ライフサイエンスコーパス: L. monocytogenes

1 L. monocytogenes 100S ribosomes were observed by sucrose

2 L. monocytogenes lacking the gene hmgR, encoding the rat

3 L. monocytogenes secA2 mutants form rough colonies, have

4 L. monocytogenes strains that lack both prsA2 and htrA e

5 L. monocytogenes survived in calyxes and stem ends of ap

6 L. monocytogenes was recovered in a dose-dependent manne

7 The 2011 L. monocytogenes cantaloupe outbreak was among the deadl

8 Intriguingly, a L. monocytogenes mutant that lacks c-di-AMP phosphodiest

9 of the PrfA regulon and complementation of a L. monocytogenes mutant lacking all PrfA-regulated genes

10 sociated HPB2262 and the invasive US Scott A L. monocytogenes strains.

11 a generalizable mechanism by finding that a L. monocytogenes strain engineered to express a flavinyl

12 Infection with a L. monocytogenes mutant impaired in c-di-AMP secretion f

13 n the interaction of extracellular, adherent L. monocytogenes with the unique subsets of myeloid-deri

14 h during early phagosome formation and after L. monocytogenes escaped the original containment vacuol

15 n to both myeloid and lymphoid cells against L. monocytogenes-induced apoptosis.

16 tical role for C5aR1 in host defense against L. monocytogenes through the suppression of type 1 IFN e

17 n to be important for early defenses against L. monocytogenes in the spleen, as well as a decrease in

18 otential or a decrease in protection against L. monocytogenes Instead, ecSOD activity enhances the pr

19 a normal robust host immune response against L. monocytogenes.

20 InlA aids L. monocytogenes transcytosis via interaction with the E

21 We created a cohort of all L. monocytogenes cases during 10 years (1998-2007) in Is

22 sion of the cell surface protein ActA allows L. monocytogenes to activate host actin regulatory facto

23 orm of intercellular trafficking that allows L. monocytogenes to move between host cells without esca

24 Although L. monocytogenes can usually be effectively treated with

25 No differences in survival amongst L. monocytogenes strains (serotypes 1/2a and 4b) from cl

26 Surprisingly, the growth of an L. monocytogenes mutant lacking the c-di-AMP-synthesizin

27 Compared with small analytes, L. monocytogenes has a larger surface and a higher numbe

28 the lowest MICs on S. aureus CMCC 26003 and L. monocytogenes CMCC 54001.

29 ype 6 had agreements of 95.7% and 85.7%, and L. monocytogenes and N. meningitidis were not observed i

30 educed the population of E. coli O157:H7 and L. monocytogenes by 1.48 and 0.47 log cfu/ml respectivel

31 oemulsion (AO75) reduced E. coli O157:H7 and L. monocytogenes count by 2.51 and 1.64 log cfu/ml, resp

32 onocytogenes DeltaactA DeltainlB (LmII), and L. monocytogenes DeltaactA DeltainlB prfA* (LmIII), we c

33 resulted in protection from C. rodentium and L. monocytogenes infection.

34 U/mL for E. coli O157:H7, S. typhimurium and L. monocytogenes.

35 P depletion suggest that P2X5-dependent anti-L. monocytogenes immunity is independent of the ATP-P2X7

36 ow that the vast majority of cell-associated L. monocytogenes in the gut were adhered to Ly6C(hi) mon

37 , Lm-RIID is as effective as live-attenuated L. monocytogenes in a therapeutic tumor model.

38 Using three attenuated L. monocytogenes vectors, L. monocytogenes DeltaactA (Lm

39 study showed that avoidance of autophagy by L. monocytogenes primarily involves PlcA and ActA and th

40 iota and promotes intestinal colonization by L. monocytogenes, as well as deeper organ infection.

41 response, which is known to be exploited by L. monocytogenes during infection.

