epidermid

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

126 ectus sheath block, may allow for diagnosing ACNES in patients with chronic abdominal pain.

127 d the magnitude of the immune response to P. acnes in the murine dermis by controlling neutrophil rec

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

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

130 eria on the skin revealed that Cutibacterium acnes induced a large increase in essential lipids inclu

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

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

133 P. acnes induced key inflammasome genes including NLRP1 and

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

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

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

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

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

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

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

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

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

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

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

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

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

147 Propionibacter acnes-induced intracutaneous inflammation showed no diff

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

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

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

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

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

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

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

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

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

157 Propionibacterium acnes induction of inflammatory responses is a major eti

158 zed to endotoxin damage by Propionibacterium acnes infection.

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

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

161 Five of the 17 rats in the C. acnes inoculated group were culture positive at euthanas

162 ACNES is a clinical diagnosis as no functional testing o

163 Cutibacterium acnes is a commensal bacterium on the skin that is gener

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

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

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

167 Propionibacterium acnes is a known cause of postneurosurgical meningitis;

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

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

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

171 Propionibacterium acnes is a skin commensal bacterium that contributes to

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

173 C acnes is also an emerging pathogen that frequently infec

174 Propionibacterium acnes is also associated with inflammatory acne vulgaris

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

176 ACNES is hardly ever considered in the differential diag

177 Propionibacterium acnes is increasingly recognized as an important agent o

178 However, it is well-known that C. acnes is not clonal on the skin of most individuals.

179 Cutibacterium acnes is one of the most common bacterial species on hum

180 Cutibacterium acnes is the most common bacterium associated with perip

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

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

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

184 Given that multiple subtypes of C. acnes isolates are present on and around the skin pilose

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

186 Clonality of C. acnes isolates from deep specimens from a potential peri

187 to consider whether further assessment of C. acnes isolates from the same joint should be performed a

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

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

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

191 Propionibacterium acnes isolates usually have relatively low virulence and

192 le samples that were culture positive for C. acnes, isolates from each sample were subjected to full

193 btilis group, Corynebacterium, Cutibacterium acnes, Lactobacillus, and Micrococcus), PPA and NPA rang

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

195 in this environment, we hypothesized that C. acnes may influence biofilm formation of S. epidermidis.

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

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

198 ve protein levels that were classified as C. acnes ODRI would be considered contaminations when accou

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

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

201 dermidis coexists with abundant Cutibacteria acnes on healthy human skin and does not typically form

202 l skin bacteria but was effective against C. acnes on pig skin and on mice.

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

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

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

206 Cutibacterium acnes orthopedic device-related infections (ODRIs) range

207 ) 7 days after heat-killed Propionibacterium acnes (P. acnes) injection into wild-type C57BL/6 (B6) m

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

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

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

211 cterial infection, notably Propionibacterium acnes (P. acnes).

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

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

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

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

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

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

218 Conspicuously, certain C. acnes phylotypes are associated with acne, whereas other

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

235 valve and prosthesis cultures positive for C acnes, retrieved from the medical microbiology databases

236 Clindamycin binding to the C. acnes ribosome interferes with both: proper orientation

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

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

239 C. acnes significantly decreased the resorption ability of

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

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

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

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

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

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

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

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

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

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

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

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

252 C. acnes strains are more stable and have a higher coloniza

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

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

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

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

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

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

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

260 Cutibacterium (previously Propionibacterium) acnes strains, and compare outcomes with non-inoculated

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

262 ce of antibiotic-resistant Propionibacterium acnes strains.

263 Staphylococcus aureus, and Propionibacterium acnes strains.

264 bited biofilm formation and, similarly to C. acnes supernatant, reduced polysaccharide synthesis by S

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

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

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

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

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

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

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

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

273 perate with the skin commensal Cutibacterium acnes to induce IL-36gamma in keratinocytes via the comb

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

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

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

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

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

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

280 that short-chain fatty acids produced by P. acnes under environmental conditions that favor fermenta

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

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

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

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

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

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

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

288 Up to four different subtypes of C. acnes were observed in the deep tissues of a single pati

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

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

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

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

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

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

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

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

297 E12) that selectively inhibited growth of C. acnes with potency greater than antibiotics commonly use

298 tients, 5 (45%) had different subtypes of C. acnes within the deep tissues even though the colony mor

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

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