ライフサイエンスコーパス: burnetii

1 dying the human innate immune response to C. burnetii.

2 restrict the intracellular replication of C. burnetii.

3 ophila, Legionella longbeachae, and Coxiella burnetii.

4 on, SCID mice were exposed to aerosolized C. burnetii.

5 early immune response against aerosolized C. burnetii.

6 old contacts were traced and screened for C. burnetii.

7 neration of human granulomas specific for C. burnetii.

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

9 genetic evidence of a functional T4SS in C. burnetii.

10 ntitis caused by a unique strain of Coxiella burnetii.

11 challenged with electron beam-inactivated C. burnetii.

12 he obligate intracellular bacterium Coxiella burnetii.

13 r is a worldwide zoonosis caused by Coxiella burnetii.

14 lar risk-factors and previous exposure to C. burnetii.

15 Q fever is an infection caused by Coxiella burnetii.

16 in mice before intranasal infection with C. burnetii.

17 rict the intracellular replication of the C. burnetii.

18 ed to decreased cytokine production after C. burnetii 3262 stimulation but not after C. burnetii Nine

19 Nine Mile and the Dutch outbreak isolate C. burnetii 3262.

20 recognition of C. burnetii Nine Mile and C. burnetii 3262.

21 Q fever is caused by Coxiella burnetii, a bacterium that persists in M2-polarized macr

22 Q fever is a zoonosis caused by Coxiella burnetii, a unique bacterium that is widespread but infr

23 Together, these results demonstrate that C. burnetii actively directs PV-autophagosome interactions

24 Earlier studies suggested that C. burnetii actively inhibited release of ROI from PMN thro

25 Recent reports suggest that C. burnetii actively recruits autophagosomes to the PV to d

26 er of 1E4 would protect SCID mice against C. burnetii aerosol infection.

27 , suggesting that neutrophils cannot kill C. burnetii and C. burnetii may be using infection of neutr

28 nomes throughout a 14-day growth cycle of C. burnetii and found that they were inversely correlated,

29 ere quantified in synchronous cultures of C. burnetii and found to closely parallel those of 16S rRNA

30 stance, mammalian pathogens such as Coxiella burnetii and Francisella tularensis, as well as Coxiella

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

32 ubstrates of the Dot/Icm system from both C. burnetii and L. pneumophila.

33 Coxiella burnetii and Legionella pneumophila are evolutionarily r

34 erial cell mass spectrometry of wild-type C. burnetii and the DeltapmrA mutant uncovered new componen

35 Studying the interaction between C. burnetii and the innate immune system can provide a mode

36 pothesize that inefficient recognition of C. burnetii and/or activation of host-defense in individual

37 eria such as Enterococcus faecalis, Coxiella burnetii, and Clostridium difficile.

38 anthracis; Francisella tularensis; Coxiella burnetii; and Ebola, Marburg, and Lassa fever viruses us

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

40 in vitro stimulation of whole blood with C. burnetii antigens.

41 primary adaptive immune response to Coxiella burnetii are not well known.

42 The effector proteins delivered by C. burnetii are predicted to have important functions durin

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

44 ne Mile phase II (NMII) clone 4 strain of C. burnetii, as a model to investigate host and bacterial c

45 moniae, Legionella longbeachae, and Coxiella burnetii, as well as the plant pathogen Ralstonia solana

46 B cells were able to phagocytose virulent C. burnetii bacteria and form Coxiella-containing vacuoles

47 Despite Coxiella burnetii being an obligate intracellular bacterial patho

48 ited when PMN were challenged with viable C. burnetii, C. burnetii extracts, or rACP but not when PMN

49 ith cardiac valve disease, infection with C. burnetii can cause a life-threatening infective endocard

50 iella-containing vacuoles (CCVs) and that C. burnetii can infect and replicate in peritoneal B1a subs

51 ates were lower than 29%, suggesting that C. burnetii can infect neutrophils, but infection is limite

52 Infection with Coxiella burnetii can lead to acute and chronic Q fever.

53 Coxiella burnetii causes human Q fever, a zoonotic disease that p

54 severity of disease following intranasal C. burnetii challenge, suggesting that keratinocyte-derived

55 volved in protecting vaccinated mice from C. burnetii challenge-induced disease.

56 to confer significant protection against C. burnetii challenge.