42 as not observed in the protrusions formed by L. monocytogenes, whose dissemination did not rely on PI

43 es to the Rab32 subnetwork in DCs induced by L. monocytogenes infection and uncovered an essential ro

44 determinants that contribute to infection by L. monocytogenes, the causative agent of the foodborne d

45 be useful in the fight against infections by L. monocytogenes and other bacteria that use similar str

46 d associate modulation of host microbiota by L. monocytogenes epidemic strains to increased virulence

47 In contrast, CD4(+) T cells primed by L. monocytogenes restricted from the cell cytoplasm are

48 tributes to efficient cell-to-cell spread by L. monocytogenes in macrophages in vitro and growth of t

49 ds to 1) promotion of cell-to-cell spread by L. monocytogenes, 2) defective leukocyte recruitment to

50 Our study uncovers a strategy used by L. monocytogenes to modulate cytotoxic LLO activity thro

51 (control), 10(3), 10(5), 10(7), or 10(9) CFU L. monocytogenes in whipping cream.

52 tericidal effect against S. aureus, E. coli, L. monocytogenes and S. Typhimurium.

53 ified among a collection of 57,820 confirmed L. monocytogenes strains isolated from a variety of sour

54 A case was defined as laboratory-confirmed L. monocytogenes infection during the period from June 1

55 xes subsequent to perforation by LLO control L. monocytogenes internalization.

56 ion, we show that Ag delivery by cytoplasmic L. monocytogenes causes selective loss of 2W1S(+) offspr

57 inks E-cadherin to F-actin, did not decrease L. monocytogenes invasion of epithelial cells in tissue

58 n and IL-1beta production and that defective L. monocytogenes killing in P2X5-deficient BMMs is subst

59 ing and cytosolic survival of DHNA-deficient L. monocytogenes RNA-seq transcriptome analysis revealed

60 found that lipoate protein ligase-deficient L. monocytogenes (DeltalplA1) mutants, which display imp

61 ealing, revealing that perforation-dependent L. monocytogenes endocytosis is distinct from the reseal

62 d-increased systemic bacterial burden during L. monocytogenes-induced enterocolitis.

63 the mechanism for IFNbeta expression during L. monocytogenes infection in human myeloid cells remain

64 and C5a modulate IFN-beta expression during L. monocytogenes infection were not examined in these in

65 arizes the requirement of neutrophils during L. monocytogenes infection by examining both neutrophil

66 ng; however, disrupting IFN signaling during L. monocytogenes-induced enterocolitis did not recapitul

67 cellular domain was sufficient for efficient L. monocytogenes invasion of epithelial cells.

68 otin and digoxigenin coding for S. enterica, L. monocytogenes and E. coli, respectively.

69 dborne infection of mice with GFP-expressing L. monocytogenes, a small percentage of CD103(neg) and C

70 EGDe) and mouse-adapted (InlA(m)-expressing) L. monocytogenes recovered from the mesenteric lymph nod

71 This toxin facilitates L. monocytogenes intracellular survival in macrophages a

72 ance of the innate immune system in fighting L. monocytogenes infection, little is known about the ro

73 Using a mouse model of foodborne L. monocytogenes infection, a reduced number of the muta

74 nd both hly and prfA genes are essential for L. monocytogenes virulence.

75 al growth in broth culture but essential for L. monocytogenes virulence.

76 trophils and macrophages, were essential for L. monocytogenes-induced fetal resorption.

77 ntified 22 host genes that are important for L. monocytogenes spread.

78 mum conditions, limit of detection (LOD) for L. monocytogenes reached as low as 3.5x10(1)CFUmL(-1) in

79 a productive intracellular growth niche for L. monocytogenes.

80 her one of these factors must be present for L. monocytogenes growth in macrophages.

81 enzymes and catalase (kat) were required for L. monocytogenes aerobic growth in rich medium.

82 CadC but not CadA is required for L. monocytogenes infection in vivo.

83 We further showed that P2X5 is required for L. monocytogenes-induced inflammasome activation and IL-

84 sults indicate that the only requirement for L. monocytogenes invasion of epithelial cells is adhesio

85 teria, PrsA2 exhibits unique specificity for L. monocytogenes target proteins required for pathogenes

86 re we report crystal structures of CdaA from L. monocytogenes in the apo state, in the post-catalytic

87 t dynamic lipid structures are released from L. monocytogenes during infection.

