ライフサイエンスコーパス: A. phagocytophilum

1 A. phagocytophilum adhesion to and infection of neutroph

2 A. phagocytophilum binding to and invasion of BMMCs do n

3 A. phagocytophilum binding to sialyl Lewis x (sLe(x)) an

4 A. phagocytophilum causes macrophage activation and hemo

5 A. phagocytophilum combats neutrophil oxidative killing

6 A. phagocytophilum evades neutrophil oxidative killing b

7 A. phagocytophilum in blood and serologic response to bo

8 A. phagocytophilum increases the binding of a repressor,

9 A. phagocytophilum induces ticks to express Ixodes scapu

10 A. phagocytophilum infection also altered the apoptotic

11 A. phagocytophilum infection induced a significant eleva

12 A. phagocytophilum infection of BMMCs depends on alpha1,

13 A. phagocytophilum infection resulted in elevated cathep

14 A. phagocytophilum infection resulted in the up- and dow

15 A. phagocytophilum infection significantly decreased pha

16 A. phagocytophilum infection was not detected in the sam

17 A. phagocytophilum lacking lpda1 revealed enlargement of

18 A. phagocytophilum major surface protein 2 [Msp2(P44)] i

19 A. phagocytophilum migrated normally from A. phagocytoph

20 A. phagocytophilum MSP2(P44) orthologs expressed by othe

21 A. phagocytophilum not only fails to activate the normal

22 A. phagocytophilum stimulated IPAK1 activity via the G p

23 A. phagocytophilum undergoes a biphasic developmental cy

24 A. phagocytophilum undergoes a biphasic developmental cy

25 A. phagocytophilum's unique tropism for neutrophils, how

26 A. phagocytophilum-induced actin phosphorylation resulte

27 A. phagocytophilum-induced actin phosphorylation was dep

28 addition, larval ticks successfully acquired A. phagocytophilum from mice that were previously infect

29 nding domains of A. phagocytophilum adhesins A. phagocytophilum invasion protein A (AipA), A. phagocy

30 with isoatp4056 mRNA significantly affected A. phagocytophilum survival and isoatp4056 expression in

31 The presence of antibodies against A. phagocytophilum did not protect mice from a challenge

32 . phagocytophilum invasion protein A (AipA), A. phagocytophilum surface protein (Asp14), and outer me

33 tick "antifreeze glycoprotein." This allows A. phagocytophilum to successfully propagate and survive

34 results reported here suggest that although A. phagocytophilum-like organisms from white-tailed deer

35 tophilum that was remarkably conserved among A. phagocytophilum strains from human granulocytic anapl

36 ctrometry identified the major protein as an A. phagocytophilum 12.5-kDa hypothetical protein, which

37 These results identify Asp14 as an A. phagocytophilum surface protein that is critical for

38 mplifying the equivalent of one-eighth of an A. phagocytophilum-infected cell and 50 borrelia spiroch

39 By using an A. phagocytophilum Himar1 transposon mutant library, we

40 tion of XA induces isoatp4056 expression and A. phagocytophilum burden in both tick salivary glands a

41 assays for the detection of A. marginale and A. phagocytophilum 16S rRNA in plasma-free bovine periph

42 The promoters in both A. marginale and A. phagocytophilum have similar structure and activity,

43 copies of 16S rRNA of both A. marginale and A. phagocytophilum in the same reaction.

44 te and precise detection of A. marginale and A. phagocytophilum infections in cattle.

45 oinfections, with two of Babesia microti and A. phagocytophilum and one of B. microti and E. chaffeen

46 throughout RNA sequencing in uninfected and A. phagocytophilum-infected I. scapularis ISE6 tick cell

47 Asp14 and outer membrane protein A, another A. phagocytophilum invasin, pronouncedly reduced infecti

48 to confirm differential modification of any A. phagocytophilum MSP2(P44) paralog and the first to pr

49 t of previously described nested PCR assays (A. phagocytophilum, 16S rRNA; B. burgdorferi, fla gene),

50 Because A. phagocytophilum is an obligate intracellular bacteriu

51 litate understanding the interaction between A. phagocytophilum and the host.

52 the complexities of the interactions between A. phagocytophilum and host myeloid cells.

53 altered, suggesting a possible link between A. phagocytophilum infection and iron metabolism.

