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 , United Kingdom, and rapidly acquired acute A. phagocytophilum infections detectable by PCR and bloo

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

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

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

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

33 Seven North American A. phagocytophilum strains were compared by PFGE.

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

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

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

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

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

39 Analysis of E. chaffeensis and A. phagocytophilum genome sequences revealed that these

40 0 cells used as hosts for E. chaffeensis and A. phagocytophilum.

41 ential transmigration of E. chaffeensis- and A. phagocytophilum-infected leukocytes and HL-60 cells c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 During A. phagocytophilum development in human promyelocytic HL

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

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

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

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

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

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

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

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

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

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

83 at a level similar to that of extracellular A. phagocytophilum and significantly (P < 0.05) beyond t

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

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

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

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

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

89 ypothesized that Msp2 acts as an adhesin for A. phagocytophilum entry into granulocytes.

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

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

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

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

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

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

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

97 PCR testing for A. phagocytophilum revealed that 5 of 263 (1.9%) from no

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

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

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

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

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

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

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

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

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

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

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

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

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

111 4 mRNA was approximately threefold higher in A. phagocytophilum-infected HL-60 cells cultured at 37 d

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

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

114 e a genomic expression site for MSP2(P44) in A. phagocytophilum.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 ata suggest that, similarly to A. marginale, A. phagocytophilum uses combinatorial mechanisms to gene

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

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

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

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

134 Notably, A. phagocytophilum uptake induced fewer perturbations in

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

136 The ability of A. phagocytophilum to trigger proinflammatory responses

137 uminescence is observed upon the addition of A. phagocytophilum to neutrophils, indicating that the b

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

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

140 Like binding of P-selectin, binding of A. phagocytophilum to human neutrophils requires express

141 Binding of A. phagocytophilum to murine neutrophils, however, requi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 DNA sequencing revealed two genotypes of A. phagocytophilum, the human granulocytic ehrlichiosis

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

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

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

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

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

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

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

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

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

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

167 sponding to the p44-1/p44-18 tandem locus of A. phagocytophilum HZ in 14 other geographically diverge

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

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

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

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

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

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

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

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

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

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

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

179 Pretreatment of A. phagocytophilum organisms with OmpA antiserum reduces

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

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

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

183 s that ruminants are efficient reservoirs of A. phagocytophilum during the acute and post-acute phase

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

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

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

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

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

189 New World strains of A. phagocytophilum have a large genome and a high degree

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

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

192 p44 gene expression loci in four strains of A. phagocytophilum were identified and it was determined

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

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

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

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

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

198 embrane proteins and neutralizing targets of A. phagocytophilum.

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

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

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

202 direct assays were further tested by use of A. phagocytophilum template DNA from both North America

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 results demonstrate that, unlike P-selectin, A. phagocytophilum binds cooperatively to a nonsulfated

222 Unlike P-selectin, A. phagocytophilum bound to cells expressing PSGL-1 in c

223 Like P-selectin, A. phagocytophilum bound to purified human PSGL-1 and to

224 of the same p44 cDNA species within a single A. phagocytophilum strain and among different strains we

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 The A. phagocytophilum burden increases in salivary glands a

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

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

247 11% of the open reading frames (ORFs) in the A. phagocytophilum genome.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

263 Thus, A. phagocytophilum mitigates mast cell activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 When A. phagocytophilum was preincubated with plasma from the

279 smigrated than uninfected monocytes, whereas A. phagocytophilum suppressed neutrophil transmigration.

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

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

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

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

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

285 neutrophils persisted for at least 18 h with A. phagocytophilum infection, whereas Escherichia coli a

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

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

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

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

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

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

292 We hypothesized that infection with A. phagocytophilum modifies the binding of neutrophils t

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

294 partially protects mice from infection with A. phagocytophilum.

295 PMN gene expression following infection with A. phagocytophilum.

296 development of histopathologic lesions with A. phagocytophilum infection.

297 mmation, and immune response that occur with A. phagocytophilum infections.

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