ライフサイエンスコーパス: skin infection

1 may enhance susceptibility to staphylococcal skin infection.

2 ilm in vivo in a murine model of superficial skin infection.

3 utrophils were dispensable for resistance to skin infection.

4 pathogenesis of the DeltafakA mutant during skin infection.

5 masome activation and immunopathology during skin infection.

6 lammation in a mouse model of staphylococcal skin infection.

7 olling the host innate response to S. aureus skin infection.

8 cally to clear vaccinia virus from a primary skin infection.

9 hogenicity of herpes simplex virus type 1 in skin infection.

10 s; 42.1% women), 22.0% reported a history of skin infection.

11 lence of USA300 in necrotizing pneumonia and skin infection.

12 key source of IL-17 in the early hours after skin infection.

13 ntion for individuals with a disseminated VV skin infection.

14 rodent models of CA-MRSA USA300 pneumonia or skin infection.

15 d with increased dermonecrosis in a model of skin infection.

16 n rodent models of necrotizing pneumonia and skin infection.

17 e lesion size in a murine model of S. aureus skin infection.

18 ce in a humanized mouse model of superficial skin infection.

19 mouse model was used to measure superficial skin infection.

20 che, while Vsp2 is associated with blood and skin infection.

21 S virulence in a murine model of necrotizing skin infection.

22 ial function in the diagnosis and therapy of skin infection.

23 of its role in the pathogenesis of S. aureus skin infection.

24 ht into how vitamin A promotes resistance to skin infection.

25 min A deficiency increases susceptibility to skin infection.

26 esions than the wild type (WT) during murine skin infection.

27 quired for vitamin-A-dependent resistance to skin infection.

28 trophils and increasing tissue damage during skin infection.

29 ss-reactive immune responses occur following skin infection.

30 cause systemic infection in a mouse model of skin infection.

31 romote host innate defense against S. aureus skin infection.

32 diathesis, and increased susceptibility for skin infections.

33 ing, as evident in both in vitro and in vivo skin infections.

34 al agent for the treatment of staphylococcal skin infections.

35 as a dose-response relationship was seen for skin infections.

36 evaluated in a mouse model of staphylococcal skin infections.

37 Exophiala species are mostly responsible for skin infections.

38 in as a topical antibacterial agent to treat skin infections.

39 common colonizer of persons with and without skin infections.

40 erbation and flare, and preventing secondary skin infections.

41 evelopment, disease chronicity, or recurrent skin infections.

42 antimicrobials currently used to treat MRSA skin infections.

43 which in turn impairs control of herpesvirus skin infections.

44 ibed a role in immunity after resolved viral skin infections.

45 rmal barrier defects and recurrent microbial skin infections.

46 s and a propensity for Staphylococcus aureus skin infections.

47 most common organism isolated from purulent skin infections.

48 taphylococcus aureus is the leading cause of skin infections.

49 ylococcus aureus (MRSA) is a common cause of skin infections.

50 rtant antiviral granule component in in vivo skin infections.

51 ccines designed to moderate severe S. aureus skin infections.

52 could provide a platform for studying human skin infections.

53 hogenesis in mouse models of lung and burned skin infections.

54 ome evidence to suggest an increased risk of skin infections.

55 , which also increases the risk of recurrent skin infections.

56 re, an effective option for the treatment of skin infections.

57 ta4(+) T cells in immunity against S. aureus skin infections.

58 nges remain in diagnosing and treating acute skin infections.

59 coccus (GAS) commonly causes pharyngitis and skin infections.

60 is responsible for the majority of bacterial skin infections.

61 non-biocide virulence inhibitors in treating skin infections.