54 The dynamic range of the assay for both A. phagocytophilum and B. burgdorferi was >/=4 logs of m

55 produce a significant respiratory burst, but A. phagocytophilum did not inhibit the neutrophil respir

56 blood from HGA patients NY36 and NY37 and by A. phagocytophilum isolates from these patients cultured

57 The illness caused by A. phagocytophilum, human granulocytic anaplasmosis, occ

58 ber of msp2(p44) transcripts is expressed by A. phagocytophilum during in vitro cultivation.

59 omplement of Msp2(P44) paralogs expressed by A. phagocytophilum during infection of sLe(x)-competent

60 r clarifying essential proteins expressed by A. phagocytophilum during transmission from ticks to mam

61 The msp2 gene was expressed by A. phagocytophilum in the blood from HGA patients NY36 a

62 ith OmpA for protecting against infection by A. phagocytophilum and other Anaplasmataceae pathogens.

63 ein is important during in vivo infection by A. phagocytophilum.

64 fied into multiple 42- to 44-kDa isoforms by A. phagocytophilum strain HGE1 during infection of HL-60

65 g cathepsin L activity is a strategy used by A. phagocytophilum to alter CDP activity and thereby glo

66 nder identical conditions in the same cells, A. phagocytophilum, but not E. coli, significantly reduc

67 Thus, characterizing A. phagocytophilum genes that affect the inflammatory pr

68 nation, we developed a novel method to clone A. phagocytophilum.

69 ling pathway plays a key role in controlling A. phagocytophilum infection in ticks by regulating the

70 The PCR also detected A. phagocytophilum DNA in blood samples obtained from 53

71 able to detect 100% of previously diagnosed A. phagocytophilum cases.

72 Caveolae-mediated endocytosis directs A. phagocytophilum and E. chaffeensis to an intracellula

73 sequence analysis of the recently discovered A. phagocytophilum msp2 gene corroborated these results.

74 During A. phagocytophilum development in human promyelocytic HL

75 y, regulates the IL-18/IFN-gamma axis during A. phagocytophilum infection through its effect on caspa

76 nal inhibition of the gp91(phox) gene during A. phagocytophilum infection, providing evidence of the

77 ssed ferritin mRNA and protein levels during A. phagocytophilum infection in vitro using HL-60 cells

78 reased dramatically at the CYBB locus during A. phagocytophilum infection, particularly around AnkA b

79 thways in neutrophils and macrophages during A. phagocytophilum invasion and highlight the importance

80 ) expression was upregulated the most during A. phagocytophilum cellular invasion.

81 (JNK2) inhibits IFN-gamma production during A. phagocytophilum infection.

82 dy, the role of tick oxidative stress during A. phagocytophilum infection was characterized through t

83 erent geographic isolates suggests that each A. phagocytophilum genome carries a set of p44 paralogs

84 ese studies provide insight into the effects A. phagocytophilum has on the ferritin levels of its hos

85 The abilities of DC- and RC-enriched A. phagocytophilum populations to bind and/or infect HL-

86 tween dietary and genetic factors facilitate A. phagocytophilum infection and up-regulate a proinflam

87 h-cholesterol diet significantly facilitated A. phagocytophilum infection in the spleen, liver, and b

88 This study identifies the first A. phagocytophilum adhesin-receptor pair and delineates

89 Here we identified APH_1387 as the first A. phagocytophilum-derived protein that associates with

90 captured by affinity purification were five A. phagocytophilum proteins, Omp85, hypothetical protein

91 nstrate that AipA and Asp14 are critical for A. phagocytophilum to productively infect mice, and immu

92 ted expression of salp16, a gene crucial for A. phagocytophilum survival.

93 data suggest similar genetic mechanisms for A. phagocytophilum variation in all hosts but worldwide

94 As therapeutic options for A. phagocytophilum and related organisms are limited, th

95 Fourteen dogs (7.6%) were PCR positive for A. phagocytophilum.

96 ultaneous and rapid screening of samples for A. phagocytophilum and Borrelia species, two of the most

97 Clinical sensitivities for A. phagocytophilum and E. chaffeensis were 93% and 84%,

98 hase of clinical signs were seropositive for A. phagocytophilum antibodies but negative for Ehrlichia

99 he assay was found to be highly specific for A. phagocytophilum and the Borrelia species tested (B. b

100 Purified DNA from A. phagocytophilum and B. burgdorferi was spiked into DN

101 ed IFN-gamma release and protected mice from A. phagocytophilum, further demonstrating the inhibitory

102 Neutrophils from A. phagocytophilum-infected mice demonstrate elevated fe

103 A. phagocytophilum migrated normally from A. phagocytophilum-infected mice to the gut of engorging

104 ilarly, the amount of p44 mRNA obtained from A. phagocytophilum-infected HL-60 cells per bacterium wa

105 zes to the AVM in neutrophils recovered from A. phagocytophilum-infected mice.

