ライフサイエンスコーパス: M. pneumoniae

1 M. pneumoniae caused a community-wide outbreak of cough

2 M. pneumoniae HA mutant II-3 lacking P30 was nonmotile,

3 M. pneumoniae induced the generation of prostaglandins P

4 M. pneumoniae infection is associated with GBS, more fre

5 M. pneumoniae possesses a cytoskeleton-like structure re

6 M. pneumoniae significantly activated SHP-1 in airway ep

7 M. pneumoniae was associated with the increased synovial

8 M. pneumoniae was cultured directly from sibling 2 autop

9 M. pneumoniae was detected by PCR in 10 of 18 asthmatics

10 M. pneumoniae was detected by PCR in 10 students with pn

11 M. pneumoniae was detected by real-time PCR in 175 (5.8%

12 M. pneumoniae was detected in bronchoalveolar lavage flu

13 M. pneumoniae was present in the lower airways of chroni

14 M. pneumoniae-infected macrophages deficient for inflamm

15 M. pneumoniae-infected mice treated with IL-12 (MpIL12 m

16 A retrospective analysis of 154 M. pneumoniae clinical isolates collected over the last

17 We examined 199 M. pneumoniae-positive specimens collected during this t

18 er surfaces of both wild-type and mutant I-2 M. pneumoniae but to a considerably lesser extent in the

19 This assay correctly identified 36 M. pneumoniae reference strains and clinical isolates fr

20 Furthermore, we screened over 3,500 M. pneumoniae transposon mutants individually to identif

21 glyA, atpA, arcC, and adk) and applied to 55 M. pneumoniae clinical isolates and the two type strains

22 l of 12 sequence types (STs) resulted for 57 M. pneumoniae isolates tested, with a discriminatory ind

23 Anti-TLR2 antibody completely abolished M. pneumoniae-induced AA release and TNFalpha secretion

24 s, SHP-1 plays a critical role in abrogating M. pneumoniae-induced IL-8 production in nonasthmatic ai

25 munologic and therapeutic responses to acute M. pneumoniae infection.

26 After M. pneumoniae lung infection, Muc18(-/-) mice exhibited

27 rts for analysis of serum antibodies against M. pneumoniae (n = 479) and GalC (n = 198).

28 All M. pneumoniae specimens (n=12) and isolates (n=10) were

29 Although M. pneumoniae was detected in schools, its transmission

30 An M. pneumoniae mini-Tn4001-integrated, clpB-null mutant w

31 notypic consequences when introduced into an M. pneumoniae topJ mutant.

32 We recently reported that an M. pneumoniae-derived ADP-ribosylating and vacuolating t

33 underscoring the correlation between crl and M. pneumoniae cytadherence.

34 nia; 5 of these specimens were cultured, and M. pneumoniae was isolated in 4.

35 sed separately and in combination to ETS and M. pneumoniae for 16 weeks.

36 n combination to cigarette smoke extract and M. pneumoniae for 48 h had elevated apical levels of GSH

37 ctionally related genes in M. genitalium and M. pneumoniae are often preceded by promoters but rarely

38 /c mice were anesthetized with metofane, and M. pneumoniae was introduced intranasally on days 0, 1,

39 cobacterium tuberculosis, S. pneumoniae, and M. pneumoniae were the most common etiologic agents.

40 Anti-M. pneumoniae immunoglobulin (Ig) M antibodies were dete

41 mens (< 10 per batch) submitted for IgM anti-M. pneumoniae testing.

42 Serum anti-M. pneumoniae immunoglobulin G titers were positive in a

43 Serum anti-M. pneumoniae immunoglobulin G was detectable in all of

44 Anti-GalC antibodies correlated with anti-M. pneumoniae antibodies (p < 0.001) and cross-reacted w

45 viously, we reported that surface-associated M. pneumoniae elongation factor Tu (EF-Tu, also called M

46 cerevisiae chromosome III and IV, bacterium M. pneumoniae, human major histocompatibility complex se

47 were found to have significantly higher BAL M. pneumoniae concentrations than those of M. pneumoniae

48 e were found to have significantly lower BAL M. pneumoniae concentrations compared with M. pneumoniae

49 ed quantitative bronchoalveolar lavage (BAL) M. pneumoniae culture, lung histopathologic score (HPS),

50 ed quantitative bronchoalveolar lavage (BAL) M. pneumoniae culture, lung histopathologic scores (HPS)

51 this study we describe interactions between M. pneumoniae and human surfactant protein-A (hSP-A).

