ライフサイエンスコーパス: C. pneumoniae

1 l-deficient mice (Kit(W-sh/W-sh) [Wsh]) with C. pneumoniae.

2 es reported previously for human isolates of C. pneumoniae.

3 le in the acceleration of atherosclerosis by C. pneumoniae.

4 sion forming units (IFU) or 5 x 10(5) IFU of C. pneumoniae.

5 in BALB/c mice after intranasal infection by C. pneumoniae.

6 an acute early inflammatory response toward C. pneumoniae.

7 ibited the growth of C. trachomatis, but not C. pneumoniae.

8 art/ascending aorta in animals infected with C. pneumoniae.

9 indefinitely retained on vacuoles containing C. pneumoniae.

10 the effect of IFN-gamma on the maturation of C. pneumoniae.

11 re medium for 72 hours before infection with C. pneumoniae.

12 onal bands from MS patients did not react to C. pneumoniae.

13 s a conformational epitope on the surface of C. pneumoniae.

14 ns C. trachomatis serovars L2, D and L2b and C. pneumoniae.

15 imilar to the proteins of C. trachomatis and C. pneumoniae.

16 ith two species of Chlamydia, C. pecorum and C. pneumoniae.

17 a more favorable replicative environment for C. pneumoniae.

18 by real-time PCR using primers specific for C. pneumoniae 16S rRNA.

19 d at least partly explain why infection with C. pneumoniae accelerates the development of atheroscler

20 Formalin and heat-inactivated C. pneumoniae activated the transcription factor nuclear

21 man peripheral blood monocytes infected with C. pneumoniae also showed the differentiation of macroph

22 ite of entry of C. muridarum, C. caviae, and C. pneumoniae, although each species similarly recruits

23 matis serovar D, C. muridarum, C. caviae and C. pneumoniae and assayed for rescue of growth repressio

24 vars L1 to L3), (iii) C. muridarum, and (iv) C. pneumoniae and C. caviae.

25 The results indicate that C. pneumoniae and C. trachomatis L2 EB-surface GAGs and

26 decreased infection rates were observed with C. pneumoniae and C. trachomatis serovar L2 in epithelia

27 tor for attachment and entry differs between C. pneumoniae and C. trachomatis.

28 o locate ArgR operators upstream of glnPQ in C. pneumoniae and Chlamydophila caviae but not Chlamydia

29 nd heart tissue were analyzed for infectious C. pneumoniae and for Chlamydophila antigen by immunohis

30 Interaction between C. pneumoniae and immune cells is important in the devel

31 We have shown that both live C. pneumoniae and inactivated C. pneumoniae induce marke

32 ncephalitogenic T cells are activated by the C. pneumoniae and myelin basic protein Ags.

33 y nested polymerase chain reaction (PCR) for C. pneumoniae and S. negevensis.

34 dies GZD1E8 and RR-402 recognize the MOMP of C. pneumoniae and that this protein is localized on the

35 In this elderly cohort, chronic H. pylori, C. pneumoniae, and CMV infections, as evidenced by serop

36 monocytic cell line cells were infected with C. pneumoniae, and the differentiation of monocytes to m

37 e known to have high titers of antibodies to C. pneumoniae, and the organism has been recovered from

38 Accentuation of EAE required live infectious C. pneumoniae, and the severity of the disease was atten

39 amydia trachomatis, the respiratory pathogen C. pneumoniae, and the zoonotic agent C. psittaci.

40 ate atherosclerotic lesions of patients with C. pneumoniae antibodies.

41 r development of CAV in patients with higher C. pneumoniae antibody titers.

42 The C. pneumoniae antiproliferative effect was linked to T c

43 and CD8(+) T cells were equally sensitive to C. pneumoniae antiproliferative effectors.

