ライフサイエンスコーパス: C. burnetii

1 C. burnetii DeltacvpB, DeltacvpC, DeltacvpD, and Deltacv

2 C. burnetii extracts and rACP were also able to inhibit

3 C. burnetii formed a prototypical PV and replicated effi

4 C. burnetii has evolved to replicate in this harsh compa

5 C. burnetii is a Gram-negative intracellular bacterium t

6 C. burnetii is considered a potential bioterrorism agent

7 C. burnetii isolates have a range of disease potentials;

8 C. burnetii lacks enzymes for de novo cholesterol biosyn

9 C. burnetii persists within and is transmitted by mammal

10 C. burnetii requires this lysosomal environment for repl

11 Over 100 C. burnetii Dot/Icm substrates have been identified, but

12 e, we compared the sequences of ankG from 37 C. burnetii isolates and classified them in three groups

13 A C. burnetii DeltacvpA mutant exhibited significant defec

14 bility of PIV to confer protection against a C. burnetii infection.

15 Here, we constructed a C. burnetii pmrA deletion mutant to directly probe PmrA-

16 e here the cloning and characterization of a C. burnetii ftsZ mutant generated by mariner-based Himar

17 e) buffers have been described that activate C. burnetii metabolism in vitro, but metabolism is short

18 associated with the production of additional C. burnetii proteins involved in host cell parasitism.

19 We predict additional C. burnetii effectors localize to the PV membrane and re

20 d significant protection against aerosolized C. burnetii, suggesting that 1E4 may be useful for preve

21 he early immune response against aerosolized C. burnetii.

22 ction, SCID mice were exposed to aerosolized C. burnetii.

23 r C. burnetii 3262 stimulation but not after C. burnetii Nine Mile stimulation.

24 6 led to decreased cytokine production after C. burnetii 3262 stimulation but not after C. burnetii N

25 ay an important role in host defense against C. burnetii infection in mice.

26 r peritoneal B cells in host defense against C. burnetii infection in vivo.

27 e of neutrophils in the host defense against C. burnetii infection remains unclear.

28 ay an important role in host defense against C. burnetii pulmonary infection.

29 f neutrophils in protective immunity against C. burnetii infection, the RB6-8C5 antibody was used to

30 r neutrophils in protective immunity against C. burnetii infection.

31 the mechanisms of pulmonary immunity against C. burnetii infection.

32 nsfer of 1E4 would protect SCID mice against C. burnetii aerosol infection.

33 manized MAb as emergency prophylaxis against C. burnetii exposure.

34 y a role in early vaccine protection against C. burnetii and contribute to antibody isotype switching

35 ble to confer significant protection against C. burnetii challenge.

36 required for PIV-mediated protection against C. burnetii infection.

37 tical role in PIV-induced protection against C. burnetii infection.

38 ibodies (Abs) can provide protection against C. burnetii natural infection, we examined if passive tr

39 phylactic measure that is protective against C. burnetii infections but is not U.S.

40 phylactic measure that is protective against C. burnetii infections but is not U.S. Food and Drug Adm

41 the induction of cytokine responses against C. burnetii in humans.

42 Designing new vaccines against C. burnetii remains a challenge and requires the use of

43 recombinant protein subunit vaccines against C. burnetii To accomplish this, we formulated C. burneti

44 ng protective and effective vaccines against C. burnetii.

45 All C. burnetii isolates carry a large, autonomously replica

46 smid, three of which are conserved among all C. burnetii isolates, suggesting that they are critical

47 oteins (CpeA, CpeB, and CpeF) encoded by all C. burnetii plasmids and IPS are Dot/Icm substrates.

48 open reading frame (CbuD1884) present in all C. burnetii isolates except the Nine Mile reference isol

49 Although C. burnetii replicates in most cell types in vitro, the

50 that neutrophils cannot kill C. burnetii and C. burnetii may be using infection of neutrophils as an

51 e positive for B. quintana, B. henselae, and C. burnetii, respectively, by the dPCR assay, which matc

52 ent recognition of C. burnetii Nine Mile and C. burnetii 3262.

53 needed for biogenesis of prototypical PV and C. burnetii replication.

