ライフサイエンスコーパス: phagosomal

1 -killed Escherichia coli, demonstrating that phagosomal acidification affects endosomal receptor-medi

2 ic fibrosis lung disease involving defective phagosomal acidification and bacterial killing in alveol

3 d not affect POS internalization but reduced phagosomal acidification and delayed POS protein clearan

4 pharmacological block of p38 activity caused phagosomal acidification and enrichment of the late endo

5 luating bacterial intracellular survival and phagosomal acidification and maturation and by testing t

6 TFEB promoted phagosomal acidification and protein degradation.

7 oxidase NOX2 in DCs, which in turn inhibited phagosomal acidification and reduced the degradation of

8 Critical to phagosomal acidification are various channels derived fr

9 summary, our results identify the control of phagosomal acidification as a novel function of Abl tyro

10 Phagosomal acidification began within 3 min of zymosan b

11 Inhibition of phagosomal acidification blocks TLR9 accumulation on pha

12 Importantly, blocking of phagosomal acidification by inhibiting vacuolar-type H(+

13 Phagosomal acidification facilitates the optimal functio

14 ng fluorescent probe that enabled imaging of phagosomal acidification in activated macrophages.

15 associated with accelerated phagocytosis and phagosomal acidification in DCs.

16 We also measured the kinetics of phagosomal acidification in J774A.1 and murine alveolar

17 The rate of phagosomal acidification in J774A.1 cells was not slowed

18 Differences in phagosomal acidification indicated that in chicken lungs

19 d NALP3 activation, and inhibition of either phagosomal acidification or cathepsin B activity impaire

20 Inhibition of macrophage phagosomal acidification resulted in a 30-fold reduction

21 phage viability and found that inhibitors of phagosomal acidification significantly impaired USA300 i

22 In addition, inhibition of phagosomal acidification significantly improved iscl(-)

23 crophages to produce cytokines is due to the phagosomal acidification that disrupts endosomal ligand-

24 Thus, human Mphi do not require phagosomal acidification to kill and degrade Hc yeasts,

25 In addition, inhibition of phagosomal acidification was detected with PIM-coated be

26 was regulated during DC maturation and that phagosomal acidification was impaired in DCs in which th

27 umulation of PtdIns4P is required for proper phagosomal acidification.

28 culosis has multiple mechanisms of resisting phagosomal acidification.

29 n be rescued bypharmacological inhibition of phagosomal acidification.

30 ly blocked by bafilomycin A, an inhibitor of phagosomal acidification.

31 target the host vacuolar ATPase to withstand phagosomal acidity, the MgtC protein acts on Salmonella'

32 e trafficking regulatory lipid essential for phagosomal acquisition of lysosomal characteristics.

33 e trafficking regulatory lipid essential for phagosomal acquisition of lysosomal constituents, is ret

34 oarabinomannan (ManLAM)] interfered with the phagosomal acquisition of the lysosomal cargo and syntax

35 Thus, a v-ATPase-dependent phagosomal activation of Cat D was required for the gene

36 ession nor Ag uptake, but rather to impaired phagosomal Ag degradation.

37 While investigating the requirement for phagosomal alkalinization in the host defense against pu

38 phagosome, this permeabilization results in phagosomal and cytoplasmic mixing and allows extracellul

39 psin D-positive lysosomes, without mixing of phagosomal and lysosomal contents.

40 polyreactive Ig and complement in directing phagosomal antigen processing for cross-presentation.

41 g the host and bacterial factors that affect phagosomal antigen processing may help facilitate new st

42 Interestingly, the phagosomal association of sortilin is critical for the d

43 Phagosomal autonomy could serve as a basis for the intra

44 fication of phagosomes and the processing of phagosomal bacterial nucleic acids and was required for

45 tments within the same cell is determined by phagosomal cargo and may affect the outcome of antigen p

46 Specific ligands present in the phagosomal cargo influence the rate of phagosome fusion

47 idence indicates that receptor engagement by phagosomal cargo, as well as inflammatory mediators and

48 Mtb specifically under conditions that mimic phagosomal cation concentrations, and further support a

49 We propose that CFTR transiently increases phagosomal chloride concentration after infection, poten

50 e, as it directly inhibits maturation of the phagosomal compartment in which the bacterium is taken u

51 thogen Listeria monocytogenes escapes from a phagosomal compartment into the cytosol by secreting the

52 lish and maintain long-term residence in the phagosomal compartment of host macrophages is critical t

53 osis, and then actively invade from within a phagosomal compartment to form a parasitophorous vacuole

54 re available for use by the brucellae in the phagosomal compartment.