44 Scc1 (CP0432) and Scc4 (CP0033) proteins of C. pneumoniae AR-39 were demonstrated to function togeth

45 mide] (M6P-PAA) inhibited the infectivity of C. pneumoniae AR-39, but not C. trachomatis serovar UW5

46 lar activities that accompany persistence of C. pneumoniae, as well as suggesting requirements for re

47 pneumoniae or heat-killed or UV-inactivated C. pneumoniae at a low multiplicity of infection for 24

48 Thus, C. pneumoniae augments the effects of oxidized LDL on ce

49 Transmission of C. pneumoniae between animals and humans has not been re

50 from some Chlamydia species (e.g. pCopN from C. pneumoniae) binds tubulin and inhibits microtubule as

51 rH-2 from C. psittaci reacted with LcrE from C. pneumoniae but not from C. trachomatis; and C. tracho

52 ropharyngeal and/or nasopharyngeal swabs for C. pneumoniae by real-time polymerase chain reaction (qP

53 Tarp orthologs from C. pneumoniae, C. muridarum, and C. caviae harbor betwee

54 We propose that infection of the CNS by C. pneumoniae can amplify the autoreactive pool of lymph

55 demia are one of the key mechanisms by which C. pneumoniae can exacerbate atherosclerotic pathology.

56 Previous studies have established that C. pneumoniae can induce cytokines in mouse and/or human

57 These findings indicate that C. pneumoniae can utilize the M6P/IGF2 receptor and that

58 Following intranasal C. pneumoniae challenge, C57BL/6 mice on a low-protein/l

59 tigations on the biology and pathogenesis of C. pneumoniae clonal genovars that could lead to new ins

60 positions 1021 and 0325, respectively, from C. pneumoniae CM-1 were used as "bait" to identify targe

61 e most extensive protein expression study of C. pneumoniae comparing the chlamydial heat shock stress

62 However, the mechanisms by which C. pneumoniae contributes to cardiovascular disease have

63 mechanistic framework for understanding the C. pneumoniae CopN-specific inhibition of microtubule as

64 ings are consistent with the conclusion that C. pneumoniae could induce a local T cell immunosuppress

65 Live, heat-killed, and UV-inactivated C. pneumoniae cultures (at multiplicities of infection [

66 This effect is mediated by C. pneumoniae-dependent degradation of TRAF3, which is i

67 eater utility as a diagnostic tool for early C. pneumoniae detection.

68 hlamydial monoclonal antibodies specific for C. pneumoniae determination.

69 This study showed that C. pneumoniae did not accelerate lesion development in m

70 We conclude that C. pneumoniae directly activates the NLRP3/ASC inflammas

71 Contrast analyses characterized severe C. pneumoniae disease as being a delayed-type hypersensi

72 ay important roles in the pathophysiology of C. pneumoniae disease.

73 tients evaluated had evidence of circulating C. pneumoniae DNA by PCR, without a statistical differen

74 Circulating C. pneumoniae DNA is detectable by PCR in up to 30% of c

75 f 30 RBC units tested showed the presence of C. pneumoniae DNA.

76 Under these wild-type conditions, C. pneumoniae do not elicit significant nitric oxide (NO

77 We found that C. pneumoniae does not grow and multiply in cultured pri

78 rate that infection of epithelial cells with C. pneumoniae does not lead to IFN-beta production.

79 ing spots to those of proteins identified in C. pneumoniae elementary bodies by matrix-assisted laser

80 GG2EE macrophage cell line, suggesting that C. pneumoniae elicits foam cell formation predominantly

81 Genome sequence analysis indicates that C. pneumoniae encodes a homologue of a chlamydial protea

82 it is shown that coculture of monocytes with C. pneumoniae enhances infection of C. pneumoniae in art

83 Our results reveal a complex network for C. pneumoniae entry involving at least six key proteins.

84 keletal muscle [GEM]) play a key role during C. pneumoniae entry, but none alone is essential to prev

85 R7, ITGB2, and PDGFB) significantly inhibits C. pneumoniae entry, but the entire network is resistant

86 sion for these modules change rapidly during C. pneumoniae entry, with cell adhesion occurring at 5 m