54 During natural infection of female animals, C. burnetii shows tropism for the placenta and is associ

55 ohydrates, and proteins; thus, it is assumed C. burnetii derives nutrients for growth from these degr

56 ic difference between virulent and avirulent C. burnetii is they have smooth and rough lipopolysaccha

57 infection in vitro and found that avirulent C. burnetii triggers sustained interleukin-1beta (IL-1be

58 Compared to wild-type bacteria, C. burnetii DeltapmrA exhibited severe intracellular gro

59 sed on understanding the interaction between C. burnetii and innate immune cells in vitro and in vivo

60 udy, we investigated the interaction between C. burnetii and other pulmonary cell types apart from th

61 Studying the interaction between C. burnetii and the innate immune system can provide a m

62 s collectively demonstrate interplay between C. burnetii and specific components of the eIF2alpha sig

63 athogen's proteome, probed with biotinylated C. burnetii genomic DNA.

64 th Fab1E4, muscFv1E4, or huscFv1E4 can block C. burnetii infection of macrophages.

65 d substrates of the Dot/Icm system from both C. burnetii and L. pneumophila.

66 PMN were challenged with viable C. burnetii, C. burnetii extracts, or rACP but not when PMN were chal

67 ned as valvular lesion potentially caused by C. burnetii: vegetation, valvular nodular thickening, ru

68 The effector proteins delivered by C. burnetii are predicted to have important functions du

69 tic tools, secretion of plasmid effectors by C. burnetii during host cell infection was confirmed usi

70 e secreted in a Dot/Icm-dependent fashion by C. burnetii during infection of human THP-1 macrophages.

71 e vesicular trafficking pathways co-opted by C. burnetii for PV development are poorly defined; howev

72 kinase pathways are most likely targeted by C. burnetii Icm/Dot effectors.

73 with L. pneumophila was also translocated by C. burnetii in a process that requires its C terminus, p

74 sponses by direct ELISpot to both whole-cell C. burnetii and individual peptides in chronic patients

75 g infection of placenta-derived JEG-3 cells, C. burnetii showed sensitivity to progesterone but not t

76 In human cells, C. burnetii generates a replication niche termed the par

77 ining a valuable approach for characterizing C. burnetii interactions with a human host.

78 Cloned C. burnetii fur complemented an Escherichia coli fur del

79 eal B cells alone may not be able to control C. burnetii infection.

80 Various formats using different C. burnetii antigens were tested.

81 effector that influences ER function during C. burnetii infection.

82 ctivity, no p62 turnover was observed during C. burnetii growth in macrophages, suggesting that the p

83 host-pathogen interactions that occur during C. burnetii infection, stable-isotope labeling by amino

84 es were differentially phosphorylated during C. burnetii infection, suggesting the pathogen uses PKA

85 and probed the role of PKA signaling during C. burnetii infection of macrophages.

86 st the enzyme may act on host sterols during C. burnetii intracellular growth.

87 is, lytic cell death did not occur following C. burnetii-triggered inflammasome activation, indicatin

88 ors, such as M6PR and LRP1, are critical for C. burnetii virulence.

89 Several effectors crucial for C. burnetii intracellular replication have been identifi

90 tion of HeLa cells, which are permissive for C. burnetii replication.

91 tiation factor alpha, which was required for C. burnetii growth.

92 te lysosomal hydrolases are not required for C. burnetii survival and growth but are needed for norma

93 sehold contacts were traced and screened for C. burnetii.

94 generation of human granulomas specific for C. burnetii.

95 gest the value of systematically testing for C. burnetii in antiphospholipid-associated cardiac valve

96 In all assay formats, C. burnetii-specific IFN-gamma production was higher (P

97 . burnetii To accomplish this, we formulated C. burnetii Ags with a novel TLR triagonist adjuvant pla

98 involved in protecting vaccinated mice from C. burnetii challenge-induced disease.

99 Importantly, axenically grown C. burnetii were highly infectious for Vero cells and ex

100 During intracellular growth, C. burnetii delivers bacterial proteins directly into th

101 xenic medium that supports sustained (>24 h) C. burnetii metabolic activity.

102 However, significantly higher C. burnetii genome copy numbers were detected in the lun

103 while raising the important question of how C. burnetii obtains essential nutrients from its host.