106 Msp2 proteins from A. platys with those from A. phagocytophilum showed sequence identities of 86.4% f

107 Furthermore, A. phagocytophilum extends the life of its otherwise sho

108 and an efficient method not only to generate A. phagocytophilum-infected ticks but also provides a to

109 efficient microinjection method to generate A. phagocytophilum-infected ticks in laboratory conditio

110 o understand the role of host cholesterol in A. phagocytophilum infection in vivo, we analyzed the ef

111 ort the view that the p44 gene conversion in A. phagocytophilum occurs through the RecF pathway.

112 ire of p44 hypervariable sequences exists in A. phagocytophilum strains in the Northeastern United St

113 ent study, however, we found an msp2 gene in A. phagocytophilum that was remarkably conserved among A

114 otein ApxR was also significantly greater in A. phagocytophilum-infected HL-60 cells than in infected

115 4 mRNA was approximately threefold higher in A. phagocytophilum-infected HL-60 cells cultured at 37 d

116 feron (IFN)- gamma causes immunopathology in A. phagocytophilum infection models.

117 ibition of procaspase-3 processing occurs in A. phagocytophilum-infected human neutrophils.

118 tion (STAT) pathway plays a critical role in A. phagocytophilum infection of ticks.

119 HL-60 cells cultured at 37 degrees C than in A. phagocytophilum-infected HL-60 cells cultured at 28 d

120 nscript of the msp2 gene was undetectable in A. phagocytophilum strain HZ in SCID mice and Ixodes sca

121 Silencing of these genes increased A. phagocytophilum infection of tick salivary glands and

122 Indeed, A. phagocytophilum rapidly detoxifies O(2)(-) in a cell-

123 A(75-205) bind to, and competitively inhibit A. phagocytophilum infection of, host cells.

124 challenge and elicit antibodies that inhibit A. phagocytophilum cellular infection in vitro These dat

125 tert-butyldimethylsilyl)-c-di-GMP, inhibited A. phagocytophilum infection in HL-60 cells.

126 oups, but not from control groups, inhibited A. phagocytophilum infection of HL-60 cells.

127 proteins have a critical role in inhibiting A. phagocytophilum infection of host cells.

128 Instead, MAb 3E65 inhibited internalized A. phagocytophilum to develop into microcolonies called

129 aled that aph_0248 (designated asp14 [14-kDa A. phagocytophilum surface protein]) expression was upre

130 apoptosis than do components of heat-killed A. phagocytophilum alone.

131 Heat-killed A. phagocytophilum caused some similar initial alteratio

132 apoptosis inhibition in live or heat-killed A. phagocytophilum-infected neutrophils.

133 g the acute phase of well-defined laboratory A. phagocytophilum infections in naive equine hosts.

134 crease mitochondrial ROS production to limit A. phagocytophilum infection, while pathogen inhibits al

135 ciation with the neutrophil plasma membrane, A. phagocytophilum stimulates NADPH oxidase assembly, as

136 Moreover, A. phagocytophilum-infected cells are inhibited in the r

137 Thus, multiple A. phagocytophilum isolates share the ability to use sLe

138 nti-Asp55 peptide sera partially neutralized A. phagocytophilum infection of HL-60 cells in vitro.

139 Notably, A. phagocytophilum uptake induced fewer perturbations in

140 This may be explained by the ability of A. phagocytophilum to functionally impair neutrophils, i

141 The ability of A. phagocytophilum to trigger proinflammatory responses

142 The addition of A. phagocytophilum, as well as Escherichia coli and seru

143 To investigate the molecular basis of A. phagocytophilum survival within neutrophils, we used

144 wed cytoplasmic inclusions characteristic of A. phagocytophilum with pleomorphic bacteria in membrane

145 ne protein family, the surface components of A. phagocytophilum are largely unknown.

146 and tick hosts for more complete control of A. phagocytophilum and its associated diseases.

147 e critical for IFN-gamma-mediated control of A. phagocytophilum infection.

148 amma plays a critical role in the control of A. phagocytophilum; however, the mechanisms that regulat

149 f detection of one genome equivalent copy of A. phagocytophilum and can reliably detect 125 bacteria/

150 The life cycle of A. phagocytophilum is biphasic, transitioning between th

151 The tricarboxylic acid (TCA) cycle of A. phagocytophilum is incomplete and requires the exogen

152 e caused a marked reduction in the degree of A. phagocytophilum infection.