52 321Q and N323D substitutions, failed to bind M. pneumoniae lipids, directly implicating the carbohydr

53 l cells, and these increases were blocked by M. pneumoniae and were also associated with increased ce

54 roduced effects similar to those elicited by M. pneumoniae in macrophages by inducing the phosphoryla

55 mechanism of mucin overproduction induced by M. pneumoniae remains unclear.

56 In asthmatic airway epithelial cells, M. pneumoniae induced significant PI3K/Akt phosphorylati

57 nd polymerase chain reaction (PCR)-confirmed M. pneumoniae infection were eligible for inclusion.

58 By contrast, M. pneumoniae persisted in the respiratory tract for the

59 e represents a superior target for detecting M. pneumoniae DNA in clinical specimens, although use of

60 assay is a useful rapid method for detecting M. pneumoniae in clinical specimens.

61 (p < 0.001) and cross-reacted with different M. pneumoniae strains.

62 cle, we show that the absence of SP-A during M. pneumoniae infection leads to increased numbers of ma

63 piratory specimens (n = 72) collected during M. pneumoniae outbreaks and sporadic cases occurring in

64 in maintenance of airway homeostasis during M. pneumoniae pulmonary infection by preventing an overz

65 is important for the immune response during M. pneumoniae acute infection.

66 lammation and BHR by reducing or eliminating M. pneumoniae in lungs.

67 The lack of IL-12 in experimental M. pneumoniae pneumonia was associated with less severe

68 Treatment of experimental M. pneumoniae pneumonia with intranasal IL-12 was associ

69 xtension analysis with E. coli RNA from five M. pneumoniae clones and two M. genitalium clones indica

70 y of 0.006 CFU and a specificity of 100% for M. pneumoniae.

71 espiratory specimens previously cultured for M. pneumoniae, when real-time PCR with bidirectional seq

72 ELISA for serum IgM and immunoblots for M. pneumoniae antibody were positive in 21 (62%) of 34 a

73 imens submitted to clinical laboratories for M. pneumoniae serology.

74 of two separate pathogenetic mechanisms for M. pneumoniae-associated neurologic disease, one related

75 ltures, EIAs, and serology were negative for M. pneumoniae.

76 50% of whom are found to be PCR positive for M. pneumoniae.

77 lacks a systematic surveillance program for M. pneumoniae.

78 multilocus sequence typing (MLST) scheme for M. pneumoniae was developed based on the sequences of ei

79 because of the lack of a "gold standard" for M. pneumoniae serology.

80 a rapid, cost-efficient laboratory test for M. pneumoniae detection that is more widely available to

81 tudies demonstrate that the AcpS enzyme from M. pneumoniae, like E. coli enzyme, exhibits a homodimer

82 ical studies show that the AcpS enzymes from M. pneumoniae and S. pneumoniae can utilize both short-

83 nsion reactions with total RNA isolated from M. pneumoniae or M. genitalium.

84 Membranes and lipoproteins from M. pneumoniae induced a 4-fold increase in arachidonic a

85 emophilus influenzae, Mycoplasma genitalium, M. pneumoniae, and Synechocystis PCC 6803, as well as on

86 A total of 365 children had M. pneumoniae detected in the cerebrospinal fluid (CSF)

87 6%) and 57 students (75%), respectively, had M. pneumoniae infection.

88 A HindIII M. pneumoniae fragment containing the lambda MP 5B52 ins

89 produce classical toxins, and precisely how M. pneumoniae injures the respiratory epithelium has rem

90 However, M. pneumoniae was detected in 2/4 synovial biopsy specim

91 ccording to strength of evidence implicating M. pneumoniae.