87 , the expression pattern of the TTS genes of C. pneumoniae examined suggests that they are temporally

88 Hence, it is likely that C. pneumoniae expresses a unique protease targeting TRAF

89 We conclude that C. pneumoniae facilitates foam cell formation via activa

90 , TLR4, MyD88, or LXRalpha intranasally with C. pneumoniae followed by feeding of a high fat diet for

91 ry, fresh human monocytes were infected with C. pneumoniae for 8 h, and the interactions between mono

92 Azithromycin-treated mice did not eliminate C. pneumoniae from lungs by 3 weeks after inoculation bu

93 n evolutionary analysis of the H. pylori and C. pneumoniae genes that encode their outer-membrane pro

94 We quantified transcripts from C. pneumoniae genes that were either rich or poor in Trp

95 n reaction (PCR) studies for the presence of C. pneumoniae genes were performed.

96 recent sequencing of the C. trachomatis and C. pneumoniae genomes.

97 an essential role of CopN in the support of C. pneumoniae growth during infection.

98 ition of the cell differentiation as well as C. pneumoniae growth in the cells, but not ICAM-1 expres

99 MS might be an infectious syndrome in which C. pneumoniae has a role in a subset of patients.

100 C. pneumoniae has also been associated with a variety of

101 To date, methods for cloning C. pneumoniae have not been reported.

102 We designated the C. pneumoniae homologue as CPAFcp.

103 trachomatis mouse pneumonitis strain and the C. pneumoniae horse N16 strain.

104 ese findings reveal a new infection site for C. pneumoniae, i.e., lymphocytes.

105 etions from the N and C termini of LcrE from C. pneumoniae identified the 50 C-terminal amino acids a

106 eumoniae IgG (HR 0.91, 95% CI 0.68 to 1.20), C. pneumoniae IgA (HR 0.65, 95% CI 0.39 to 1.07), and CM

107 itivity to H. pylori IgG, C. pneumoniae IgG, C. pneumoniae IgA, and CMV IgG was 60%, 45%, 11%, and 69

108 . pylori IgG (HR 1.09, 95% CI 0.81 to 1.46), C. pneumoniae IgG (HR 0.91, 95% CI 0.68 to 1.20), C. pne

109 We measured serum H. pylori IgG, C. pneumoniae IgG and IgA, and CMV IgG levels in Framing

110 C. pneumoniae IgG titer correlates with severity of allo

111 Seropositivity to H. pylori IgG, C. pneumoniae IgG, C. pneumoniae IgA, and CMV IgG was 60

112 moniae-associated illness and no episodes of C. pneumoniae illness, suggesting that these bacteria do

113 For every twofold increase in geometric mean C. pneumoniae immunoglobulin (Ig)G titer, the odds ratio

114 TAC testing detected C. pneumoniae in 4 (57%) inmates; no other causative pat

115 e VD4 assay and one nested PCR each detected C. pneumoniae in a single, but different, PBMC specimen.

116 These results indicate that the growth of C. pneumoniae in alveolar macrophages may be restricted.

117 tes with C. pneumoniae enhances infection of C. pneumoniae in arterial smooth-muscle cells 5.3-fold a

118 rved when rats were immunized with sonicated C. pneumoniae in CFA.

119 PCR assays and may improve the detection of C. pneumoniae in clinical specimens.

120 and endothelial cells promotes infection of C. pneumoniae in endothelial cells and that the enhancem

121 to inhibit attachment and internalization of C. pneumoniae in endothelial cells but did not inhibit a

122 tine and acetylcholine altered the growth of C. pneumoniae in epithelial HEp-2 cells.

123 detailed roles of Chlamydia trachomatis and C. pneumoniae in induction of spondyloarthritis have not

124 ns (6.1%) showed evidence of the presence of C. pneumoniae in one or more tests.