55 nter during their prolonged residence in the phagosomal compartment.

56 form an activation-induced Rab7(+) endosomal/phagosomal compartment.

57 mice exhibit decreased copper transport into phagosomal compartments and a reduced ability to kill Sa

58 equired for mycobacterial retention in early phagosomal compartments and that an inadequate supply of

59 Cs to CD4(+) T cells in the endosomal versus phagosomal compartments of Ms versus DCs.

60 ns indicate that the composition of distinct phagosomal compartments within the same cell is determin

61 y using liposomal model membranes that mimic phagosomal compartments.

62 i to vesicles that partially overlapped with phagosomal compartments.

63 phagosome maturation and trafficked to late phagosomal compartments.

64 lysosome formation and that USA300 may sense phagosomal conditions and upregulate expression of a key

65 and maturation and by testing the impact of phagosomal conditions on bacterial viability.

66 Macrophages sample the phagosomal content and orchestrate the innate immune res

67 tion', which leads to the degradation of the phagosomal content.

68 Ctr1) and ATP7A, a transporter implicated in phagosomal Cu compartmentalization, respectively.

69 l recruitment of YFP-tagged p67(phox) to the phagosomal cup, and, after phagosome internalization, a

70 tion of which migrated toward and within the phagosomal cup.

71 get particle, is transiently enriched in the phagosomal cup.

72 accumulated at extending pseudopodia and in phagosomal cups in trophozoites exposed to erythrocytes

73 nd actin rearrangements for engulfment; have phagosomal cysteine proteases active at low pH; and can

74 environment accidentally, for example, upon phagosomal damage, whereas pathogens routinely accessing

75 ies used by bacteria to resist antimicrobial phagosomal defenses and transiently pass through this co

76 by which the bacteria might evade macrophage phagosomal defenses are unclear.

77 is more sensitive to lysozyme, we show that phagosomal degradation and release of intracellular liga

78 The rapid cleavage of the microgels leads to phagosomal disruption through a colloid osmotic mechanis

79 are all dispersed among the bacteria, after phagosomal disruption, within both human macrophages and

80 mes and become acidified before the onset of phagosomal disruption.

81 particles confirmed a major role for GILT in phagosomal disulfide reduction in both resting and inter

82 Assessment of phagosomal disulfide reduction upon internalization of I

83 s that the depletion of Mg(2+) observed upon phagosomal engulfment may act to trigger isoTb biosynthe

84 ism that triggers edaxadiene production upon phagosomal engulfment.

85 mably, isoTb production should be induced by phagosomal entry.

86 sis is its ability to escape the destructive phagosomal environment and inhibit the host cell respira

87 sured the shear modulus and viscosity of the phagosomal environment concurrently with the phagosomal

88 her intracellular pathogens that control the phagosomal environment use specialized protein export sy

89 riptome thus served as a bioprobe of the MTB phagosomal environment, showing it to be nitrosative, ox

90 ditions designed to simulate features of the phagosomal environment.

91 ze cytosolic and phagosomal pH, and regulate phagosomal enzymatic activities.

92 Furthermore, activation of a phagosomal enzyme, inducible nitric oxide synthase, whic

93 (LLO) is a pore-forming toxin that mediates phagosomal escape and cell-to-cell spread of the intrace

94 tion significantly delayed but did not block phagosomal escape and cytosolic replication, indicating

95 ve and proliferate within phagocytes through phagosomal escape and cytosolic replication.

96 gh an intracellular life cycle that includes phagosomal escape and extensive proliferation within the

97 e production in the early FCP and restricted phagosomal escape and intracellular growth in an NADPH o

98 enicity island (FPI) mutant, is deficient in phagosomal escape and intracellular growth, whereas F. n

99 ied IgG enhanced phagocytosis but restricted phagosomal escape and intracellular proliferation.

100 ia through phagocytic pathways that restrict phagosomal escape and intracellular proliferation.

101 d macrophages by opsonization that inhibited phagosomal escape and resulted in phagolysosomal killing

102 ing phagosome (FCP) is important for optimal phagosomal escape and subsequent intracellular growth.