57 Monocytes migrated toward C. burnetii-coated beads independently of the presence of T

58 the obligate intracellular pathogen Coxiella burnetii contains a large number of selfish genetic elem

59 ing genes were recently discovered on the C. burnetii cryptic QpH1 plasmid, three of which are conser

60 A C. burnetii DeltacvpA mutant exhibited significant defects

61 and PV generation, whereas the growth of C. burnetii DeltacvpB and DeltacvpC was rescued upon cohabi

62 C. burnetii DeltacvpB, DeltacvpC, DeltacvpD, and DeltacvpE

63 Compared to wild-type bacteria, C. burnetii DeltapmrA exhibited severe intracellular growth

64 he intracellular bacterial pathogen Coxiella burnetii directs biogenesis of a parasitophorous vacuole

65 he intracellular bacterial pathogen Coxiella burnetii directs biogenesis of a phagolysosome-like para

66 Based on [(35)S]Cys-Met incorporation, C. burnetii displayed optimal metabolic activity in citrate

67 The obligate intracellular pathogen Coxiella burnetii displays antiapoptotic activity which depends o

68 These data suggest that C. burnetii does not actively inhibit phagolysosome functio

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

70 critical virulence factor that regulates C. burnetii Dot/Icm secretion.

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

72 translocation of effector proteins by the C. burnetii Dot/Icm system occurs after acidification of th

73 he identification of 32 substrates of the C. burnetii Dot/Icm system using a fluorescence-based beta-

74 tools, secretion of plasmid effectors by C. burnetii during host cell infection was confirmed using

75 Replication of C. burnetii during infection has been shown to be increased

76 ecreted in a Dot/Icm-dependent fashion by C. burnetii during infection of human THP-1 macrophages.

77 We show that a unique C. burnetii effector from the ankyrin repeat (Ank) family c

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

79 e a beta-lactamase enzyme (BlaM) fused to C. burnetii effector proteins to study protein translocatio

80 We predict additional C. burnetii effectors localize to the PV membrane and regul

81 ed a machine-learning approach to predict C. burnetii effectors, and examination of 20 such proteins

82 To identify novel C. burnetii effectors, we applied a machine-learning approa

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

84 Collectively, these results indicate that C. burnetii encodes a large repertoire of T4SS substrates t

85 The human pathogen Coxiella burnetii encodes a type IV secretion system called Dot/I

86 Collectively, these data indicate C. burnetii encodes multiple effector proteins that target

87 Coxiella burnetii endocarditis is considered to be a late complic

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

89 ized MAb as emergency prophylaxis against C. burnetii exposure.

90 increased interleukin 10 production with C. burnetii exposure.

91 C. burnetii extracts and rACP were also able to inhibit PMA

92 vely accumulated around beads coated with C. burnetii extracts, and complete granulomas were generate

93 issue culture host cells or axenic media, C. burnetii extracts, or purified recombinant ACP (rACP) wa

94 were challenged with viable C. burnetii, C. burnetii extracts, or rACP but not when PMN were challen

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

96 esicular trafficking pathways co-opted by C. burnetii for PV development are poorly defined; however,

97 s Brucella spp., Toxoplasma gondii, Coxiella burnetii, Francisella tularensis, and Neospora caninum,

98 pression profiling, allowed the rescue of C. burnetii from its host cell to regain the axenic growth

99 quintana, Bartonella henselae, and Coxiella burnetii from surgical heart valve tissue specimens with

100 L-1 may be important for the clearance of C. burnetii from the lungs following intranasal infection.

101 ere the cloning and characterization of a C. burnetii ftsZ mutant generated by mariner-based Himar1 t

102 Cloned C. burnetii fur complemented an Escherichia coli fur deleti

103 hila as a surrogate host, reveals a novel C. burnetii gene (IcaA) involved in the inhibition of caspa

104 In human cells, C. burnetii generates a replication niche termed the parasi

105 s revealed multiple transpositions in the C. burnetii genome and rescue cloning identified 30 and 5 i

106 However, significantly higher C. burnetii genome copy numbers were detected in the lungs

107 While C. burnetii genomes are highly syntenous, recombination bet

108 ogen's proteome, probed with biotinylated C. burnetii genomic DNA.

109 Moreover, correlations between C. burnetii genomic groups and human disease presentation (

110 vity, no p62 turnover was observed during C. burnetii growth in macrophages, suggesting that the path

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

112 To define conditions that support C. burnetii growth, we systematically evaluated the organis

113 C. burnetii has evolved to replicate in this harsh compartm

114 nase pathways are most likely targeted by C. burnetii Icm/Dot effectors.