104 However, we do not understand how C. burnetii evades the intracellular immune surveillance

105 duction increased during infection; however, C. burnetii actively prevented CHOP nuclear translocatio

106 In humans, C. burnetii infects alveolar macrophages and promotes ph

107 ological responses to infection with phase I C. burnetii isolates from the following four genomic gro

108 ed by using (i) a genetic screen to identify C. burnetii proteins interacting with DotF, a component

109 To determine if C. burnetii cultured in ACCM-2 retains immunogenicity, w

110 (convalescents) to promiscuous HLA class II C. burnetii epitopes, providing the basis for a novel T-

111 oring virulent phase I or avirulent phase II C. burnetii variants in human mononuclear phagocytes.

112 In C. burnetii, we found that four different types of coval

113 itical role for extrachromosomal elements in C. burnetii pathogenesis.

114 Expression of a subset of repair genes in C. burnetii was monitored and, in contrast to the non-in

115 /Thr kinase), a protein kinase identified in C. burnetii by in silico analysis.

116 results suggest a versatile role for PKA in C. burnetii infection and indicate virulent organisms us

117 ws the expression of recombinant proteins in C. burnetii as TEM fusion products.

118 tism and opens the door for a renaissance in C. burnetii research.

119 d ERK led to decreased cytokine responses in C. burnetii-stimulated human PBMCs.

120 ect genetic evidence of a functional T4SS in C. burnetii.

121 ce of clathrin-coated vesicle trafficking in C. burnetii infection and define a role for CvpA in subv

122 re challenged with electron beam-inactivated C. burnetii.

123 rotective efficacies of formalin-inactivated C. burnetii Nine Mile phase I (PIV) and phase II (PIIV)

124 rotective efficacy of a formalin-inactivated C. burnetii Nine Mile phase I vaccine (PIV) in beta(2)-m

125 Collectively, these data indicate C. burnetii encodes multiple effector proteins that targ

126 n and viability are not impaired, indicating C. burnetii does not require by-products of hydrolase de

127 After human inhalation, C. burnetii is engulfed by alveolar macrophages and tran

128 uscFv1E4, and huscFv1E4 were able to inhibit C. burnetii infection in mice but that their ability to

129 accinated WT mouse sera were able to inhibit C. burnetii infection in vivo, but only IgM from PIV-vac

130 esults indicate that 1E4 was able to inhibit C. burnetii infection in vivo, suggesting that 1E4 is a

131 41920-KLH-immunized mice was able to inhibit C. burnetii infection in vivo, suggesting that m1E41920

132 on in mice but that their ability to inhibit C. burnetii infection was lower than that of 1E4.

133 v1E4) retained the ability of 1E4 to inhibit C. burnetii infection.

134 CD4(+) T cell-deficient mouse sera inhibited C. burnetii infection.

135 l antibody (MAb) 1E4 significantly inhibited C. burnetii infection in mice, suggesting that 1E4 is a

136 n by siRNA treatment significantly inhibited C. burnetii replication.

137 Interestingly, C. burnetii inside neutrophils can infect and replicate

138 the severity of disease following intranasal C. burnetii challenge, suggesting that keratinocyte-deri

139 n the current study, we further investigated C. burnetii manipulation of host cell signaling and apop

140 By investigating C. burnetii effector proteins containing eukaryotic-like

141 tii Nine Mile and the Dutch outbreak isolate C. burnetii 3262.

142 ges, suggesting that neutrophils cannot kill C. burnetii and C. burnetii may be using infection of ne

143 We evaluated our top candidates in a live C. burnetii aerosol challenge model in C56BL/6 mice and

144 In human alveolar macrophages, C. burnetii uses a Dot/Icm type IV secretion system (T4S

145 he lack of methods to genetically manipulate C. burnetii significantly impedes the study of this orga

146 n tissue culture host cells or axenic media, C. burnetii extracts, or purified recombinant ACP (rACP)

147 The low rate of phase I and II Nine Mile C. burnetii growth in murine lungs may be a direct resul

148 doses of both phase I and phase II Nine Mile C. burnetii multiply and are less readily cleared from t

149 gments of an LPS-specific MAb can neutralize C. burnetii infection and appears to be a promising step

150 To establish this unique niche, C. burnetii requires the Dot/Icm type IV secretion syste

151 Our data reveal IcaA as a novel C. burnetii effector protein that is secreted by the Dot

152 mophila as a surrogate host, reveals a novel C. burnetii gene (IcaA) involved in the inhibition of ca

153 To identify novel C. burnetii effectors, we applied a machine-learning app

154 stantial growth (approximately 3 log(10)) of C. burnetii in a 2.5% oxygen environment.