125 Deletion of C. pneumoniae in Red Blood Cell (RBC) units was accompli

126 a marked reduction of leukocytes as well as C. pneumoniae in terms of bacterial number and positive

127 Persistence of C. pneumoniae in the oropharynx creates challenges for o

128 W3965 was added to macrophages infected with C. pneumoniae in the presence of oxidized LDL.

129 KO mice, treated them with live or UV-killed C. pneumoniae in the presence or absence of oxidized LDL

130 dal antibiotic known to be effective against C. pneumoniae, in a double-blind, randomized, placebo-co

131 tion may adversely impact the fitness of the C. pneumoniae inclusion for chlamydial replication.

132 odies did not cross-react with IncA, a known C. pneumoniae inclusion membrane protein, although the a

133 o be a sensitive method for identifying rare C. pneumoniae inclusions and was useful in the detection

134 -651) partially inhibited the development of C. pneumoniae inclusions in EGFP.

135 rachomatis inclusions but not C. psittaci or C. pneumoniae inclusions.

136 e macrophages with both live and inactivated C. pneumoniae increased the ATP content of the cells.

137 that both live C. pneumoniae and inactivated C. pneumoniae induce markers of cell death prior to comp

138 C. pneumoniae induced decreases in both KCl- and u46619-

139 Both live and UV-killed C. pneumoniae induced IRF3 activation and promoted foam

140 We tested the hypothesis that C. pneumoniae-induced acceleration of atherosclerosis in

141 However, C. pneumoniae-induced acceleration of atherosclerosis in

142 le of the IL-17A in high-fat diet (HFD)- and C. pneumoniae-induced acceleration of atherosclerosis.

143 ay a significant role in the pathogenesis of C. pneumoniae-induced chronic inflammatory lung diseases

144 tor 2 (TLR-2) but not TLR-4 are resistant to C. pneumoniae-induced death.

145 C. pneumoniae-induced foam cell formation was significan

146 LXR agonist GW3965, which in turn inhibited C. pneumoniae-induced IRF3 activation, suggesting a bidi

147 ut it is not known how cHSP60 contributes to C. pneumoniae-induced lung inflammation.

148 ation of amphiphysin IIm function results in C. pneumoniae-induced NO production and in the steriliza

149 adaptor molecule MyD88 in host responses to C. pneumoniae-induced pneumonia in mice.

150 ted the role of IL-1 in host defense against C. pneumoniae-induced pneumonia using mice deficient in

151 n bacterial protein expression were found in C. pneumoniae-infected cells due to IFN-gamma treatment.

152 n0308 was detected in inclusion membranes of C. pneumoniae-infected cells using antibodies raised wit

153 Upon delivery into live C. pneumoniae-infected cells, Cpn0585(628-651)-specific

154 In vitro studies showed that C. pneumoniae-infected GFP-macrophages adhered better th

155 In C. pneumoniae-infected HEp-2 cells transfected with enha

156 The ex vivo studies showed that C. pneumoniae-infected macrophages adhered better than u

157 In contrast, adherence of C. pneumoniae-infected macrophages to the aortas of inte

158 s crucial for activation of the adherence of C. pneumoniae-infected macrophages to the endothelium.

159 In C. pneumoniae-infected monocyte-derived macrophages, gro

160 C. pneumoniae-infected monocytes can contribute to the d

161 We conclude that C. pneumoniae infection accelerates atherosclerosis in h

162 This study evaluated association between C. pneumoniae infection and accelerated graft arterioscl

163 Thus, MyD88 is essential to recognize C. pneumoniae infection and initiate a prompt and effect

164 at mast cells play a detrimental role during C. pneumoniae infection by facilitating immune cell infi

165 These findings indicate that C. pneumoniae infection can directly alter the vascular

166 y less acceleration of lesion size following C. pneumoniae infection compared with WT control despite

167 However, unlike oxidized LDL, C. pneumoniae infection does not activate caspase 3 or i

168 Murine C. pneumoniae infection enhanced insulin resistance deve

169 We hypothesize that C. pneumoniae infection favors the recruitment of monocy

170 In contrast, C. pneumoniae infection had only a minimal effect on ath

171 f immune cells, particularly lymphocytes, to C. pneumoniae infection has not been reported, even thou

172 roviding additional evidence for the role of C. pneumoniae infection in cardiovascular disease.

