ライフサイエンスコーパス: C. pneumoniae

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

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

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

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

5 an acute early inflammatory response toward C. pneumoniae.

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

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

8 a more favorable replicative environment for C. pneumoniae.

9 indefinitely retained on vacuoles containing C. pneumoniae.

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

11 the effect of IFN-gamma on the maturation of 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 re medium for 72 hours before infection with C. pneumoniae.

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

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

17 ith two species of Chlamydia, C. pecorum and 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 y nested polymerase chain reaction (PCR) for C. pneumoniae and S. negevensis.

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

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

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

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

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

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

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

40 composite reference standard (CRS) for anti-C. pneumoniae antibody status of human sera, the top-per

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 Importantly, C. trachomatis and C. pneumoniae are Trp auxotrophs and are starved for thi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 Human C. pneumoniae (Cpn) and C. trachomatis (Ctr) seroreactiv

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

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

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

70 hlamydial monoclonal antibodies specific for C. pneumoniae determination.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 We designated the C. pneumoniae homologue as CPAFcp.

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

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

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

107 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

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

109 . 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

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

111 significantly higher than 4 commercial anti-C. pneumoniae IgG ELISAs (36-12% sensitivity at 95% spec

112 C. pneumoniae IgG titer correlates with severity of allo

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

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

115 cell epitopes to 48 peptide antigens from 12 C. pneumoniae immunodominant proteins.

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

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

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

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

120 or involved in regulating the endocytosis of C. pneumoniae in an EGFR- and SNX9-dependent manner.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 C. pneumoniae-induced foam cell formation was significan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 Murine C. pneumoniae infection enhanced insulin resistance deve

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

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

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

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

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

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

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

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

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

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

181 C. pneumoniae infection markedly accelerated atheroscler

182 C. pneumoniae infection may accelerate the death of cell

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

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

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

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

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

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

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

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

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

192 ve the potential to improve serodiagnosis of C. pneumoniae infection.

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

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

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

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

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

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

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

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

201 NX9 is found at bacterial entry sites, where C. pneumoniae is internalized via EGFR-mediated endocyto

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

222 C. pneumoniae often coexists with other etiologic agents

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 C. pneumoniae replication showed a dose-dependent decrea

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

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

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

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

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

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

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 tisera, we expanded 18 previously discovered C. pneumoniae-specific B-cell epitopes to 48 peptide ant

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 C. pneumoniae was also recovered from the central nervou

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

287 C. pneumoniae was first identified solely in human popul

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

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

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

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

292 For specific detection of antibodies against C. pneumoniae, we developed novel ELISAs with strongly r

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