92 In M. pneumoniae, transcription of the six genes terminates

93 (WT) mice to determine the role of IL-12 in M. pneumoniae respiratory disease.

94 in gliding in other organisms are absent in M. pneumoniae, random transposon mutagenesis was employe

95 ranscription-PCR analysis of this cluster in M. pneumoniae shows that mRNA levels for all six genes v

96 expression of p30 and an hmw3-cat fusion in M. pneumoniae, while deletion of the promoter-like regio

97 the cytadherence-associated protein HMW1 in M. pneumoniae.

98 s cognate phosphatase gene (prpC; MPN247) in M. pneumoniae resulted in significant and contrasting ef

99 gnized unique RepMP1 sequences found only in M. pneumoniae.

100 rmed ORF1 and ORF2 herein) conserved only in M. pneumoniae.

101 est that PrkC and PrpC work in opposition in M. pneumoniae to influence gliding frequency.

102 and assembly of the attachment organelle in M. pneumoniae are poorly understood, and no counterparts

103 ype, indicating an important role for P30 in M. pneumoniae biology.

104 red CARDS toxin mRNA and protein profiles in M. pneumoniae during distinct in vitro growth phases.

105 y elevated airway methacholine reactivity in M. pneumoniae-inoculated mice compared with that in cont

106 proteins having direct or indirect roles in M. pneumoniae cytadherence have been previously localize

107 and translational analyses of heat shock in M. pneumoniae indicated that clpB is significantly upreg

108 e proposed pathogenic role of CARDS toxin in M. pneumoniae-mediated pathologies.

109 (2)alpha (cPLA(2)alpha) completely inhibited M. pneumoniae-induced AA release from macrophages.

110 from immune cells suggest that SP-A inhibits M. pneumoniae-induced DC maturation by regulating HMGB-1

111 Interestingly, M. pneumoniae ClpB does not use dual translational start

112 Consistent with its M. pneumoniae counterpart, MGA_1199 (renamed PlpA) was d

113 ce of numerous copies of four distinct large M. pneumoniae repetitive elements (RepMPs).

114 Evidence links M. pneumoniae respiratory disease severity with interleu

115 Evidence links M. pneumoniae respiratory disease severity with interleu

116 that surfactant protein-A (SP-A) binds live M. pneumoniae and mycoplasma membrane fractions (MMF) wi

117 We reported earlier that surface-localized M. pneumoniae elongation factor Tu (EF-Tu(Mp)) mediates

118 e genomes of Mycoplasma genitalium (0.6 Mb), M. pneumoniae (0.8 Mb) and M. mycoides subspecies capri

119 Murine M. pneumoniae respiratory infection can lead to chronic

120 genes was detected in M. genitalium but not M. pneumoniae.

121 tance was identified in approximately 10% of M. pneumoniae infections occurring during this time peri

122 R or both identified four episodes (0.8%) of M. pneumoniae-associated illness and no episodes of C. p

123 , antagonized the proinflammatory actions of M. pneumoniae, Pam3Cys, and MALP-2 by reducing the produ

124 Analysis of M. pneumoniae-infected mouse lung tissue revealed high e

125 present study, we determined that binding of M. pneumoniae EF-Tu to Fn is primarily mediated by the E

126 ram is necessary to understand the burden of M. pneumoniae disease in the United States, facilitate c

127 oculated once intranasally with 10(7) CFU of M. pneumoniae.

128 xpand our understanding of the complexity of M. pneumoniae gliding and the identity of possible eleme

129 characterize the neurologic complications of M. pneumoniae in children using stringent diagnostic cri

130 , by its ability to reduce concentrations of M. pneumoniae in lung tissue.

131 The addition of SP-A to cultures of M. pneumoniae markedly attenuated the growth of the orga

132 e formation in detail in growing cultures of M. pneumoniae.