103 hagosomal maturation is required for optimal phagosomal escape and that the early FCP provides cues o

104 variety of acid phosphatases, whose roles in phagosomal escape and virulence have been documented yet

105 s than wild-type Schu S4 and were capable of phagosomal escape but exhibited reduced intracellular gr

106 were transcribed during the period of active phagosomal escape but that tlyA and pat1 were not.

107 st a role for tlyC and pld in the process of phagosomal escape by R. prowazekii.

108 Addition of biotin complemented the phagosomal escape defect of the FTN_0818 mutant, demonst

109 f endosomal acidification mimicked the early phagosomal escape defects caused by mutation of the FPI-

110 The key role of biotin in phagosomal escape implies biotin may be a limiting facto

111 Phagosomal escape is a multistep process characterized b

112 The contribution of host factors to Listeria phagosomal escape is incompletely defined.

113 unaffected, suggesting that ESX-1-dependent phagosomal escape is not required for CD8(+) T-cell prim

114 Recent studies indicate that phagosomal escape may have a major impact on the nature

115 that a bacterial metabolite is required for phagosomal escape of an intracellular pathogen, providin

116 rence, invasion, intracellular survival, and phagosomal escape of the bipC mutant.

117 acpA, acpB, and acpC deletions affected the phagosomal escape or cytosolic growth of Schu S4 in muri

118 The mechanism underlying rickettsial phagosomal escape remains unknown, although the genomic

119 analyses indicated that the period of active phagosomal escape was between 30 and 50 min postinfectio

120 include cellular uptake and internalization, phagosomal escape, and intracellular cargo concentration

121 this interlacing is essential to secretion, phagosomal escape, and intracellular replication.

122 malarial drug, inhibits Burkholderia growth, phagosomal escape, and subsequent MNGC formation.

123 orted to play important roles in Francisella phagosomal escape, inhibition of the respiratory burst,

124 e precisely regulated in order to facilitate phagosomal escape, intracellular growth, and cell-to-cel

125 VgrG and IglI are required for F. tularensis phagosomal escape, intramacrophage growth, inflammasome

126 These results reveal a crucial role for phagosomal escape, not for delivery of antigen to the cl

127 la-containing phagosome (FCP) and restricted phagosomal escape, while FcgammaR-dependent phagocytosis

128 ults on the timing and extent of Francisella phagosomal escape.

129 olipase D activity, has been associated with phagosomal escape.

130 ltaFTT1103 mutant bacteria were defective in phagosomal escape.

131 III secretion apparatus (T3SA) in mediating phagosomal escape.

132 brane protrusions, actin polymerization, and phagosomal escape.

133 regulated by bacterial genes associated with phagosomal escape.

134 asmic pathogens, including Shigella, mediate phagosomal escape.

135 The phenomenon of "phagosomal extrusion" indicates the existence of a previ

136 dy was to assess the effect of GILT on major phagosomal functions with an emphasis on proteolytic eff

137 ii infects alveolar macrophages and promotes phagosomal fusion with autophagosomes and lysosomes, est

138 Phagosomal fusion with late endosomes and lysosomes enha

139 stinctive Zn sequestration strategy elevated phagosomal H(+) channel function and triggered reactive

140 e to killing, which suggests the presence of phagosomal immune evasion molecules.

141 D4(+) T cells maintained during a persistent phagosomal infection progressively deteriorates.

142 CD4(+) T cells maintained during persistent phagosomal infection.

143 s play a critical role in protection against phagosomal infections.

144 Our data demonstrate that a phagosomal inflammatory response of microglia is leading

145 A phagosomal integrity assay and lysosome-associated membr

146 Slc11a1 encodes a phagosomal ion transporter, Nramp1, that affects resista

147 viable filamentous L. pneumophila to escape phagosomal killing in a length-dependent manner.

148 o-BCFAs enhance bacterial resistance against phagosomal killing in macrophages.

149 Mg(2+) (0.43 mM), shifting Mtb to media with phagosomal levels (0.1 mM) led to a significant ( approx

150 s to phagosomes and the acidification of the phagosomal lumen.

151 se of infection in both humans and mice, how phagosomal M. tuberculosis Ags are processed and present

152 iquitin-mediated autophagy pathway access to phagosomal M. tuberculosis.