153 cations for the maintenance and detection of A. phagocytophilum in its vector and early pathogen inte

154 s a major improvement for early diagnosis of A. phagocytophilum in human patients and suggest a role

155 The binding domains of A. phagocytophilum adhesins A. phagocytophilum invasion

156 early demonstrates multifactorial effects of A. phagocytophilum infection on NB4 promyelocytic leukem

157 We therefore examined the effects of A. phagocytophilum infection on neutrophil NADPH oxidase

158 or 1 (IRF-1) and PU.1 in nuclear extracts of A. phagocytophilum-infected cells.

159 nally induced during transmission feeding of A. phagocytophilum-infected ticks on mice and is upregul

160 n was induced during transmission feeding of A. phagocytophilum-infected ticks on mice and was upregu

161 The dense-core (DC) form of A. phagocytophilum was isolated from in vitro cultures a

162 ralogous copies of msp2 within the genome of A. phagocytophilum Our novel RPA assay targeting this se

163 the amount obtained from salivary glands of A. phagocytophilum-infected Ixodes scapularis nymphs.

164 differential expression and glycosylation of A. phagocytophilum Msp2(P44).

165 We assessed the impact of A. phagocytophilum infection in NB4 promyelocytic leukem

166 Here, we demonstrate the importance of A. phagocytophilum outer membrane protein A (OmpA) APH_0

167 The zoonotic importance of A. phagocytophilum should support an increase in surveil

168 Although ingestion of A. phagocytophilum did not elicit significant PMN ROS, p

169 Importantly, ingestion of A. phagocytophilum failed to trigger the neutrophil apop

170 ed with one of the two sympatric isolates of A. phagocytophilum via tick bite and challenged 16 weeks

171 survival, we first assessed the kinetics of A. phagocytophilum entry into neutrophils by using doubl

172 UV cross-linking of A. phagocytophilum lysate with c-di-[(32)P]GMP detected

173 a donor p44 and the p44 expression locus of A. phagocytophilum was detected in an HL-60 cell culture

174 However, the mechanisms of A. phagocytophilum survival in neutrophils and the inhib

175 onstrate that the isolated outer membrane of A. phagocytophilum has porin activity, as measured by a

176 its predicted structural homology to OmpA of A. phagocytophilum (ApOmpA), an adhesin that uses key ly

177 n the obligatory intracellular parasitism of A. phagocytophilum and their biochemical activities were

178 ajor components in the early pathogenesis of A. phagocytophilum infection.

179 allenge (PCH) and tested for the presence of A. phagocytophilum as freshly molted nymphs.

180 Neutrophils in the presence of A. phagocytophilum did not produce a significant respira

181 We now show that the presence of A. phagocytophilum in I. scapularis ticks increases thei

182 bility shift assays revealed the presence of A. phagocytophilum proteins that interact with the promo

183 trophil respiratory burst in the presence of A. phagocytophilum was assessed by a kinetic cytochrome

184 Pretreatment of A. phagocytophilum organisms with OmpA antiserum reduces

185 phic 44-kDa major outer membrane proteins of A. phagocytophilum are dominant antigens recognized by p

186 To identify the major surface proteins of A. phagocytophilum, a membrane-impermeable, cleavable bi

187 The present study investigated regulation of A. phagocytophilum p44 genes, which encode the P44 major

188 lts demonstrate that the respective roles of A. phagocytophilum DCs and RCs are consistent with analo

189 way, Italy, and Switzerland and 4 samples of A. phagocytophilum-like organisms obtained from white-ta

190 rvariable region of each p44 cDNA species of A. phagocytophilum in naturally infected ticks and in di

191 amount of p44 mRNA obtained from spleens of A. phagocytophilum-infected SCID mice was approximately

192 Sequence variation between strains of A. phagocytophilum (90 to 100% identity at the nucleotid

193 expression site is present in all strains of A. phagocytophilum investigated.

194 information but did differentiate strains of A. phagocytophilum obtained from ruminants from those ob

195 hat msp2 is functional in various strains of A. phagocytophilum, and relative expression ratios of ms

196 d other gene expression profiling studies of A. phagocytophilum-infected neutrophils and promyelocyti

197 The surface of A. phagocytophilum plays a crucial role in subverting th

198 PH_1387 is not detectable on the surfaces of A. phagocytophilum dense core organisms bound at the HL-

199 e expression interfered with the survival of A. phagocytophilum that entered ticks fed on A. phagocyt

200 embrane proteins and neutralizing targets of A. phagocytophilum.