173 However, the involvement of C. pneumoniae infection in such steps is not clear.

174 We demonstrate that C. trachomatis and C. pneumoniae infection in vitro elicits the externaliza

175 xamined the susceptibility of lymphocytes to C. pneumoniae infection in vitro.

176 Furthermore, C. pneumoniae infection in WT but not in IL-17A(-/-) mic

177 In obese C57BL/6 mice, C. pneumoniae infection induced significantly increased

178 As expected, C. pneumoniae infection led to a significant increase in

179 C. pneumoniae infection markedly accelerated atheroscler

180 C. pneumoniae infection may accelerate the death of cell

181 These results indicate that C. pneumoniae infection may directly induce the differen

182 crophages, designated "MH-S," as an in vitro C. pneumoniae infection model.

183 To test this hypothesis, the impact of C. pneumoniae infection on the death of lipid-loaded mou

184 tant because of the high prevalence of human C. pneumoniae infection worldwide.

185 ro system to further characterize persistent C. pneumoniae infection, employing both ultrastructural

186 ne cells showed an obvious susceptibility to C. pneumoniae infection, indicating that T cells could b

187 uced atherosclerotic lesion development, and C. pneumoniae infection-mediated acceleration of atheros

188 t previously been reported to be affected by C. pneumoniae infection.

189 s required for MHC antigen expression during C. pneumoniae infection.

190 is unclear what role mast cells play during C. pneumoniae infection.

191 ate and reduce the proatherogenic effects of C. pneumoniae infection.

192 C. pneumoniae infections of humans are a common cause of

193 Thus, typical C. pneumoniae infections of humans are consistent with a

194 This MAb is potent in the neutralization of C. pneumoniae infectivity in vitro.

195 with their genetic relatedness, LcrH-2 from C. pneumoniae interacted with LcrE produced from the thr

196 was started after infection, indicating that C. pneumoniae is a co-risk factor with hyperlipidemia fo

197 noprecipitation, indicating that the MOMP of C. pneumoniae is an immunogenic protein.

198 Detection of C. pneumoniae is inconsistent, and standardized PCR assa

199 The pathogenicity of C. pneumoniae is thought to depend on its ability to cau

200 A key question is how C. pneumoniae is transferred from the site of primary in

201 line, ciprofloxacin, and enrofloxacin for 10 C. pneumoniae isolates from these bandicoots ranged from

202 Thirty-nine C. pneumoniae isolates obtained from widely distributed

203 ant intrastrain polymorphism exists for some C. pneumoniae isolates.

204 These data suggest that C. pneumoniae kills cells by a caspase-independent pathw

205 ith neural antigens, systemic infection with C. pneumoniae led to the dissemination of the organism i

206 tive method to significantly reduce resident C. pneumoniae levels in RBC components but may not be co

207 We describe C. pneumoniae lower respiratory tract infection in a 19-

208 ic chlamydial plasmid of the koala strain of C. pneumoniae (LPCoLN) using the whole-genome shotgun me

209 or (TNF)-alpha produced in response to acute C. pneumoniae lung colonization exacerbated insulin resi

210 t of patients had evidence of infection with C. pneumoniae, M. pneumoniae, or both, there was no rela

211 These findings suggest that C. pneumoniae may activate macrophages through OMP2, Cpn

212 Our results suggest that infection with C. pneumoniae may be more severe in old animals.

213 the activation of endothelial NF-kappaB, and C. pneumoniae may contribute to atherogenesis without ac

214 Finally, reassessing previous C. pneumoniae microarray data based on codon content, we

215 the discrepancies between C. trachomatis and C. pneumoniae MOMP exposure on intact chlamydiae and imm

216 s directed to conformational epitopes of the C. pneumoniae MOMP.