62 A safety outcome was number of skin infections.

63 fections (UTIs, 1.41; 95% CI, 1.35 to 1.45), skin infections (1.50; 95% CI, 1.45 to 1.55), septicemia

64 ds ratio 6.21, 95% CI 3.25-11.85), recurrent skin infections (2.87, 1.10-7.45), and severe pneumonia

65 promoter showed increased resistance to GAS skin infection (50% smaller necrotic ulcers and 60% fewe

66 In a model of MRSA skin infection, ACE 10/10 mice had 50-fold less bacteria

67 moisturizer often used in the prevention of skin infections after ambulatory surgeries and as a main

68 Although a common cause of community-onset skin infections among Indigenous populations in northern

69 component alone is ineffectual in preventing skin infection and bacteremia due to CovR/S mutants but

70 matory skin disease associated with frequent skin infection and impaired skin barrier function.

71 n and p300/CBP binding are important for VZV skin infection and may be targeted for antiviral drug de

72 he diabetic environment influences S. aureus skin infection and observed an increased susceptibility

73 ciated with niche-specific infections, i.e., skin infection and pharyngitis-induced acute rheumatic f

74 ve strain in murine models of staphylococcal skin infection and pneumonia, we expanded upon recent st

75 at staphylococcal alpha-toxin promotes viral skin infection and provides a mechanism by which S aureu

76 CA-MRSA PSMs contribute to skin infection and recruit and lyse neutrophils, and tru

77 Staphylococcus aureus is a frequent cause of skin infection and sepsis in humans.

78 nate susceptibility to Staphylococcus aureus skin infection and that bone marrow neutrophils (BMN) fr

79 that liver infection is predicated on severe skin infection and that death requires significant liver

80 ration can persist after resolution of local skin infection and that the cytokine environment within

81 the ORF25 deleted virus infects fish through skin infection and then spreads to internal organs as re

82 Skin infections and acute skin breakdown were common amo

83 MCG-2 strains were mostly obtained from skin infections and affected patients with a mean age of

84 of disease manifestations from pulmonary to skin infections and are notoriously difficult to treat,

85 disseminated systemic diseases, particularly skin infections and arthritis in severely immunocompromi

86 and higher rates of both secondary bacterial skin infections and genital ulcers.

87 ayer in cutaneous innate immune responses to skin infections and injury.

88 s aureus (MRSA) has become a common cause of skin infections and invasive infections in community dwe

89 reat potential for topical treatment of MRSA skin infections and lays the foundation for further anal

90 ts role against bacterial strains related to skin infections and mechanism of action is not well unde

91 We investigated whether skin infections and nasal colonization in travelers cont

92 Skin infections and previous infection or inflammation o

93 rovide new insights into the pathogenesis of skin infections and suggest potential roles for MCs and

94 s and children after treatment for S. aureus skin infections and their household contacts in Los Ange

95 study of adults and children with S. aureus skin infections and their household contacts in Los Ange

96 ain developed fatal sepsis, extensive tissue skin infection, and abscess-forming deep-seeded thigh mu

97 ng PLHIV, recent injection drug use, current skin infection, and HIV care at outpatient clinic A that

98 patients, recent injection drug use, current skin infection, and HIV care at outpatient Clinic A that

99 itis, joint surgery, hip or knee prosthesis, skin infection, and human immunodeficiency virus type 1

100 tamine use, unstable housing, current/recent skin infection, and recent injection drug use were predi

101 tamine use, unstable housing, current/recent skin infection, and recent injection drug use were predi

102 bscess, abscess size, the number of sites of skin infection, and the presence of nonpurulent cellulit

103 cluding overnight hospitalization, recurrent skin infections, and similar infection in household cont

104 l produce large SAg numbers, consistent with skin infections, and that certain SAgs will be overrepre

105 kin (IL)-6 autoantibodies and staphylococcal skin infection; and anti-IL-17A, anti-IL-17F, or anti-IL

106 (aOR 1.19), age >85 years (aOR 1.17), prior skin infection (aOR 1.14), recent high white blood cell

107 ew, skin anatomy and its barriers along with skin infection are discussed.

108 nitiation and termination of inflammation in skin infection are incompletely understood.