133 ay that enables rapid, low-cost detection of M. pneumoniae from nucleic acid extracts and directly fr

134 estations and IgM response, and detection of M. pneumoniae in the CSF, but not the respiratory tract.

135 sponse in peripheral blood, and detection of M. pneumoniae in the respiratory tract, but not the CSF,

136 A postmortem diagnosis of M. pneumoniae infection was obtained for the first patie

137 Disruption of M. pneumoniae open reading frame MPN311 results in loss

138 ter insight into the genetic distribution of M. pneumoniae strains.

139 The strain diversity of M. pneumoniae associated with this outbreak setting was

140 current understanding of the epidemiology of M. pneumoniae and may ultimately lead to a more effectiv

141 xist in multiple copies within the genome of M. pneumoniae.

142 nd specific method for the identification of M. pneumoniae and was helpful for the detection and moni

143 ans to investigate the immunopathogenesis of M. pneumoniae infection and its possible role in reactiv

144 lammatory, and pulmonary function indices of M. pneumoniae pneumonia in IL-12 (p35) knockout (KO) mic

145 lammatory, and pulmonary function indices of M. pneumoniae pneumonia in mice.

146 nterface culture to study the interaction of M. pneumoniae with differentiated airway epithelium.

147 Libraries of M. pneumoniae and M. genitalium DNA constructed in pGFPU

148 to better understand the basic mechanisms of M. pneumoniae pathogenesis.

149 ease/asthma, a comprehensive murine model of M. pneumoniae lower respiratory infection was establishe

150 , we utilized in vitro and in vivo models of M. pneumoniae infection to characterize the role of the

151 Most non-cytadhering mutants of M. pneumoniae isolated to date exhibit defects in the ar

152 tion has yielded insights into the nature of M. pneumoniae cell division and the role of gliding moti

153 ast 50 years and a limited (n = 4) number of M. pneumoniae-positive primary specimens acquired by the

154 s undertaken during a very large outbreak of M. pneumoniae pneumonia at a facility for developmentall

155 s of cases, small clusters, and outbreaks of M. pneumoniae infections that were supported by the Cent

156 be useful during institutional outbreaks of M. pneumoniae pneumonia.

157 toxin as well as for the major adhesin P1 of M. pneumoniae.

158 lung epithelial cells in the pathogenesis of M. pneumoniae infection and provide a better understandi

159 ailed analysis of observed epidemic peaks of M. pneumoniae infection.

160 What emerges is a picture of M. pneumoniae cytadherence as a multifactorial process t

161 d to play a role in asthma, the potential of M. pneumoniae to establish chronic respiratory infection

162 from sibling 2 demonstrated the presence of M. pneumoniae organisms and community-acquired respirato

163 ologic analysis to determine the presence of M. pneumoniae, Chlamydia pneumoniae, and seven respirato

164 response and influencing the progression of M. pneumoniae during acute infection.

165 The 65-kDa hSP-A binding protein of M. pneumoniae was identified by sequence analysis as a n

166 identified a 65-kDa hSP-A binding protein of M. pneumoniae.

167 Whole-cell radioimmunoprecipitation of M. pneumoniae with antibodies directed against the proli

168 es a powerful tool for greater resolution of M. pneumoniae strains and could be useful during outbrea

169 Students with positive results of M. pneumoniae IgM serologic testing and no alternative d

170 This case prompted us to unravel the role of M. pneumoniae in GBS in a case-control study.

171 However, the role of M. pneumoniae in the pathogenesis of chronic asthma has

172 ave been reported in some cases, the role of M. pneumoniae in the pathogenesis of GBS remains unclear

173 Although the entire genomic sequence of M. pneumoniae has been completed, the functions of many

174 s obtained from the whole genome sequence of M. pneumoniae.

175 t and NF-kappaB activation in the setting of M. pneumoniae infection in nonasthmatic cells, but it di

176 Here we analyzed a clinical strain of M. pneumoniae designated S1 isolated from a 1993 outbrea

177 L M. pneumoniae concentrations than those of M. pneumoniae-infected mice treated with placebo (MpP mi

178 an ADP-ribosylating and vacuolating toxin of M. pneumoniae, designated Community Acquired Respiratory

179 ays implicated the household transmission of M. pneumoniae among all 5 siblings and both parents.