88 Case patients had L. monocytogenes with </=3 SNPs (the outbreak strain) is

89 e previously infected with a relatively high L. monocytogenes dose displayed highly similar Ag-specif

90 of NEAT domains and provide insight into how L. monocytogenes captures heme iron.

91 Among the three identified L. monocytogenes evolutionary lineages, lineage I strain

92 stitutively virulent state strongly impaired L. monocytogenes performance in soil, the natural habita

93 and interleukin 6 expression, thus impairing L. monocytogenes survival in macrophages.

94 on resulted in altered metabolic activity in L. monocytogenes.

95 that GpsB, PBP A1 and PgdA form a complex in L. monocytogenes and identified the regions in PBP A1 an

96 enes CdaA is the sole diadenylate cyclase in L. monocytogenes, making this enzyme an attractive targe

97 fy LLS as the first bacteriocin described in L. monocytogenes and associate modulation of host microb

98 fatty acid incorporation was not detected in L. monocytogenes unless the pathway was partially inacti

99 To understand the role(s) of DHNA in L. monocytogenes intracellular survival and virulence, w

100 and IFN-beta were significantly elevated in L. monocytogenes-infected C5aR1(-/-) mice.

101 equency, PrfA(-)/LLO(-) mutational events in L. monocytogenes lead to niche restriction and open an e

102 HPF is required for ribosome hibernation in L. monocytogenes.

103 t whether this same mechanism is involved in L. monocytogenes, or even whether similar ion channels w

104 ontaneous virulence-attenuating mutations in L. monocytogenes Sixty nonhemolytic isolates were identi

105 assium uptake seems to be less pronounced in L. monocytogenes than in other Firmicutes.

106 ntified a novel transcriptional regulator in L. monocytogenes and determined that its metabolic regul

107 ctors responsible for lysozyme resistance in L. monocytogenes.

108 in-associated virulence and organ tropism in L. monocytogenes isolates from well-defined ruminant cas

109 rtance for cell wall growth and viability in L. monocytogenes and S. pneumoniae.

110 for normal cell morphology and virulence in L. monocytogenes; however, the mechanism of export via t

111 clearance of pathogenic organisms, including L. monocytogenes The diverse roles of neutrophils during

112 es infection was largely caused by increased L. monocytogenes-induced apoptosis of myeloid and lympho

113 and blocking neutrophil proteases increased L. monocytogenes intracellular survival.

114 e before low dose oral inoculation increases L. monocytogenes growth in the intestine.

115 steriolysin O (LLO), is sufficient to induce L. monocytogenes internalization into human epithelial c

116 We propose that LLO-induced L. monocytogenes internalization requires a Ca2+ - and K

117 asma membrane resealing process, LLO-induced L. monocytogenes internalization requires both Ca2+ and

118 try with a high prevalence of HIV infection, L. monocytogenes caused disproportionate illness among p

119 a cell type that inefficiently internalized L. monocytogenes With bone marrow-derived in vitro cultu

120 r, but the small proportion of intracellular L. monocytogenes is essential for dissemination to the M

121 t cell lamellipodin (Lpd) with intracellular L. monocytogenes detectable 6 h postinfection of epithel

122 on protein internalin A (InlA) are involved, L. monocytogenes can cross the gut barrier in their abse

123 improved nor worsened compared with isogenic L. monocytogenes-primed control mice.

124 obial activity against Campylobacter jejuni, L. monocytogenes, and Pseudomonas fluorescens.

125 of storage, significantly (p < 0.05) larger L. monocytogenes populations were recovered from apples

126 sponse to different types of systemic (LCMV, L. monocytogenes) and/or localized (influenza virus) inf

127 espite the established role of NOX2 limiting L. monocytogenes infection in mice, the underlying mecha

128 visualize intracellular cdiA levels in live L. monocytogenes strains and to determine the catalytic

129 against virulent challenges, similar to live L. monocytogenes vaccines.