109 linking epidermal barrier defects and viral skin infection are not well understood.

110 Bacterial skin infections are a major societal health burden and a

111 Skin infections are frequently caused by Staphylococcus

112 gh their roles in immunity against localized skin infections are less well defined.

113 Group A Streptococcus (GAS) skin infections are particularly prevalent in developing

114 he dual roles of staphylokinase in S. aureus skin infections as promoting the establishment of infect

115 in identifying acceptable levels of risk for skin infections associated with sand exposures.

116 .2 percentage points; 95% CI, -8.2 to -2.2), skin infections at new sites (3.1% vs. 10.3%; difference

117 Among 588 household contacts, 10% reported a skin infection by month 3 and 13% by month 6.

118 soprostol improved host defense against MRSA skin infection by restoring DC migration to draining lym

119 as targeting the Hla might prevent invasive skin infection by staphylococci.

120 mice, which have increased susceptibility to skin infection by Streptococcus.

121 that enables CA-MRSA to produce necrotizing skin infections by allowing the bacteria to escape from

122 patients are prone to chronic bacteremia and skin infections by Helicobacter and related species such

123 y and are important for host defense against skin infections by some bacterial and viral pathogens.

124 on of C57BL/6 mice, impairs the clearance of skin infections by Streptococcus pyogenes and Staphyloco

125 We report here a case of disseminated skin infection caused by Mucor velutinosus, a recently d

126 Skin infections caused by bacteria, viruses and fungi ar

127 osum virus, a dermatotropic poxvirus causing skin infections common in children and immunocompromised

128 gher in patients with established B. garinii skin infection compared to patients with other Borrelia

129 iotic-induced expression of mecA during MRSA skin infection contributes to immunopathology by alterin

130 t of skin breakdown and early recognition of skin infection could prevent iGAS infections in these pa

131 However, skin infection decreased Mphi half-life, thereby limitin

132 ts, skin puncture, extreme temperatures, and skin infections-eg, cellulitis) increase the risk of bre

133 beta-lactam treatment of MRSA skin infection exacerbates immunopathology, which is IL-

134 A murine MRSA skin infection experiment confirmed that simvastatin sig

135 For skin infections, Florida had higher risk-adjusted revisi

136 of sepsis was greatest for UTI, followed by skin infection, followed by RTI.

137 These models also support human skin infection following intradermal inoculation with co

138 cormycosis with a high prevalence of primary skin infection following trauma and a prognosis signific

139 in mice that localized vaccinia virus (VACV) skin infection generates long-lived non-recirculating CD

140 reus (MRSA) in the United States, visits for skin infections greatly increased.

141 Patients with AD with skin infections had higher CD4(+) IL-22(+) and IL-17(+)

142 isms that provide durable protection against skin infections has the potential to guide the developme

143 ctious disease, particularly with respect to skin infection, has not been addressed.

144 Revisit rates varied by diagnosis, with skin infections having the highest rate (23.1% [95% CI,

145 +) skin T(RM) cells are both generated after skin infection; however, CD8(+) T(CM) cells recirculate

146 A history of skin infection identified a state of enhanced susceptibi

147 analog isotretinoin, which protected against skin infection in a RELMalpha-dependent manner.

148 We report a case of Macrophomina phaseolina skin infection in an immunocompromised child with acute

149 plex virus (HSV-1) is a major cause of viral skin infection in humans.

150 ctional PTS is not required for subcutaneous skin infection in mice; however, it does play a role in

151 oup A Streptococcus pyogenes (GAS) cutaneous skin infection in mice; this was accompanied by increase

152 site, antibiotic use in the prior year, and skin infection in the prior 3 months.

153 L), could account for the high rates of MRSA skin infection in this region.

154 ia formation translated to severely impaired skin infection in vivo.

155 protein E genes, and the pathogenesis of VZV skin infection in vivo.

156 letion reduced cell-cell spread in vitro and skin infection in vivo.