155 genome reduction suggests the adaptation of C. burnetii to an obligate intracellular lifestyle is a

156 likely reflect a unique repair adaptation of C. burnetii to its hostile niche.

157 oaerosols via the air, the aerosolization of C. burnetii in the shower, and the air filtration effici

158 t IL-1 may be important for the clearance of C. burnetii from the lungs following intranasal infectio

159 biogenesis, were examined in the context of C. burnetii infection.

160 Axenic cultivation of C. burnetii will facilitate studies of the organism's pa

161 s were quantified in synchronous cultures of C. burnetii and found to closely parallel those of 16S r

162 genomes throughout a 14-day growth cycle of C. burnetii and found that they were inversely correlate

163 le for TNF produced upon immune detection of C. burnetii NMII by TLRs, rather than cytosolic PRRs, in

164 ing and apoptosis by examining the effect of C. burnetii infection on activation of 15 host proteins

165 Unexpectedly, examination of C. burnetii growth in GNPTAB(-/-) HeLa cells revealed re

166 bserved and more apparent with expression of C. burnetii RecAG159D mutant protein.

167 The ?2 Mb genome of C. burnetii is about twice the size of genomes of most o

168 wth and PV generation, whereas the growth of C. burnetii DeltacvpB and DeltacvpC was rescued upon coh

169 fampin are effective at preventing growth of C. burnetii in axenic media, with moxifloxacin and doxyc

170 ychloroquine is thought to inhibit growth of C. burnetii in vivo by raising the pH of typically acidi

171 In this study, we investigated the impact of C. burnetii infection on activation of the three arms of

172 eventing progesterone-mediated inhibition of C. burnetii activity.

173 Dominant-negative inhibition of C. burnetii RecA by recA mutant alleles, modelled after

174 The mechanisms of C. burnetii intracellular survival are poorly defined an

175 Moreover, icaA(-) mutants of C. burnetii failed to suppress the caspase-11-mediated i

176 imics the intracellular replicative niche of C. burnetii and allows axenic growth of the bacteria.

177 variant (NMI) or phase II variant (NMII) of C. burnetii.

178 a T4SS are implicated in the pathogenesis of C. burnetii in flies.

179 characterized a thiol-specific peroxidase of C. burnetii that belongs to the atypical 2-cysteine subf

180 , genomic rearrangements, and pseudogenes of C. burnetii isolates are consistent with genome structur

181 hypothesize that inefficient recognition of C. burnetii and/or activation of host-defense in individ

182 known about their role in the recognition of C. burnetii in humans.

183 ing finding was the divergent recognition of C. burnetii Nine Mile and C. burnetii 3262.

184 with a known role in initial recognition of C. burnetii were included.

185 Replication of C. burnetii during infection has been shown to be increa

186 at restrict the intracellular replication of C. burnetii.

187 expression profiling, allowed the rescue of C. burnetii from its host cell to regain the axenic grow

188 is factor (TNF) produced upon TLR sensing of C. burnetii NMII was required to control bacterial repli

189 The sensitivity of C. burnetii to progesterone, but not structurally relate

190 did not significantly affect the severity of C. burnetii infection-induced diseases in both severe co

191 Nine Mile phase II (NMII) clone 4 strain of C. burnetii, as a model to investigate host and bacteria

192 h this study, we have expanded the subset of C. burnetii immunoreactive proteins validated by enzyme-

193 tem for testing antibiotic susceptibility of C. burnetii in axenic media was set up to evaluate the i

194 The initial target of C. burnetii is the alveolar macrophage.

195 ar (pppy), hence the risk of transmission of C. burnetii through inhalation of drinking water aerosol

196 s are the aeration process, the transport of C. burnetii in bioaerosols via the air, the aerosolizati

197 In addition, treatment of C. burnetii with Fab1E4, muscFv1E4, or huscFv1E4 can blo

198 Interestingly, treatment of C. burnetii with huscFv1E4 can significantly reduce C. b

199 dy has further enhanced our understanding of C. burnetii pathogenesis, the host-pathogen interactions

200 To provide a more-complete understanding of C. burnetii's genetic diversity, evolution, and pathogen

201 t bactericidal or bacteriostatic activity on C. burnetii in axenic media, suggesting that raising pH

202 rmined to have a direct inhibitory effect on C. burnetii replication.