130 s vectors, L. monocytogenes DeltaactA (LmI), L. monocytogenes DeltaactA DeltainlB (LmII), and L. mono

131 m perforation and contributes to maintaining L. monocytogenes in a bactericidal phagosome from which

132 findings are consistent with the ability of L. monocytogenes to switch between terminal oxidases und

133 To explain the absence of L. monocytogenes survival in neutrophils, we hypothesize

134 portance of considering clonal background of L. monocytogenes isolates in surveillance, epidemiologic

135 In addition, significantly lower burdens of L. monocytogenes were recovered from the colon, spleen,

136 longed to phylogenetically diverse clades of L. monocytogenes, and most were identified among nonclin

137 Finally, CCL8-mediated enhanced clearance of L. monocytogenes was dependent on gamma/delta T cells.

138 the presence of ecSOD decreases clearance of L. monocytogenes while increasing the recruitment of neu

139 that are required for ultimate clearance of L. monocytogenes, including neutrophils, macrophages, de

140 efinition of a foodborne outbreak cluster of L. monocytogenes.

141 e bacteria for functional complementation of L. monocytogenes mutants lacking prsA2.

142 invaded organs and higher concentrations of L. monocytogenes in almost all organs than nonpregnant a

143 ion of any host cell death in the context of L. monocytogenes infection inhibited the generation of p

144 T cells leads to a deficiency in control of L. monocytogenes expansion in the spleen.

145 ore, fail to replicate the natural course of L. monocytogenes infection.

146 The intracellular life cycle of L. monocytogenes deficient in inlP (DeltainlP) was not i

147 The intracellular life cycle of L. monocytogenes is considered to be its primary virulen

148 cceeded in inactivating over 5 log cycles of L. monocytogenes and maximizing inactivation of PPO and

149 tance are highly upregulated determinants of L. monocytogenes pathogenesis that are required for avoi

150 viously infected with a relative low dose of L. monocytogenes CD44(hi)CD4(+) T cells from I-A(100%) a

151 animals, however, can tolerate high doses of L. monocytogenes without developing systemic disease.

152 Here, we assessed the dynamics of L. monocytogenes infection in primary human decidual org

153 tablished that the major virulence factor of L. monocytogenes, the pore-forming toxin listeriolysin O

154 are not a niche for intracellular growth of L. monocytogenes during intestinal infection of mice.

155 -CSF readily supported exponential growth of L. monocytogenes Flt3 ligand-induced cultures yielded CD

156 ages fully supported intracellular growth of L. monocytogenes In contrast, inflammatory monocytes tha

157 cient to support the intracellular growth of L. monocytogenes Our results show that FabI is the prima

158 phagy was required to restrict the growth of L. monocytogenes, an intracellular pathogen that damages

159 vation prevented the intracellular growth of L. monocytogenes, showing that neither FabK nor the inco

160 is essential for the intracellular growth of L. monocytogenes.

161 More than half of L. monocytogenes strains with cas9 contain at least one

162 ts achieved higher levels of inactivation of L. monocytogenes and of the oxidative enzymes, succeedin

163 ted with a rapid decline in the incidence of L. monocytogenes ST6 infections.

164 BMMs) exhibit defective cytosolic killing of L. monocytogenes We further showed that P2X5 is required

165 y resembled cDC, with only a modest level of L. monocytogenes replication.

166 that NMHC-IIA limits intracellular levels of L. monocytogenes, and this is dependent on the phosphory

167 ing differences between the four lineages of L. monocytogenes we have detected differences in the rec

168 c-di-AMP), a secondary messenger molecule of L. monocytogenes, in J774A.1 macrophage-like cells and i

169 Lpd resulted in an increase in the number of L. monocytogenes-containing protrusions (listeriopods).

170 ified the LLO-dependent endocytic pathway of L. monocytogenes and support a novel model for pathogen

171 choline-specific phospholipase C (PC-PLC) of L. monocytogenes, is a potent inhibitor of intra- and ex

172 ovel factors for the colonization process of L. monocytogenes.