157 envelopment, efficient cell-cell spread, and skin infection in vivo.

158 e recovered from patients with uncomplicated skin infections in 10 different countries during five ph

159 rapidly and specifically diagnose bacterial skin infections in a contact-less manner, allowing for i

160 This outbreak of MRSA skin infections in an otherwise-healthy, well-defined, m

161 Recurrent skin infections in extrinsic atopic dermatitis (EAD) may

162 by S. aureus, promoted the establishment of skin infections in humans and increased bacterial penetr

163 temic disease in fish but produces localized skin infections in humans.

164 (Hla) contributes to the severity of USA300 skin infections in mice and determined whether vaccinati

165 Agr contribute to the pathogenesis of USA300 skin infections in rabbits, whereas a role for PVL could

166 o have increased exposure to antibiotics and skin infections in the home.

167 tem has a crucial role in the development of skin infections in the most prevalent CA-MRSA strain USA

168 ng the prevention and treatment of bacterial skin infections in the newborn period.

169 ertenue and another bacterium known to cause skin infections in the Pacific islands-Haemophilus ducre

170 Emergency department visits for skin infections in the United States have increased with

171 ely absent, perhaps accounting for recurrent skin infections in this disease.

172 profile, for the treatment of uncomplicated skin infections, including both cellulitis and abscesses

173 itive and gram-negative pathogens that cause skin infections, including those resistant to other anti

174 ctive against resistant pathogens that cause skin infections-including dalbavancin, tedizolid phospha

175 Staphylococcus aureus skin infection is a frequent and recurrent problem in ch

176 Thus, the clinical severity of S. aureus skin infection is driven by the inflammatory response to

177 ontribution in a murine model of necrotizing skin infection is largely driven by its ability to neutr

178 for the life cycle of the virus because VZV skin infection is necessary for viral transmission and p

179 s), but whether they target hookworms during skin infection is unknown.

180 at contribute to the pathogenesis of CA-MRSA skin infections is incomplete.

181 The US burden of acute skin infections is substantial.

182 rrow-derived monocytes during staphylococcal skin infection leading to transiently increased resistan

183 To recapitulate the various types of human skin infections, many different mouse models have been d

184 population, exposure to alpha-toxin through skin infection may modulate the establishment of T cell-

185 trate that MC presence protects mice from VV skin infection, MC degranulation is required for protect

186 In a murine skin infection model, an insertion mutation in the respo

187 Using a murine skin infection model, we compared T helper cell response

188 Using a Candida albicans skin infection model, we have shown that direct presenta

189 ly supported in studies using a low-inoculum skin infection model, where low levels of PVL augmented

190 the size of lesions caused by S. aureus in a skin infection model.

191 vival on skin was tested in an adapted mouse skin infection model.

192 -1 human keratinocyte cell line and a rabbit skin infection model.

193 models; an acute lung infection model and a skin infection model.

194 a high-density Staphylococcus aureus murine skin infection model.

195 and suppresses microbial growth in a topical skin infection model.

196 S. aureus virulence was studied in a murine skin infection model.

197 To this end, mouse skin infection models allow researchers to examine host

198 In this article, we will describe these skin infection models in detail along with their advanta

199 f vancomycin in MRSA mouse and human ex vivo skin infection models, with no acute in vivo toxicity in

200 d had reduced virulence in murine sepsis and skin infection models.

201 In an S. aureus skin infection mouse model, we found that the IL-17 resp

202 y against HSV-1 was examined using the flank skin infection mouse model.

203 ct in the previous month with someone with a skin infection; multiple infiltrates or cavities on ches

204 nage) and matched control subjects without a skin infection (n = 147 each) presenting to 10 U.S. emer

205 dache (n=1 [2%]), lung infection (n=1 [2%]), skin infection (n=1 [2%]), pleural effusion (n=1 [2%]),

206 Skin infections (n = 103) were reported from 67 individu

207 Although most strains caused severe skin infection, not every strain caused systemic infecti

208 Skin infections occurred in 36/142 (25%) and 39/141 (28%

209 Adverse events, such as skin infection, occurred more frequently with placebo; n

210 d having a roommate in training with a prior skin infection (odds ratio [OR] = 3.44) or having a fami

211 a (odds ratio, 0.76 [CI, 0.64 to 0.91]), and skin infections (odds ratio, 0.64 [CI, 0.46 to 0.89]).