203 sms in TLRs and Nod-like receptors (NLRs) on C. burnetii-induced cytokine production was assessed.

204 a was set up to evaluate the impact of pH on C. burnetii growth and survival in the presence and abse

205 Indeed, insight from early work on C. burnetii metabolism, along with new information gaine

206 Moreover, a CstK-overexpressing C. burnetii strain displayed a severe CCV development ph

207 predictors of progression toward persistent C. burnetii endocarditis.

208 plied a machine-learning approach to predict C. burnetii effectors, and examination of 20 such protei

209 uolar effector proteins, a list of predicted C. burnetii T4BSS substrates was compiled using bioinfor

210 ossibility of using humanized 1E4 to prevent C. burnetii infection, we examined whether the Fab fragm

211 esting that 1E4 may be useful for preventing C. burnetii natural infection.

212 ion is a novel diagnostic assay for previous C. burnetii infection and shows similar performance and

213 e of B cells in host defense against primary C. burnetii infection remains unclear.

214 portant role in host defense against primary C. burnetii infection.

215 portant role in host defense against primary C. burnetii infection.

216 d effector protein CvpA was found to promote C. burnetii intracellular growth and PV expansion.

217 ne responses in the lung following pulmonary C. burnetii infection is lacking.

218 etii with huscFv1E4 can significantly reduce C. burnetii infectivity in human macrophages.

219 s a critical virulence factor that regulates C. burnetii Dot/Icm secretion.

220 We have developed a safe and reproducible C. burnetii aerosol challenge in three different animal

221 In this study, C. burnetii-specific interferon gamma (IFN-gamma) produc

222 To define conditions that support C. burnetii growth, we systematically evaluated the orga

223 d maintenance of the organelle that supports C. burnetii intracellular replication.

224 Formation of a PV that supports C. burnetii replication requires a Dot/Icm type 4B secre

225 Coxiella-containing vacuoles (CCVs) and that C. burnetii can infect and replicate in peritoneal B1a s

226 Together, these results demonstrate that C. burnetii actively directs PV-autophagosome interactio

227 In contrast, our finding that C. burnetii infection induced more-severe splenomegaly a

228 Collectively, these results indicate that C. burnetii encodes a large repertoire of T4SS substrate

229 Recent studies have indicated that C. burnetii likely originated from a tick-associated anc

230 The data show that C. burnetii does not grow in axenic media at pH 6.0 or h

231 Here, we show that C. burnetii inhibits caspase-1 activation in primary mou

232 Previous studies showed that C. burnetii replicates efficiently in primary human alve

233 Recent reports suggest that C. burnetii actively recruits autophagosomes to the PV t

234 These data suggest that C. burnetii does not actively inhibit phagolysosome func

235 Collectively, these data suggest that C. burnetii isolates translocate distinct subsets of the

236 Collectively, these results suggest that C. burnetii plasmid-encoded T4SS substrates play importa

237 Earlier studies suggested that C. burnetii actively inhibited release of ROI from PMN t

238 n rates were lower than 29%, suggesting that C. burnetii can infect neutrophils, but infection is lim

239 The C. burnetii NMII T4SS translocates bacterial products in

240 ted that particular amino acids activate the C. burnetii PmrA/B two-component system.

241 of genetic systems, protein transfer by the C. burnetii Dot/Icm has not been demonstrated.

242 s, translocation of effector proteins by the C. burnetii Dot/Icm system occurs after acidification of

243 the T4SS effector repertoire encoded by the C. burnetii QpH1, QpRS, and QpDG plasmids that were orig

244 on and the engagement of this pathway by the C. burnetii type 4B secretion system substrate Coxiella

245 proteins injected into the host cell by the C. burnetii type IVB secretion system (T4BSS) are requir

246 ysis revealed multiple transpositions in the C. burnetii genome and rescue cloning identified 30 and

247 Indeed, the C. burnetii PmrA/B regulon, responsible for transcriptio

248 may play an important role in inhibiting the C. burnetii infection-induced inflammatory response.

249 t the identification of 32 substrates of the C. burnetii Dot/Icm system using a fluorescence-based be

250 Further assessment of the C. burnetii growth niche showed that macrophages mounted

251 ere identified upon genome sequencing of the C. burnetii Nine Mile reference isolate, which is associ

252 a similar role for PmrA in regulation of the C. burnetii T4BSS has been proposed.