153 This promoted phagosomal maturation (EEA-1/Lamp-3) and autophagy (LC3-

154 teract M. tuberculosis-induced inhibition of phagosomal maturation and promote host-induced autophagy

155 of M. tuberculosis correlates strongly with phagosomal maturation and that the inducible GFP express

156 and discovered WhiB3 as crucial mediator of phagosomal maturation arrest and acid resistance in M. t

157 Furthermore, we also performed a phagosomal maturation assay and observed that the activa

158 S. iniae does not alter neutrophil phagosomal maturation but instead is able to adapt to th

159 parable capacity for phagocytosis and normal phagosomal maturation compared to wild-type macrophages.

160 key aspects in phagocytic cup remodeling and phagosomal maturation could be influenced by target morp

161 YN-1 leads to common as well as differential phagosomal maturation defects.

162 inhibition of Rab7 acquisition and arrest of phagosomal maturation depends on Rab22a.

163 echanisms used by M. tuberculosis to inhibit phagosomal maturation differ from the mechanisms involve

164 he data are consistent with a model in which phagosomal maturation events associated with the acquisi

165 gnition and triggering of Th17 responses, to phagosomal maturation has not been defined.

166 Mycobacterium tuberculosis arrests phagosomal maturation in infected macrophage, and, apart

167 culosis, edaxadiene, whose ability to arrest phagosomal maturation in isolation presumably contribute

168 ies annually rests with its ability to block phagosomal maturation into the phagolysosome in infected

169 We conclude that the default pathway of phagosomal maturation into the phagolysosome includes te

170 We show that this block in phagosomal maturation is in part due to WhiB3-dependent

171 gether, these results demonstrate that early phagosomal maturation is required for optimal phagosomal

172 rophages phagocytose Mucor yeast, subsequent phagosomal maturation occurs, indicating host cells resp

173 ation of invading microbes by macrophages is phagosomal maturation through heterotypic endosomal fusi

174 induces inflammatory cytokines and controls phagosomal maturation through spleen tyrosine kinase act

175 r active TRIF signaling events, thus linking phagosomal maturation to specific TLR signaling pathways

176 Importantly, in the absence of MUNC13-4, phagosomal maturation was impaired as observed by the de

177 MUNC13-4 in selective vesicular trafficking, phagosomal maturation, and intracellular bacterial killi

178 ort that under certain conditions, including phagosomal maturation, possible actin depolymerization,

179 oss of functional Lyst leads to dysregulated phagosomal maturation, resulting in a failure to form an

180 In the process of blocking phagosomal maturation, the intracellular pathogen Mycoba

181 increase in EEA1 association and its role in phagosomal maturation, the pharmacological block of p38

182 status of M. tuberculosis and the degree of phagosomal maturation.

183 n in vitro, and contributes to inhibition of phagosomal maturation.

184 pression of innate immune genes and blocking phagosomal maturation.

185 populations relies on its ability to inhibit phagosomal maturation.

186 is product responsible for the inhibition of phagosomal maturation.

187 equire Dectin-1-dependent Syk activation for phagosomal maturation.

188 h many T4SS substrates being retained on the phagosomal membrane adjacent to the poles of the bacteri

189 Therefore, L. pneumophila disrupts the phagosomal membrane and becomes cytoplasmic at the last

190 ime after uptake, F. tularensis disrupts its phagosomal membrane and escapes into the cytoplasm.

191 " indicating that F. tularensis disrupts its phagosomal membrane by a mechanism that does not require

192 cated by the Dot/Icm complex across the host phagosomal membrane can also be transferred from one bac

193 while activation of the NADPH oxidase at the phagosomal membrane generates reactive oxygen species wi

194 gering of TLR9 recruitment to the macrophage phagosomal membrane is a conserved feature of fungi of d

195 Penetration of the phagosomal membrane is initiated by the secreted haemoly

196 g and fusion of the virion envelope with the phagosomal membrane is likely facilitated by clustering

197 rastic spatial redistribution of TLR9 to the phagosomal membrane of A. fumigatus-containing phagosome

198 It also promotes phagosomal membrane permeabilization, allowing dsDNA and

199 m tuberculosis, induce type I IFNs following phagosomal membrane perturbations.

200 of-function mutations in Nramp1 (SLC11A1), a phagosomal membrane protein that controls iron export fr

201 que E3 ubiquitin ligase family important for phagosomal membrane remodeling by L. pneumophila.