212 0.77], P < .001), and receiving services for skin infections or endocarditis (adjusted ORs: HIV, 0.91

213 ecially male rural residents with claims for skin infections or endocarditis, commonly associated wit

214 verse events such as hypo/hyperpigmentation, skin infection, or recurrence were reported.

215 During a CO-MRSA skin infection outbreak in Alaska, we assessed risk fact

216 se in the incidence of outpatient visits for skin infections, peaking in 2010-2013, followed by a pla

217 Mean number of skin infections per child in year 1 was 0.23 (SD 0.68) i

218 are prescribed commonly and increasingly for skin infections, perhaps due, in part, to lack of experi

219 oorly understood whether localized S. aureus skin infections persistently alter the resident Mphi sub

220 s causes a variety of human diseases such as skin infections, pneumonia, and endocarditis.

221 e aetiological agent of both respiratory and skin infections, produces numerous exotoxins to establis

222 s recombinant IL-17A injected at the site of skin infection promoted more rapid healing of candidiasi

223 ose that the production of SLS by GAS during skin infection promotes invasive outcomes by triggering

224 In skin infections, R1 at 64 muM was the most effective var

225 te, diabetes, recent hospitalization, recent skin infection, recent cephalexin use, and household S.

226 pe colonizing household contacts were recent skin infection, recent cephalexin use, and USA300 geneti

227 de calculation suggests that 155 000-540 000 skin infections related to IDU occur annually.

228 Another review on severe staphylococcal skin infections reminds us of the importance of covering

229 Staphylococcus aureus skin infections represent a significant public health th

230 ential for the development of bacteremia and skin infection, representing major types of acute S. aur

231 ocompromised mice might be used in bacterial skin infection research.

232 ells generated as a result of localized VACV skin infection reside not only in the site of infection,

233 3.1% for those with and without a history of skin infection, respectively (unadjusted hazard ratio (H

234 sed approaches to protect against Hla during skin infection restored the T cell response.

235 Bacterial skin infections result in significant morbidity and have

236 and control mice had similar GAS numbers at skin infection sites and similar abilities to select Spe

237 obust neutrophil infiltration at the edge of skin infection sites and throughout infection sites at 2

238 aused changes in the histological pattern at skin infection sites could be complemented.

239 Skin infection sites of streptolysin S-deficient MGAS222

240 , while there was no MGAS2221 clearance from skin infection sites.

241 g the genotypic biomarkers for throat versus skin infection specialists.

242 In skin infections, SPMs enhanced vancomycin clearance of S

243 ration) and larger lesion size in a model of skin infection (subcutaneous administration).

244 response against Staphylococcus aureus (SA) skin infection substantially improved systemic host defe

245 oth forms of AD have increased propensity to skin infection, suggesting a novel mechanism for infecti

246 skin neutrophils and are prone to bacterial skin infections, suggesting that allergic inflammation c

247 to determine colonization at enrollment, and skin infection swabs over 17 months were assessed for S.

248 By examining the relationships between skin infection, systemic liver infection, and presumptiv

249 etes are more prone to Staphylococcus aureus skin infection than healthy individuals.

250 the expression of hasA than spyCEP in mouse skin infection than wild-type GAS did.