201 Transstadial transmission of A. phagocytophilum from larvae to nymphal stage was also

202 orthwestern Wisconsin, local transmission of A. phagocytophilum has not to date been documented.

203 ay that may be targeted for the treatment of A. phagocytophilum infection.

204 to promote bacterial survival: 1) uptake of A. phagocytophilum fails to trigger the apoptosis differ

205 DNA was recovered from the Ap-ha variant of A. phagocytophilum, associated exclusively with human in

206 reduced apolipoprotein E (apoE) activity on A. phagocytophilum infection in mice.

207 nfection, we conducted proteomic analyses on A. phagocytophilum organisms purified from HL-60 cells.

208 wn of isoatp4056 expression had no effect on A. phagocytophilum acquisition from the murine host but

209 A. phagocytophilum that entered ticks fed on A. phagocytophilum-infected mice.

210 sera but not with A. platys-negative sera or A. phagocytophilum-positive sera.

211 orylation, replaced by alanine) or two other A. phagocytophilum recombinant response regulators.

212 Because it was unknown whether other A. phagocytophilum isolates share this ability, we exten

213 fected or infected with low- or high-passage A. phagocytophilum and assayed for hepatic histopatholog

214 Compared to high-passage A. phagocytophilum-infected mice, low-passage A. phagocy

215 Low-passage A. phagocytophilum-infected mice also showed significant

216 . phagocytophilum-infected mice, low-passage A. phagocytophilum-infected mice had more severe hepatic

217 patic histopathology severity in low-passage A. phagocytophilum-infected mice peaked on day 2 at the

218 ed, thereby verifying 23.7% of the predicted A. phagocytophilum proteome.

219 at blocking APH_1235 with antibodies reduced A. phagocytophilum infection levels in mammalian cell cu

220 d that a c-di-GMP-receptor complex regulates A. phagocytophilum intracellular infection.

221 ast, AnkA orthologues in the closely related A. phagocytophilum and Ehrlichia chaffeensis have been s

222 Remarkably, A. phagocytophilum induced the expression of iafgp, ther

223 n conserved and may be unique to the species A. phagocytophilum.

224 We conclude that A. phagocytophilum does not suppress a global respirator

225 We demonstrate that A. phagocytophilum binds and/or infects murine bone marr

226 We now demonstrate that A. phagocytophilum modifies the I. scapularis microbiota

227 Previous results demonstrated that A. phagocytophilum does not induce the production of ROS

228 We have previously demonstrated that A. phagocytophilum organisms of the NCH-1 strain that ut

229 aper presents the first direct evidence that A. phagocytophilum actively modifies its host cell-deriv

230 y shift assays provide further evidence that A. phagocytophilum and XA influences isoatp4056 expressi

231 We investigated the hypotheses that A. phagocytophilum invades mast cells and inhibits mast

232 t-pathogen coevolution by hypothesizing that A. phagocytophilum utilizes common molecular mechanisms

233 These data define a mechanism that A. phagocytophilum uses to selectively alter arthropod g

234 Our Affymetrix data revealed that A. phagocytophilum altered the expression of transcripti

235 We now show that A. phagocytophilum induces expression of the Ixodes scap

236 We show that A. phagocytophilum induces the phosphorylation of actin

237 We now show that A. phagocytophilum infection also enhances the binding o

238 In this study, we show that A. phagocytophilum specifically up-regulates I. scapular

239 A during pathogen infection, and showed that A. phagocytophilum modifies I. scapularis tick cell miRN

240 Sukumaran et al. recently showed that A. phagocytophilum uses a tick salivary protein, Salp16,

241 These data suggest that A. phagocytophilum may alter selected host pathways in o

242 These results suggest that A. phagocytophilum strains from ruminants could share so

243 is in western Washington State suggests that A. phagocytophilum infection should be considered in dif

244 rophils and tick cells, thus supporting that A. phagocytophilum uses common mechanisms for infection

245 The A. phagocytophilum burden increases in salivary glands a

246 p22(phox) were significantly reduced at the A. phagocytophilum phagosome after 1 and 4 h of incubati

247 hways, of recombination were detected in the A. phagocytophilum genome.

248 11% of the open reading frames (ORFs) in the A. phagocytophilum genome.