202 h LAMPs but without cathepsin D and that the phagosomal membrane subsequently becomes morphologically

203 re the sifA null mutant phenotype of loss of phagosomal membrane to sifA sseJ null double mutants, su

204 By remodeling the phagosomal membrane, the type III secretion system encod

205 the reduced recruitment of the endosomal and phagosomal membrane-tethering molecule called early endo

206 gh the action of regulatory molecules on the phagosomal membrane.

207 of resting PMNs and was up-regulated to the phagosomal membrane.

208 and transiently in the actin-poor region of phagosomal membrane.

209 proceeds despite physical disruption of the phagosomal membrane.

210 ellularly to translocate proteins across the phagosomal membrane.

211 mporally organized cyclical waves of PI3P on phagosomal membranes and that this process is targeted f

212 In many cases, these coated phagosomal membranes appeared to bud, vesiculate, and fr

213 iated reduction in cholesterol levels within phagosomal membranes counteract M. tuberculosis-induced

214 Endoplasmic reticulum (ER) contribution to phagosomal membranes is thought to provide antigen acces

215 e, SidC, was shown to translocate across the phagosomal membranes to the cytoplasmic face of the L. p

216 ith dysfunctional recruitment of retromer to phagosomal membranes, reduced retromer levels, and impai

217 LLO mediates rupture of phagosomal membranes, thereby releasing bacteria into th

218 onfocal imaging and direct patch clamping of phagosomal membranes, we found that particle binding ind

219 the only kinase that produces PtdIns(3)P in phagosomal membranes.

220 CpG-containing compartments and A. fumigatus phagosomal membranes.

221 ed ratios of PI(3,4,5)P(3) to PI(3,4)P(2) on phagosomal membranes.

222 -3-phosphate (PI(3)P), which is generated in phagosomal membranes.

223 ase activity by altering oxidase assembly on phagosomal membranes.

224 ce P(1B)-ATPases appear key to overcome high phagosomal metal levels and are required for the assembl

225 hagosome biogenesis and in adaptation to the phagosomal microenvironment.

226 al phagocytes generate ROS primarily via the phagosomal NADPH oxidase machinery.

227 agocytic process directs M.tb to its initial phagosomal niche, thereby enhancing survival in human ma

228 itive phagosomes, concomitantly potentiating phagosomal NOX activity.

229 burnetii, and F. tularensis to assess their phagosomal nutrient supply before committing to reenter

230 phate, a regulator of both NOX2 function and phagosomal or endosomal fusion.

231 teria interfere with the dynamics of PI3P on phagosomal organelles by altering the timing and charact

232 monella in vitro, in part due to inefficient phagosomal oxidant production, when compared with WT BMM

233 of complement, antibody and lytic peptides, phagosomal pathogens pose a unique problem for the innat

234 ssential for macrophage host defense against phagosomal pathogens, including Mycobacterium tuberculos

235 we found that bafilomycin A did not prevent phagosomal permeabilization by F. tularensis LVS or viru

236 Here we show that phagosomal permeabilization mediated by the bacterial ES

237 eactive oxygen species (ROS), which regulate phagosomal pH and processing of particulate antigens for

238 n, BDCA1(+) and BDCA3(+) DCs display similar phagosomal pH and similar production of reactive oxygen

239 neutrophils occurs by neutralization of the phagosomal pH by NADPH oxidase.

240 regulator Cl- channel (CFTR) participates in phagosomal pH control and has bacterial killing capacity

241 Following phagocytosis, the phagosomal pH dropped rapidly to <6.5 in Ms but remained

242 capsulatum mutants that experience decreased phagosomal pH have not been identified.

243 ), we demonstrated that a modest decrease in phagosomal pH is sufficient to generate redox heterogene

244 Here, the neutralization of phagosomal pH reduces protease activity, which preserves

245 a Tmem176b-dependent cation current controls phagosomal pH, a critical parameter in cross-presentatio

246 membrane potentials, optimize cytosolic and phagosomal pH, and regulate phagosomal enzymatic activit

247 egments (POS), proteolysis of POS rhodopsin, phagosomal pH, phagosome fusion with early and late endo

248 otropic agent LysoTracker as an indicator of phagosomal pH, we obtained evidence that in the absence

249 phagosomal environment concurrently with the phagosomal pH.

250 trating that this response is independent of phagosomal pH.

251 ells, and release DNA rapidly in response to phagosomal pH.