180 Although two genetically distinct types of M. pneumoniae are known, variants of each also exist.

181 ection and provide a better understanding of M. pneumoniae pathology at the cellular level.

182 lcholines did not have significant effect on M. pneumoniae-induced AA release.

183 ay of asthma treatment, but their effects on M. pneumoniae and associated airway inflammation and BHR

184 adherence to host cells, but their impact on M. pneumoniae gliding has not been investigated.

185 mice received aerosolized sham solution plus M. pneumoniae, sham solution alone, or FP alone.

186 In addition, the ETS-plus-M. pneumoniae-exposed mice had elevated levels of oxidiz

187 ad evidence of infection with C. pneumoniae, M. pneumoniae, or both, there was no relationship betwee

188 ction and appropriate responses to potential M. pneumoniae outbreaks and clusters within the communit

189 No vaccine to prevent M. pneumoniae infection currently exists, since the mech

190 Biochemical characterization of purified M. pneumoniae recombinant ClpB revealed casein- and lysi

191 both recombinant EF-Tu(Mp) and radiolabeled M. pneumoniae cell binding to Fn.

192 FP reduced M. pneumoniae by up to 20-fold in lung tissue but not in

193 omes of M. genitalium and its close relative M. pneumoniae were determined by sequencing across the j

194 We report a cluster of macrolide-resistant M. pneumoniae cases among a mother and two daughters.

195 Isolates from several M. pneumoniae community outbreaks within the United Stat

196 These results demonstrate that M. pneumoniae EF-Tu and PDH-B, in addition to their majo

197 In this study, we demonstrate that M. pneumoniae infection also induces proinflammatory cyt

198 These findings demonstrate that M. pneumoniae is likely to be recognized by SP-D in the

199 Collectively, these data demonstrate that M. pneumoniae stimulates the production of eicosanoids f

200 We demonstrated that M. pneumoniae induced the expression of mucins MUC5AC an

201 ollectively, these studies demonstrated that M. pneumoniae induces airway mucus hypersecretion by mod

202 and antibody blocking methods, we found that M. pneumoniae cytoadherence is important for the inducti

203 Evidence is provided that M. pneumoniae was readily transmitted to all members of

204 immunofluorescence microscopy revealed that M. pneumoniae readily expressed CARDS toxin during infec

205 Finally, our biochemical studies show that M. pneumoniae AcpS is kinetically a very sluggish enzyme

206 We show that M. pneumoniae MPN372 encodes a 68-kDa protein that posse

207 Further studies showed that M. pneumoniae exposure blocked ETS-induced increases in

208 Previous studies have shown that M. pneumoniae can induce proinflammatory cytokines in se

209 These studies suggest that M. pneumoniae infection synergizes with ETS and suppress

210 inatory than both MLVA and P1 typing for the M. pneumoniae isolates examined, providing a method for

211 In the M. pneumoniae cytadherence mutant I-2, loss of HMW2 resu

212 of ELF GSH levels, which was blocked in the M. pneumoniae-exposed mice.

213 The proteins of the M. pneumoniae AO share compositional features with prote

214 ew, I discuss recent work on the role of the M. pneumoniae attachment organelle (AO), a structure req

215 _0928, the M. gallisepticum homologue of the M. pneumoniae cytoskeletal protein HMW3, were identified

216 Analysis of the M. pneumoniae genome sequence indicated that this promot

217 Here we explored the molecular nature of the M. pneumoniae gliding machinery, utilizing fluorescent p

218 ing frames widely distributed throughout the M. pneumoniae genome; 30 of these were dispensable for c

219 rotein with 40.9 and 31.4% identity with the M. pneumoniae P30 and M. genitalium P32 cytadhesins, res

220 We here cultured, for the first time, M. pneumoniae from a GBS patient with antibodies against

221 detect immunoglobulin M (IgM) antibodies to M. pneumoniae.