253 es required for endocytic trafficking of the C. burnetii-containing vacuole to the lysosome.

254 estrict the intracellular replication of the C. burnetii.

255 coding genes were recently discovered on the C. burnetii cryptic QpH1 plasmid, three of which are con

256 Here we show that the C. burnetii secreted effector Coxiella vacuolar protein

257 of cytokines shows that cells exposed to the C. burnetii nopA::Tn or a Dot/Icm-defective dotA::Tn mut

258 Thirty-three C. burnetii proteins, previously identified as immunorea

259 Within whole lung tissue, C. burnetii preferentially replicated in hAMs.

260 first evidence of exposure of polar bears to C. burnetii, N. caninum, and F. tularensis.

261 well as designing vaccine countermeasures to C. burnetii aerosol transmission.

262 scular risk-factors and previous exposure to C. burnetii.

263 have a beta-lactamase enzyme (BlaM) fused to C. burnetii effector proteins to study protein transloca

264 PI-WVC stimulates protective immunity to C. burnetii in mice through stimulation of migratory beh

265 critical role in vaccine-induced immunity to C. burnetii infection by producing protective antibodies

266 udies suggested that Ab-mediated immunity to C. burnetii phase I LPS (PI-LPS) is protective.

267 8 (IL-8), neutrophil-attracting response to C. burnetii and ultimately shifted to an M2-polarized ph

268 vel of interleukin-10 (IL-10) in response to C. burnetii infection in vitro suggest that B1a cells ma

269 not play essential roles in the response to C. burnetii infection.

270 mechanisms of the innate immune response to C. burnetii natural infection, SCID mice were exposed to

271 studying the human innate immune response to C. burnetii.

272 TLR1, increased interleukin 10 responses to C. burnetii in individuals carrying the risk allele may

273 at adult Drosophila flies are susceptible to C. burnetii NMII infection and that this bacterial strai

274 se functions, some of which may be unique to C. burnetii pathotypes.

275 Monocytes migrated toward C. burnetii-coated beads independently of the presence o

276 Following aerosol-mediated transmission, C. burnetii replicates in alveolar macrophages in a uniq

277 acterial cell mass spectrometry of wild-type C. burnetii and the DeltapmrA mutant uncovered new compo

278 se, as opposed to cells exposed to wild-type C. burnetii or the corresponding nopA complemented strai

279 We show that a unique C. burnetii effector from the ankyrin repeat (Ank) famil

280 study provides further clarity on the unique C. burnetii-lung dynamic during early stages of human ac

281 To test this model, viable C. burnetii propagated in tissue culture host cells or a

282 hibited when PMN were challenged with viable C. burnetii, C. burnetii extracts, or rACP but not when

283 rred significant protection against virulent C. burnetii as early as 7 days postvaccination, which su

284 Both virulent C. burnetii Nine Mile phase I (NMI) and avirulent Nine M

285 s also required for PV formation by virulent C. burnetii isolates during infection of primary human a

286 al B cells were able to phagocytose virulent C. burnetii bacteria and form Coxiella-containing vacuol

287 These data support a model in which C. burnetii eludes the primary ROI killing mechanism of

288 creation of the specialized vacuole in which C. burnetii replicates represents a two-stage process me

289 While C. burnetii genomes are highly syntenous, recombination

290 ter in vitro stimulation of whole blood with C. burnetii antigens.

291 ssively accumulated around beads coated with C. burnetii extracts, and complete granulomas were gener

292 Whole blood incubated for 24 hours with C. burnetii Nine Mile showed optimal performance.

293 e with cardiac valve disease, infection with C. burnetii can cause a life-threatening infective endoc

294 We report on evidence of infection with C. burnetii in a small group of regular consumers of raw

295 During infection with C. burnetii, both TFEB and TFE3 were activated, as demon

296 ils in mice before intranasal infection with C. burnetii.

297 inea pigs were infected intratracheally with C. burnetii Nine Mile phase I (NMI) and demonstrated sus

298 Following inoculation of the lungs with C. burnetii Nine Mile phase I (NMI), SCID mice developed

299 rmine that the infection of macrophages with C. burnetii inhibits the caspase-11-mediated non-canonic

300 wed increased interleukin 10 production with C. burnetii exposure.

301 nonuclear cells (PBMCs) were stimulated with C. burnetii Nine Mile and the Dutch outbreak isolate C.