217 s infectivity upon subsequent challenge with C. pneumoniae more effectively than all other protein sp

218 DCs) were generated and stimulated with live C. pneumoniae (multiplicity of infection [MOI], 5), UVCP

219 a bactericidal antibiotic effective against C. pneumoniae, no reduction in the rate of cardiovascula

220 C. pneumoniae often coexists with other etiologic agents

221 erved increase in cell death, the effects of C. pneumoniae on ATP concentrations within mouse macroph

222 The effect of C. pneumoniae on monocyte MMPs was mediated through the

223 Heat or UV inactivation of C. pneumoniae only partially reduced the cytokine respon

224 , including patients with elevated titers to C. pneumoniae or C-reactive protein.

225 with C. trachomatis inclusions but not with C. pneumoniae or C. muridarum inclusions, while the oppo

226 Subsequent infection with either live C. pneumoniae or heat-killed or UV-inactivated C. pneumo

227 Conversely, C. pneumoniae or Pam, but not E. coli LPS, induced foam

228 e induced by Escherichia coli LPS but not by C. pneumoniae or Pam.

229 In HUVECs infected with C. pneumoniae or stimulated with TNF-alpha, both azithro

230 rophage RAW 264.7 cells either infected with C. pneumoniae or treated with the TLR4 ligand E. coli li

231 We found that C. pneumoniae organisms inhibited activated but not nona

232 to be secreted into the host cell cytosol by C. pneumoniae organisms.

233 re, CPAFcp was secreted into host cytosol by C. pneumoniae organisms.

234 We investigated a C. pneumoniae outbreak at a federal correctional facilit

235 ls exposed to each of the three TLR ligands (C. pneumoniae, Pam, and E. coli LPS).

236 ated indoleamine 2,3-dioxygenase activity on C. pneumoniae persistence in HEp-2 cells, inclusion morp

237 Protein expression patterns of C. pneumoniae persistence indicates a strong stress comp

238 to synthetic peptides representing analogous C. pneumoniae PorB sequences.

239 We also show that human sera from C. pneumoniae-positive donors consistently recognize the

240 nt study defined a homing mechanism by which C. pneumoniae promotes the adherence of mononuclear phag

241 ced the cytokine response, and inhibition of C. pneumoniae protein or DNA synthesis did not affect it

242 Thus, Cpn0797 represents the third C. pneumoniae protein secreted into the host cell cytoso

243 Upregulation of C. pneumoniae proteins involved in diverse functions dur

244 y, we examined, by proteomics, expression of C. pneumoniae proteins labeled intracellularly with [(35

245 More than 20 Chlamydia trachomatis and C. pneumoniae proteins were detected within the cytoplas

246 We determined the expression patterns of 52 C. pneumoniae proteins, representing nine functional sub

247 The assays were compared by testing C. pneumoniae purified elementary bodies, animal tissues

248 This pattern suggests that, in C. pneumoniae, recombination events have broken up the l

249 These compounds interfered with C. pneumoniae replication in mammalian cells, presumably

250 C. pneumoniae replication showed a dose-dependent decrea

251 f our knowledge, this is the first report of C. pneumoniae respiratory infection after stem cell or m

252 We previously observed that C. pneumoniae responds to this stress by globally increa

253 Infection of MH-S cells with C. pneumoniae resulted in the development of typical inc

254 e observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tiss

255 The data suggest that C. pneumoniae retains amphiphysin IIm on the vacuole to

256 ltrastructural analysis of IFN-gamma-treated C. pneumoniae revealed atypical inclusions containing la

257 Depletion of the C. pneumoniae-secreted CPAFcp with specific antibodies c

258 presence or absence of diabetes mellitus, or C. pneumoniae serologic status at baseline.