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

116 h L. pneumophila was also translocated by C. burnetii in a process that requires its C terminus, prov

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

118 t the value of systematically testing for C. burnetii in antiphospholipid-associated cardiac valve di

119 re the aeration process, the transport of C. burnetii in bioaerosols via the air, the aerosolization

120 4SS are implicated in the pathogenesis of C. burnetii in flies.

121 wn about their role in the recognition of C. burnetii in humans.

122 e induction of cytokine responses against C. burnetii in humans.

123 R1, increased interleukin 10 responses to C. burnetii in individuals carrying the risk allele may con

124 rosols via the air, the aerosolization of C. burnetii in the shower, and the air filtration efficienc

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

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

127 of clathrin-coated vesicle trafficking in C. burnetii infection and define a role for CvpA in subvert

128 sults suggest a versatile role for PKA in C. burnetii infection and indicate virulent organisms usurp

129 is a novel diagnostic assay for previous C. burnetii infection and shows similar performance and pra

130 st Rho GTPases for establishment of Coxiella burnetii infection and virulence in mammalian cell cultu

131 tical role in vaccine-induced immunity to C. burnetii infection by producing protective antibodies.

132 Fv1E4, and huscFv1E4 were able to inhibit C. burnetii infection in mice but that their ability to inh

133 ntibody (MAb) 1E4 significantly inhibited C. burnetii infection in mice, suggesting that 1E4 is a pro

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

135 of interleukin-10 (IL-10) in response to C. burnetii infection in vitro suggest that B1a cells may p

136 inated WT mouse sera were able to inhibit C. burnetii infection in vivo, but only IgM from PIV-vaccin

137 lts indicate that 1E4 was able to inhibit C. burnetii infection in vivo, suggesting that 1E4 is a pro

138 20-KLH-immunized mice was able to inhibit C. burnetii infection in vivo, suggesting that m1E41920 may

139 eritoneal B cells in host defense against C. burnetii infection in vivo.

140 In contrast, our finding that C. burnetii infection induced more-severe splenomegaly and

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

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

143 d probed the role of PKA signaling during C. burnetii infection of macrophages.

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

145 f neutrophils in the host defense against C. burnetii infection remains unclear.

146 f B cells in host defense against primary C. burnetii infection remains unclear.

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

148 were differentially phosphorylated during C. burnetii infection, suggesting the pathogen uses PKA sig

149 eutrophils in protective immunity against C. burnetii infection, the RB6-8C5 antibody was used to dep

150 ibility of using humanized 1E4 to prevent C. burnetii infection, we examined whether the Fab fragment

151 not significantly affect the severity of C. burnetii infection-induced diseases in both severe combi

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

153 4) retained the ability of 1E4 to inhibit C. burnetii infection.

154 mechanisms of pulmonary immunity against C. burnetii infection.

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

156 ity of PIV to confer protection against a C. burnetii infection.

157 al role in PIV-induced protection against C. burnetii infection.

158 t play essential roles in the response to C. burnetii infection.

159 tant role in host defense against primary C. burnetii infection.

160 fector that influences ER function during C. burnetii infection.

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

162 tant role in host defense against primary C. burnetii infection.

163 eutrophils in protective immunity against C. burnetii infection.

164 i with huscFv1E4 can significantly reduce C. burnetii infectivity in human macrophages.

165 In humans, C. burnetii infects alveolar macrophages and promotes phago

166 Coxiella burnetii infects mononuclear phagocytes, where it direct

167 Here, we show that C. burnetii inhibits caspase-1 activation in primary mouse

168 ne that the infection of macrophages with C. burnetii inhibits the caspase-11-mediated non-canonical

169 Interestingly, C. burnetii inside neutrophils can infect and replicate wit

170 ng a valuable approach for characterizing C. burnetii interactions with a human host.

171 ffector protein CvpA was found to promote C. burnetii intracellular growth and PV expansion.