252 These results support a model in which phagosomal PI3K generates PI(3,4,5)P(3) necessary for la

253 (DAG) was not generated uniformly across the phagosomal population, varying in a manner that directly

254 requires MyD88, Syk, and PI3K signaling and phagosomal processing to activate IRF1 and IRF3/IRF7 and

255 hat NOX2 activity not only affects levels of phagosomal proteolysis as previously shown, but also the

256 Phagosomal proteolysis of AM was assessed with fluorogen

257 WASH is required for efficient phagosomal proteolysis, and proteomic analysis demonstra

258 Furthermore we observed a decrease in early phagosomal proteolytic efficiency in GILT-deficient macr

259 ps-34 completely abolishes the production of phagosomal PtdIns(3)P and disables phagosomes from recru

260 Remarkably, persistent appearance of phagosomal PtdIns(3)P, as a result of inactivating mtm-1

261 plays a novel and crucial role in producing phagosomal PtdIns(3)P.

262 idase response correlates with inhibition of phagosomal PtdIns3P accumulation and overlaps with the r

263 isappearance coincides with the emergence of phagosomal PtdIns3P.

264 phagosomes, little is known about how these phagosomal Rab proteins influence phagosome maturation.

265 cross-presentation requires Sec22b-mediated phagosomal recruitment of the peptide loading complex fr

266 monstrate that silica particles can generate phagosomal ROS independent of NOX activity, and we propo

267 and appeared in parallel with an increase in phagosomal ROS, as well as several hours later associate

268 ments of individual organelles indicate that phagosomal SHIP-1 enhances the early oxidative burst thr

269 ition of diverse ligands; in the case of Bb, phagosomal signaling involves a cooperative interaction

270 Atg23 localizes to the pre-auto-phagosomal structure but also to other cytosolic punctat

271 erial cell integrity: it associates with the phagosomal surface, promotes replication vacuole formati

272 efficient removal of Lys63 linkages from the phagosomal surface.

273 e found that these proteins were enriched on phagosomal surfaces through association with PtdIns(3)P

274 We propose that UNC-108 acts on phagosomal surfaces to promote phagosome maturation and

275 tiator, to strengthen DYN-1's association to phagosomal surfaces, and facilitates the maintenance of

276 transient enrichment of the RAB-5 GTPase to phagosomal surfaces, only the self-assembly mutation but

277 tates the maintenance of the RAB-7 GTPase on phagosomal surfaces.

278 es failure in recruiting the RAB-7 GTPase to phagosomal surfaces.

279 e and actin cytoskeleton and MyD88-dependent phagosomal TLR signaling, but not phagolysosome formatio

280 The capacity to trigger phagosomal TLR9 recruitment was not affected by a loss o

281 tracellular locations and is mediated by the phagosomal trafficking molecule adaptor protein-3 (AP-3)

282 Our studies further elucidate the effects of phagosomal trafficking on tailoring immune responses in

283 the NADPH oxidase complex, facilitating its phagosomal trafficking to induce a burst of reactive oxy

284 which M.tb inhibits both the activation and phagosomal translocation of SK1 to block the localized C

285 To characterize the mechanism of phagosomal translocation, live cell confocal microscopy

286 results suggest that preventing centripetal phagosomal transport delays the onset of acidification.

287 Suppression of the host phagosomal transport systems and the pathogen transporte

288 irst report of manipulation of intracellular phagosomal transport without interfering with the underl

289 ransporters, and the nine-member Francisella phagosomal transporter (Fpt) subfamily possesses homolog

290 The phagosomal transporter (Pht) family of the major facilit

291 or superfamily transporters, here named Pht (phagosomal transporter), that also is conserved in two o

292 ligands and TLR stimulation, the late-onset phagosomal tubules are not essential for delivery of pha

293 Our data show that phagosomal tubules in DCs are functionally distinct from

294 oth LST-4 and SNX-1 promote the extension of phagosomal tubules to facilitate the docking and fusion

295 reveal that this IFN-beta induction requires phagosomal uptake and processing but bypasses the endoso

296 Therefore, avoidance of phagosomal uptake or subsequent escape from the phagosom

297 s with binding, uptake, and formation of the phagosomal vacuole, whereas recruitment of both TLR2 and

298 acid pH and reduced survival in an acidified phagosomal vacuole.

299 o invade host cells and promptly escape from phagosomal vacuoles into the host cell cytosol, thereby

300 , and that PLD1 actively translocates to the phagosomal wall after particle ingestion.