173 emic infection, the massive proliferation of L. monocytogenes in Perforin-2(-/-)mice leads to a rapid

174 ntrolling the intracellular proliferation of L. monocytogenes.

175 malian infection; however, the proportion of L. monocytogenes that is intracellular in vivo has not b

176 thesis by 80% and lowered the growth rate of L. monocytogenes in laboratory medium.

177 mplications for innate immune recognition of L. monocytogenes in the gut and highlight the need for a

178 not the result of an enhanced recruitment of L. monocytogenes to the gestational uterus but rather is

179 ssential for control of early replication of L. monocytogenes in the intestine as well as for restric

180 stigate whether intracellular replication of L. monocytogenes was essential during the intestinal pha

181 cking Ab resulted in near-complete rescue of L. monocytogenes-induced mortality.

182 that GpsB influences lysozyme resistance of L. monocytogenes as mutant strains lacking gpsB showed a

183 myeloid cells specifically near the sites of L. monocytogenes replication within the MLN to restrict

184 ial for dissemination and systemic spread of L. monocytogenes In this article, we show that the vast

185 ased movement and the cell-to-cell spread of L. monocytogenes.

186 cally involved in the cell-to-cell spread of L. monocytogenes.

187 bstantially decreased cell-to-cell spread of L. monocytogenes.

188 A mutant strain of L. monocytogenes expressing the cysteine-to-alanine vari

189 Here we used a recombinant strain of L. monocytogenes that efficiently invades the intestinal

190 ria monocytogenes Using a modified strain of L. monocytogenes that mimics human gastrointestinal list

191 ddress this question, we designed strains of L. monocytogenes that robustly activate necrosis, apopto

192 Combining infection studies of L. monocytogenes wild type and isogenic mutants together

193 esis, is essential for cytosolic survival of L. monocytogenes independent from its role in respiratio

194 g with wax facilitates prolonged survival of L. monocytogenes on whole apples is novel and reveals ga

195 ation is implicated in cytosolic survival of L. monocytogenes.

196 la infection blocked xenophagic targeting of L. monocytogenes by a RavZ-dependent mechanism.

197 G, and other downstream molecular targets of L. monocytogenes-generated c-di-AMP.

198 counting for the more rapid translocation of L. monocytogenes to its replicative niche in the cytosol

199 compared i.v. and foodborne transmission of L. monocytogenes in mice lacking the common type I IFN r

200 owing i.v. but not foodborne transmission of L. monocytogenes.

201 Moreover, treatment of L. monocytogenes-infected HeLa cells with a formin FH2-d

202 tractant leukotriene B4, decreased uptake of L. monocytogenes by PMN, and inhibited the respiratory b

203 use of opsonized bacteria enhanced uptake of L. monocytogenes in CD64(-) monocytes, but very few bact

204 r functional complementation of a variety of L. monocytogenes PrsA2-associated phenotypes central to

205 also affected the intracellular velocity of L. monocytogenes, with a reduction in Lpd corresponding

206 tial for cytosolic survival and virulence of L. monocytogenes Furthermore, we have identified a novel

207 icroscopy revealed that deposition of LC3 on L. monocytogenes-containing vacuoles via noncanonical au

208 PgdA and OatA, confer lysozyme resistance on L. monocytogenes; however, these enzymes are also conser

209 In this study, the only L. monocytogenes diadenylate cyclase gene, dacA, was del

210 t radically changed following secondary oral L. monocytogenes infection.

211 C. violaceum 12472, PAO1, L. monocytogenes, E. coli.

212 rol group of mice vaccinated with the parent L. monocytogenes strain not expressing LJM11.

213 facultative intracellular bacterial pathogen L. monocytogenes.