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

173 Several effectors crucial for C. burnetii intracellular replication have been identified,

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

175 Coxiella burnetii is a Gram-negative bacterium that causes acute

176 Coxiella burnetii is a Gram-negative, obligate intracellular bact

177 Coxiella burnetii is a highly infectious bacterium that promotes

178 Coxiella burnetii is a widespread zoonotic bacterial pathogen tha

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

180 Coxiella burnetii is an intracellular bacterial pathogen that cau

181 Coxiella burnetii is an intracellular Gram-negative bacterium tha

182 Coxiella burnetii is an obligate intracellular bacterial pathogen

183 Coxiella burnetii is an obligate intracellular bacterium that cau

184 Coxiella burnetii is an obligate intracellular bacterium that dir

185 Coxiella burnetii is an obligate intracellular Gram-negative bact

186 Coxiella burnetii is the bacterial agent of human Q fever, an acu

187 Coxiella burnetii is the causative agent of Q fever, a zoonotic d

188 er, an infectious disease caused by Coxiella burnetii, is associated with granuloma formation.

189 enomic rearrangements, and pseudogenes of C. burnetii isolates are consistent with genome structures

190 All C. burnetii isolates carry a large, autonomously replicatin

191 lso required for PV formation by virulent C. burnetii isolates during infection of primary human alve

192 n reading frame (CbuD1884) present in all C. burnetii isolates except the Nine Mile reference isolate

193 gical responses to infection with phase I C. burnetii isolates from the following four genomic groups

194 C. burnetii isolates have a range of disease potentials; is

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

196 d, three of which are conserved among all C. burnetii isolates, suggesting that they are critical for

197 C. burnetii lacks enzymes for de novo cholesterol biosynthe

198 ia (Bartonella spp., Brucella spp., Coxiella burnetii, Leptospira spp., Rickettsia spp., Salmonella e

199 Recent studies have indicated that C. burnetii likely originated from a tick-associated ancest

200 Coxiella burnetii load was high on-farm (2009), and lower off-far

201 he current study, we further investigated C. burnetii manipulation of host cell signaling and apoptos

202 t neutrophils cannot kill C. burnetii and C. burnetii may be using infection of neutrophils as an eva

203 ic medium that supports sustained (>24 h) C. burnetii metabolic activity.

204 buffers have been described that activate C. burnetii metabolism in vitro, but metabolism is short-li

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

206 es of both phase I and phase II Nine Mile C. burnetii multiply and are less readily cleared from the

207 st evidence of exposure of polar bears to C. burnetii, N. caninum, and F. tularensis.

208 chanisms of the innate immune response to C. burnetii natural infection, SCID mice were exposed to ae

209 dies (Abs) can provide protection against C. burnetii natural infection, we examined if passive trans

210 ing that 1E4 may be useful for preventing C. burnetii natural infection.

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

212 uclear cells (PBMCs) were stimulated with C. burnetii Nine Mile and the Dutch outbreak isolate C. bur

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

214 nt study demonstrated that virulent Coxiella burnetii Nine Mile phase I (NMI) is capable of infecting

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

216 identified upon genome sequencing of the C. burnetii Nine Mile reference isolate, which is associate

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

218 . burnetii 3262 stimulation but not after C. burnetii Nine Mile stimulation.

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

220 adult Drosophila flies are susceptible to C. burnetii NMII infection and that this bacterial strain,

221 The C. burnetii NMII T4SS translocates bacterial products into

222 factor (TNF) produced upon TLR sensing of C. burnetii NMII was required to control bacterial replicat

223 cal role for extrachromosomal elements in C. burnetii pathogenesis.

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

225 C. burnetii persists within and is transmitted by mammalian

226 mechanisms of formalin-inactivated Coxiella burnetii phase I (PI) vaccine (PIV)-induced protection,

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

228 Collectively, these results suggest that C. burnetii plasmid-encoded T4SS substrates play important

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

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

231 ron present in the 23S rRNA gene of Coxiella burnetii, possesses a unique 3'-terminal adenine in plac

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

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

234 present the first published case of Coxiella burnetii prosthetic joint infection.

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

236 ociated with the production of additional C. burnetii proteins involved in host cell parasitism.

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

238 e T4SS effector repertoire encoded by the C. burnetii QpH1, QpRS, and QpDG plasmids that were origina

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

240 absence of LexA, co-protease activity for C. burnetii RecA was demonstrated.

241 rved and more apparent with expression of C. burnetii RecAG159D mutant protein.

242 burg, the Netherlands, reported 220 Coxiella burnetii-related abortions in 450 pregnant goats.

243 aused by the intracellular pathogen Coxiella burnetii, relies mainly on serology and, in prevaccinati

244 Following aerosol-mediated transmission, C. burnetii replicates in alveolar macrophages in a unique

245 The Q fever bacterium Coxiella burnetii replicates inside host cells within a large Cox

246 ation of the specialized vacuole in which C. burnetii replicates represents a two-stage process media

247 Coxiella burnetii replicates within permissive host cells by empl

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

249 n of HeLa cells, which are permissive for C. burnetii replication.