222 whom had neurologic disease attributable to M. pneumoniae.

223 -13, increased dramatically upon exposure to M. pneumoniae.

224 ect role in antibody-independent immunity to M. pneumoniae by interacting with lipid ligands expresse

225 There was no discrete seasonality to M. pneumoniae infections.

226 We compared the ImmunoCard with two M. pneumoniae IgM-specific assays (immunofluorescence as

227 dified Tn4001 and transformed into wild-type M. pneumoniae and into a non-cytadhering mutant lacking

228 microscopy analyses of cores from wild-type M. pneumoniae and mutants producing HMW2 derivatives.

229 developing airway cells, comparing wild-type M. pneumoniae and mutants thereof with moderate to sever

230 EGFP) and expressed this fusion in wild-type M. pneumoniae and the hmw2- mutant I-2.

231 ts were morphologically similar to wild-type M. pneumoniae but failed to localize P1 to the attachmen

232 Wild-type M. pneumoniae cells are generally elongated, tapering to

233 Gliding ceases in wild-type M. pneumoniae during terminal organelle development, whi

234 a polar localization like that in wild-type M. pneumoniae in all mutants having normal levels of HMW

235 base of the terminal organelle in wild-type M. pneumoniae, functions in the late stages of assembly,

236 d gliding capacity quickly, unlike wild-type M. pneumoniae.

237 ssociated with the cell surface in wild-type M. pneumoniae.

238 idate in mice after challenge with wild-type M. pneumoniae.

239 Upon M. pneumoniae infection of mammalian cells, increased ex

240 moniae induces mucus hypersecretion by using M. pneumoniae infection of mouse lungs, human primary br

241 Also, adherence of viable M. pneumoniae cells to hSP-A was inhibited by recombinan

242 Adherence of viable M. pneumoniae to immobilized Fn was inhibited by antirEF

243 Initially, we found that viable M. pneumoniae cells bound to immobilized hSP-A in a dose

244 ously ascribed to infection with WT virulent M. pneumoniae.

245 The present study examined whether M. pneumoniae infections synergize with environmental to

246 dy aimed to determine the mechanism by which M. pneumoniae induces mucus hypersecretion by using M. p

247 On the other hand, while M. pneumoniae protein synthesis and DNA synthesis do not

248 itis, also colonizes airway cells along with M. pneumoniae.

249 y and inflammatory responses associated with M. pneumoniae infection in humans and animals.

250 ar damage and other sequelae associated with M. pneumoniae infections in humans.

251 postinfectious autoimmunity associated with M. pneumoniae-mediated pathologies.

252 toxin per mycoplasma cell when compared with M. pneumoniae cells grown in SP-4 medium alone.

253 L M. pneumoniae concentrations compared with M. pneumoniae-infected WT mice.

254 The interaction of rat and human SP-D with M. pneumoniae was unaffected by the presence of surfacta

255 version to MPN372 in patients diagnosed with M. pneumoniae-associated pneumonia, indicating that this

256 Mice infected with M. pneumoniae (no FP) developed significant lung inflamm

257 gene expression in macrophages infected with M. pneumoniae C57BL/6 mice deficient for NLRP3 expressio

258 IL-12 (p35) KO mice infected with M. pneumoniae were found to have significantly lower BAL

259 iagnosis were considered to be infected with M. pneumoniae.

260 etectable in all of the mice inoculated with M. pneumoniae and was inversely correlated with HPS (r =

261 ys, however, 78% of the mice inoculated with M. pneumoniae demonstrated abnormal histopathology chara

262 BALB/c mice were inoculated with M. pneumoniae or SP4 broth.

263 mice were intranasally inoculated once with M. pneumoniae and examined at 109, 150, 245, 368, and 53

264 mice were intranasally inoculated once with M. pneumoniae and sacrificed at 0 to 42 days postinocula

265 ies were not only found in GBS patients with M. pneumoniae infection, but also in patients without ne