214 The human pathogen L. monocytogenes and the animal pathogen L. ivanovii, to

215 improve the chances of creating a persistent L. monocytogenes infection in an actively extruding epit

216 se, are less capable of killing phagocytosed L. monocytogenes, and have decreased oxidative burst.

217 h a RavZ-deficient strain of L. pneumophila, L. monocytogenes was targeted by the host xenophagy syst

218 and neither agglutinate bacteria nor prevent L. monocytogenes invasion.

219 rane sculpting F-BAR protein PACSIN2 promote L. monocytogenes protrusion engulfment during spread, an

220 f human neutrophils and is unable to protect L. monocytogenes from intracellular killing.

221 ve identified and characterized the putative L. monocytogenes' potassium transporters KimA, KtrCD, an

222 pecific CD8(+) T cells primed by recombinant L. monocytogenes is associated with reductions in circul

223 We previously revealed L. monocytogenes cadC as highly expressed during mouse i

224 ribe a new vaccine platform, termed Lm-RIID (L. monocytogenes recombinase-induced intracellular death

225 t evolutionarily distinct bacterial species, L. monocytogenes and Shigella flexneri, exploit the acce

226 We studied L. monocytogenes and its secreted pore-forming toxin lis

227 ry strains are imperfect models for studying L. monocytogenes pathogenesis.

228 ellular electron transfer system and support L. monocytogenes growth.

229 ytogenes exposure in the gut did not support L. monocytogenes growth.

230 ized clusters with myeloid cells surrounding L. monocytogenes replication foci only after a secondary

231 ticle, we report that NOX2 controls systemic L. monocytogenes spread through modulation of the type I

232 In a model of systemic L. monocytogenes infection, we show that mice lacking th

233 ly (within 3-6 d) susceptibility to systemic L. monocytogenes infection.

234 aR2, in the host immune response to systemic L. monocytogenes infection.

235 and statistical modeling to demonstrate that L. monocytogenes cell-to-cell spread proceeds anisotropi

236 Here, we demonstrate that L. monocytogenes has two terminal oxidases, a cytochrome

237 Our findings demonstrate that L. monocytogenes uses EVs for toxin release and implicat

238 ntial for aerobic growth, demonstrating that L. monocytogenes SpxA1 likely regulates a distinct set o

239 Therefore, we hypothesized that L. monocytogenes would hijack these types of host protei

240 Thus, our results indicate that L. monocytogenes cell-to-cell spread is heterogeneous, a

241 uman primate LD50s, but the observation that L. monocytogenes-induced stillbirths can be seen in guin

242 Thus, contrary to the perception that L. monocytogenes can infect virtually all cell types, ne

243 We propose that L. monocytogenes uses CadC to repress lspB expression du

244 We report that L. monocytogenes perforates the host cell plasma membran

245 Here we report that L. monocytogenes produces EVs with diameters ranging fro

246 Scanning electron microscopy revealed that L. monocytogenes EPS is cell surface-bound.

247 Here we show that L. monocytogenes CadC is a sequence-specific, DNA-bindin

248 Here, we summarize the strategies that L. monocytogenes employs to circumvent the intestinal ep

249 The L. monocytogenes CodY protein was functionally similar t

250 The L. monocytogenes intracellular life cycle is critical fo

251 The L. monocytogenes PrsA2 chaperone thus appears evolutiona

252 are highly conserved in Firmicutes, and the L. monocytogenes genome contains two paralogues, spxA1 a

253 these data indicate that the majority of the L. monocytogenes burden in the gastrointestinal tract is

254 e present the first crystal structure of the L. monocytogenes CdaA diadenylate cyclase domain that is

255 idates expressing r30 linked in frame to the L. monocytogenes listeriolysin O signal sequence and dri

256 a decrease in CD8(+) T cell response to the L. monocytogenes vaccine.

257 In support of this, L. monocytogenes is a potent inducer of neutrophil degra

258 Thus, L. monocytogenes promotes its dissemination in a host by

259 if LLO could confer a survival advantage to L. monocytogenes in neutrophils.