259 Blood specimens were examined for C. pneumoniae serology and DNA detection by polymerase c

260 genes and SNPs against the human isolates of C. pneumoniae show that the LPCoLN isolate is basal to h

261 In this study, heparin treatment of C. pneumoniae significantly reduced its ability to induc

262 cytes could be vehicles for dissemination of C. pneumoniae since the organism has been detected in pe

263 The intracellular growth rate of C. pneumoniae slows dramatically during chronic infectio

264 We present here a description of C. pneumoniae species-specific monoclonal antibody (MAb)

265 Another previously described C. pneumoniae species-specific monoclonal antibody, RR-4

266 CSF have shown no significant difference in C. pneumoniae-specific DNA or antibody between MS and co

267 work has revealed intrathecal production of C. pneumoniae-specific IgG in only 24% of MS patients co

268 ure and staining of the resected tissue with C. pneumoniae-specific monoclonal antibodies, and azithr

269 re confirmed to be Chlamydia pneumoniae by a C. pneumoniae-specific ompA-based real-time PCR assay an

270 Analyses of additional C. pneumoniae strains showed that although some Pmps are

271 e sequences of two H. pylori strains and two C. pneumoniae strains, we identify multiple independent

272 Upon infection of HEp-2 cells with C. pneumoniae, the expression of these genes was followe

273 In cells treated with inactivated C. pneumoniae, the increase in ATP content was smaller t

274 In cells infected with live C. pneumoniae, the increase was inversely proportional t

275 h Chlamydia trachomatis (C. trachomatis) and C. pneumoniae, the PmpD protein is proteolytically cleav

276 ll mice by day 28 postinfection, with higher C. pneumoniae titers in old animals than in young animal

277 ence of spread to the heart, although higher C. pneumoniae titers were observed in the hearts from ol

278 ve revealed a unique molecular mechanism for C. pneumoniae to evade host adaptive immunity that may a

279 The capacity of C. pneumoniae to increase the ATP content was ablated in

280 n this study, we investigated the ability of C. pneumoniae to induce IL-1beta secretion.

281 re, the differentiation-inducing activity of C. pneumoniae to monocytes was examined.

282 ice inoculated with 5 x 10(5) IFU, spread of C. pneumoniae to the heart was evident by day 14, with n

283 HEp-2 cells were infected with C. pneumoniae (TW-183) at a multiplicity of infection of

284 th recombinant cHSP60 (50 microg), UV-killed C. pneumoniae (UVCP; 5 x 10(6) inclusion-forming units/m

285 indings have potential implications for both C. pneumoniae vaccine and diagnostic assay development.

286 C. pneumoniae was also recovered from the central nervou

287 Among 40 inmates followed prospectively, C. pneumoniae was detected for up to 8 weeks.

288 C. pneumoniae was first identified solely in human popul

289 In addition, expression was analyzed when C. pneumoniae was grown in the presence of human gamma i

290 onclusion, use of antibiotics active against C. pneumoniae was not associated with a decreased risk o

291 antibiotic use or use of antibiotics against C. pneumoniae was not associated with multiple sclerosis

292 We found that C. pneumoniae was unique among the other Chlamydia speci

293 Two real-time PCR assays specific for C. pneumoniae were developed by using the fluorescent dy

294 cted zoonotically by an animal isolate(s) of C. pneumoniae which adapted to humans primarily through

295 a 20-mer peptide from a protein specific to C. pneumoniae which shares a 7-aa motif with a critical

296 ed infections and preventable blindness, and C. pneumoniae, which infects the respiratory tract and i

297 ental cycle was independent of the growth of C. pneumoniae, while sustained induction required live o

298 We show by immunoprecipitation of C. pneumoniae with GZD1E8 and RR-402 MAbs and by mass sp

299 We also found that the destruction of C. pneumoniae within infected macrophages resulted in a

300 In this study we focused on survival of C. pneumoniae within PBMCs isolated from the blood of he