249 found, and all of these had orthologs in the A. phagocytophilum HZ strain genome that shared 95 to 10

250 The msp2 gene in the A. phagocytophilum strain HZ genome was a single-copy ge

251 that a single transposon insertion into the A. phagocytophilum dihydrolipoamide dehydrogenase 1 gene

252 The expression of the A. phagocytophilum 16S rRNA, sdhC, and sdhD genes was ex

253 ication enzymes, suggesting that most of the A. phagocytophilum cells were no longer dividing.

254 Interestingly, transcription of the A. phagocytophilum gene encoding the DNA binding protein

255 The recently completed sequence of the A. phagocytophilum genome confirmed our findings and ind

256 (phox) was present on 20, 14, and 10% of the A. phagocytophilum phagosomes, whereas p22(phox) was pre

257 most completely blocked the infection of the A. phagocytophilum population that predominantly express

258 is work represents an extensive study of the A. phagocytophilum proteome, discerns the complement of

259 While the conservation of the A. phagocytophilum Sdh proteins, including the residues

260 Asp14 localized to the A. phagocytophilum surface and was expressed during in v

261 cted by the bites of ticks infected with the A. phagocytophilum NTN-1 strain or of naturally infected

262 lum-derived protein that associates with the A. phagocytophilum-occupied vacuolar membrane (AVM).

263 Thus, A. phagocytophilum employs at least two strategies to pr

264 Thus, A. phagocytophilum mitigates mast cell activation.

265 Thus, A. phagocytophilum needs to usurp and acquire various co

266 ere more susceptible than control animals to A. phagocytophilum infection due to the absence of IL-18

267 neutrophils and promyelocytic HL-60 cells to A. phagocytophilum are linked to bacterial usage of P-se

268 gs to Bartonella and the exposure of dogs to A. phagocytophilum in this study.

269 higher in groups of control mice exposed to A. phagocytophilum for the first time than in mice reinf

270 effect was initially mediated by exposure to A. phagocytophilum components in heat-killed bacteria.

271 ctivation of the p38 MAPK pathway leading to A. phagocytophilum-delayed neutrophil apoptosis is bypas

272 The resistance of jnk2-null mice to A. phagocytophilum infection was due to elevated levels

273 scriptional response of human neutrophils to A. phagocytophilum infection.

274 white-tailed deer may be closely related to A. phagocytophilum, they could be more diverse.

275 However, differences in ROS response to A. phagocytophilum infection between human and tick cell

276 Antibody response to A. phagocytophilum, but not B. burgdorferi, was decrease

277 ired for IFN-gamma production in response to A. phagocytophilum.

278 n a2-deficient mice were more susceptible to A. phagocytophilum infection and showed splenomegaly, th

279 These ticks successfully transmitted A. phagocytophilum to the murine host.

280 ntimicrobial peptides is highly induced upon A. phagocytophilum infection of tick salivary glands.

281 When A. phagocytophilum was preincubated with plasma from the

282 To explore the mechanism by which A. phagocytophilum increases CDP activity, we assessed t

283 potentially represent a novel means by which A. phagocytophilum usurps host defense mechanisms and sh

284 g domains in alum followed by challenge with A. phagocytophilum The bacterial peripheral blood burden

285 for IFN-gamma secretion upon challenge with A. phagocytophilum.

286 These results suggest that coinfection with A. phagocytophilum and B. burgdorferi modulates pathogen

287 poptotic interleukin 8 (IL-8) expressed with A. phagocytophilum infection was excluded by the use of

288 sts its role in innate immune induction with A. phagocytophilum infections.

289 n be used to identify patients infected with A. phagocytophilum and is the microbiologic gold standar

290 uman promyelocytic HL-60 cells infected with A. phagocytophilum demonstrate increased transcription o

291 tron microscopy of neutrophils infected with A. phagocytophilum or Escherichia coli revealed that NAD

292 tissue of C3H mice previously infected with A. phagocytophilum.

293 mice were more refractory to infection with A. phagocytophilum and produced increased levels of IFN-

294 mune response to a tick-borne infection with A. phagocytophilum provides protection against homologou

295 partially protects mice from infection with A. phagocytophilum.

296 PMN gene expression following infection with A. phagocytophilum.

297 development of histopathologic lesions with A. phagocytophilum infection.

298 IFN-gamma after in vitro restimulation with A. phagocytophilum.

299 In neutrophils incubated simultaneously with A. phagocytophilum and E. coli for 30, 60, and 90 min, g

300 d of all seven dogs that were tested yielded A. phagocytophilum after a comparison to bacterial seque