260 genes PrsA2-associated phenotypes central to L. monocytogenes pathogenesis and bacterial cell physiol

261 gnancy outcomes in gerbils orally exposed to L. monocytogenes, to compare the dose-response data to t

262 ncreased susceptibility of C3aR(-/-) mice to L. monocytogenes infection was largely caused by increas

263 increased bacterial growth and mortality to L. monocytogenes.

264 isolated that restored swarming motility to L. monocytogenes secA2 mutants.

265 the bone marrow of BALB/c/By/J mice prior to L. monocytogenes exposure in the gut did not support L.

266 on expansion of LLO56 T cells in response to L. monocytogenes in vivo.

267 n a specific tyrosine residue in response to L. monocytogenes infection.

268 a signaling on the innate immune response to L. monocytogenes may be an artifact of the i.v. infectio

269 been reported to impede the host response to L. monocytogenes through the promotion of splenocyte dea

270 suppress IFN-beta production in response to L. monocytogenes via cyclic di-AMP (c-di-AMP), a seconda

271 known to be critical in the host response to L. monocytogenes, including IFN-gamma and TNF-alpha.

272 e normal monocyte recruitment in response to L. monocytogenes, P2X5-deficient bone marrow-derived mac

273 Comparison of responses to L. monocytogenes by WT and Tim-3 knockout (KO) mice show

274 nsic role of Tim-3, we analyzed responses to L. monocytogenes infection by WT and Tim-3 KO TCR-transg

275 cates that gerbils are not more sensitive to L. monocytogenes invasion.

276 and C3aR(-/-) mice are highly susceptible to L. monocytogenes infection as a result of increased IFN-

277 cking the Ccl8 gene were more susceptible to L. monocytogenes infection than were wild-type mice.

278 rvation of the TA inhibitory activity toward L. monocytogenes, the possibility of being magnetically

279 g infection by priming leukocytes to undergo L. monocytogenes-mediated apoptosis.

280 ins undergoing tyrosine phosphorylation upon L. monocytogenes infection.

281 ional modification event and show that, upon L. monocytogenes infection, Src phosphorylates NMHC-IIA

282 fective cell-mediated immune responses using L. monocytogenes-based immunotherapeutic platforms.

283 rotection against fetal wastage and in utero L. monocytogenes invasion was maintained even when CXCR3

284 g three attenuated L. monocytogenes vectors, L. monocytogenes DeltaactA (LmI), L. monocytogenes Delta

285 InlP is conserved in virulent L. monocytogenes strains but absent in Listeria species

286 Finally, in vitro BMM killing and in vivo L. monocytogenes infection experiments employing either

287 neumophila infection of macrophages, whereas L. monocytogenes short-circuits this pathway by producin

288 While L. monocytogenes virulence hinges on cell-to-cell spread

289 equencing (IDAP-Seq) to identify genome-wide L. monocytogenes chromosomal DNA regions that CodY binds

290 nalysis of wild-type (WT) mice infected with L. monocytogenes revealed that Tim-3 was transiently exp

291 responses to gastrointestinal infection with L. monocytogenes and identify STAT4 as a central modulat

292 and IL-12p70 during in vitro infection with L. monocytogenes compared with splenocytes from C5aR2(+/

293 memory CD8 T-cells following infection with L. monocytogenes either expressing or not cognate Ag.

294 urvival roles during systemic infection with L. monocytogenes In our current study, we have examined

295 12 and IFN-gamma early during infection with L. monocytogenes is protective to the host, and we belie

296 Following oral infection with L. monocytogenes, Rc3h1(gt/gt) --> NL chimeras had more

297 in the first few minutes of interaction with L. monocytogenes, granules can fuse with the plasma memb

298 In pregnant women, L. monocytogenes infection leads to abortion and severe

299 nd that, upon access to the host cytosol, WT L. monocytogenes utilized PLCs and ActA to avoid subsequ

300 t shortly after phagocytosis, wild-type (WT) L. monocytogenes escaped from a noncanonical autophagic