251 m is a potentially fatal, disseminated viral skin infection that develops in individuals with atopic

252 eczema vaccinatum (EV), a disseminated viral skin infection that follows inoculation with vaccinia vi

253 e evidence using a murine model of S. aureus skin infection that the effects mediated by rsr reduce d

254 immune response, and susceptibility to viral skin infections that are normally restrained by a T(H)1

255 Acute skin infections that involve mixed gram-positive and gra

256 trains have been known to be associated with skin infections, the Nudix hydrolase and its associated

257 We hypothesized that MC help protect against skin infection through the expression of cathelicidin.

258 ing the initiation and progression from mild skin infection to a severe disseminated infection remain

259 During the transition from a throat or skin infection to an invasive infection, GAS must adapt

260 We used a mouse model of skin infection to compare the virulence of methicillin-r

261 hylococcus infections range from superficial skin infections to deep-seated invasive infections such

262 ide spectrum of diseases, ranging from minor skin infections to fatal necrotizing pneumonia.

263 ns, causing infections from mild superficial skin infections to lethal bacteremia and endocarditis.

264 any infectious diseases, ranging from benign skin infections to life-threatening endocarditis and tox

265 humans, from relatively mild pharyngitis and skin infections to life-threatening necrotizing fasciiti

266 es an array of infections ranging from minor skin infections to more serious infections, including os

267 nother acute care hospital varied from 1.3% (skin infection) to 5.1% (septicemia).

268 The response to VV skin infection under conditions of TNF-alpha deficiency,

269 rsus those without a past medical history of skin infection using Cox proportional hazards models.

270 e of and species responsible for a bacterial skin infection using differences in Mie scatter spectra

271 78 (1,966-2,686) in women; the NNT following skin infection was 503 (398-646) in men and 784 (602-1,0

272 This defect in adaptive immunity following skin infection was associated with a loss of DCs, attrib

273 cell responses, we demonstrated that primary skin infection was associated with impaired development

274 in-resistant Staphylococcus aureus (CA-MRSA) skin infections was observed in a population of U.S. mil

275 In a mouse model of S. aureus skin infection, we found that lesion size did not correl

276 In contrast to previous findings of skin infection, we observed that clearance of SA from th

277 odel for infection that closely mimics human skin infection, we show that the vaccine can protect aga

278 ntacts, independent predictors of subsequent skin infection were Chicago site, antibiotic use in the

279 ongitudinal study, patients with a S. aureus skin infection were more likely to suffer a recurrence i

280 Recurrent skin infections were common, particularly in childhood (

281 Skin infections were more common in Thailand (P = .001),

282 Skin infections were more common in Thailand (P=0.001) w

283 increased neutrophil recruitment and reduced skin infection, whereas in trans expression of SsE(M28)

284 Deletion of ORF12 had no effect on skin infection, whereas replication of POKADelta11, POKA

285 We enrolled outpatients with uncomplicated skin infections who had cellulitis, abscesses larger tha

286 munity, comparing 34 case patients with MRSA skin infection with 94 control subjects.

287 ealing and decreased IL-17A production after skin infection with C. albicans compared with wild-type

288 g epicutaneous sensitization with hapten and skin infection with Candida albicans.

289 In this study, we used a skin infection with HSV-1 characterized by the successiv

290 Using a murine model that supports extensive skin infection with Leishmania donovani, spatial analyse

291 At 8 months after surgery, the patient had a skin infection with phaeohyphomycosis due to Alternaria

292 Furthermore, treatment of a USA300 MRSA skin infection with retapamulin ointment resulted in up

293 istant S. aureus strains most commonly cause skin infections with abscess formation.

294 to expedite specific treatment of bacterial skin infections with narrow-spectrum antibiotics, rather

295 pneumonias; recurrent Staphylococcus aureus skin infections with otitis externa; recurrent, severe h

296 This review examines neonatal bacterial skin infections with respect to host immunity, bacterial

297 Skin infections with ulceration are a major health probl

298 Using skin infections with vaccinia virus (VacV)-expressing mo

299 nificantly attenuated in our animal model of skin infection, with significant reductions observed in

300 aviruses (HPVs) cause near ubiquitous latent skin infection within long-lived hair follicle (HF) kera