250 y siRNA treatment significantly inhibited C. burnetii replication.

251 ded for biogenesis of prototypical PV and C. burnetii replication.

252 C. burnetii requires this lysosomal environment for replica

253 lonization by the Q fever pathogen, Coxiella burnetii, requires translocation of effector proteins in

254 m and opens the door for a renaissance in C. burnetii research.

255 ositive for B. quintana, B. henselae, and C. burnetii, respectively, by the dPCR assay, which matched

256 provide a more-complete understanding of C. burnetii's genetic diversity, evolution, and pathogenic

257 Here we show that the C. burnetii secreted effector Coxiella vacuolar protein B (

258 These results suggest that C burnetii should be added to the list of bacteria that pr

259 lack of methods to genetically manipulate C. burnetii significantly impedes the study of this organis

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

261 In this study, C. burnetii-specific interferon gamma (IFN-gamma) productio

262 RK led to decreased cytokine responses in C. burnetii-stimulated human PBMCs.

263 ignificant protection against aerosolized C. burnetii, suggesting that 1E4 may be useful for preventi

264 imilar role for PmrA in regulation of the C. burnetii T4BSS has been proposed.

265 ar effector proteins, a list of predicted C. burnetii T4BSS substrates was compiled using bioinformat

266 racterized a thiol-specific peroxidase of C. burnetii that belongs to the atypical 2-cysteine subfami

267 The 23S rRNA gene of Coxiella burnetii, the agent of Q fever in humans, contains an un

268 Growth of Coxiella burnetii, the agent of Q fever, is strictly limited to c

269 Coxiella burnetii, the causative agent of human Q (Query) fever,

270 For over seven decades, Coxiella burnetii, the causative agent of human Q fever, has been

271 Coxiella burnetii, the causative agent of Q fever, establishes a

272 Coxiella burnetii, the causative agent of Q fever, is a human int

273 Coxiella burnetii, the causative agent of Q fever, is a zoonotic

274 ccessful macrophage colonization by Coxiella burnetii, the cause of human Q fever, requires pathogen-

275 Coxiella burnetii, the etiological agent of acute and chronic Q f

276 Coxiella burnetii, the etiological agent of human Q fever, occupi

277 Coxiella burnetii, the etiological agent of Q fever in humans, is

278 Coxiella burnetii, the etiological agent of Q fever, is a small,

279 (pppy), hence the risk of transmission of C. burnetii through inhalation of drinking water aerosols i

280 nome reduction suggests the adaptation of C. burnetii to an obligate intracellular lifestyle is a rec

281 ely reflect a unique repair adaptation of C. burnetii to its hostile niche.

282 ellular bacterial agent of Q fever, Coxiella burnetii, translocates effector proteins into its host c

283 lytic cell death did not occur following C. burnetii-triggered inflammasome activation, indicating a

284 fection in vitro and found that avirulent C. burnetii triggers sustained interleukin-1beta (IL-1beta)

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

286 In human alveolar macrophages, C. burnetii uses a Dot/Icm type IV secretion system (T4SS)

287 ng virulent phase I or avirulent phase II C. burnetii variants in human mononuclear phagocytes.

288 C. burnetii was coelectroporated with a plasmid encoding th

289 C burnetii was detected in CD68(+) macrophages within both

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

291 Serodiagnosis for Coxiella burnetii was performed for all patients.

292 The presence of Coxiella burnetii was tested using immunofluorescence and fluores

293 male and female mice infected with Coxiella burnetii, we hypothesized that circadian genes are diffe

294 Importantly, axenically grown C. burnetii were highly infectious for Vero cells and exhib

295 th a known role in initial recognition of C. burnetii were included.

296 membrane protein similar to Com1 of Coxiella burnetii, which we designate as dsbA2.

297 Axenic cultivation of C. burnetii will facilitate studies of the organism's patho

298 In addition, treatment of C. burnetii with Fab1E4, muscFv1E4, or huscFv1E4 can block

299 Interestingly, treatment of C. burnetii with huscFv1E4 can significantly reduce C. burn

300 tudy demonstrated that treatment of Coxiella burnetii with the phase I lipopolysaccharide (PI-LPS)-ta