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 elicited more potent simian immunodefic

3 L. monocytogenes is the only pathogen known to possess b

4 L. monocytogenes secA2 mutants form rough colonies, have

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

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

7 cept a step further, vaccination of C57BL/6 (L. monocytogenes-resistant) and BALB/c (L. monocytogenes

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

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

13 inflammatory cytokines triggered early after L. monocytogenes infection in controlling PDL-1-mediated

14 a, TNF-alpha, IL-4, IL-17, or perforin after L. monocytogenes infection, and some effector Vgamma2Vde

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 L-23 is required for host resistance against L. monocytogenes and for neutrophil recruitment to the l

20 y dynamic during the innate response against L. monocytogenes and that the protective IL-6 function i

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

22 onal Vgamma2Vdelta2 T cell responses against L. monocytogenes.

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

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

25 Although L. monocytogenes can usually be effectively treated with

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

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

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

29 ach of the target species of S. enterica and L. monocytogenes, along with five strains of the non-tar

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 not been performed to investigate human anti-L. monocytogenes immune responses, including those of Ag

36 aking it interesting to explore in vivo anti-L. monocytogenes immune responses of Vgamma2Vdelta2 T ce

37 atory responses to invading microbes such as L. monocytogenes.

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

39 genous and overexpressed OCRL are present at L. monocytogenes invasion foci; live-cell imaging additi

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

41 ic infection and reinfection with attenuated L. monocytogenes uncovered the ability of Vgamma2Vdelta2

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

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

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

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

46 012; P < .001) and emergence of infection by L. monocytogenes genotype sequence type 6 (ST6; 4% in 19

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

48 ance of zinc acquisition during infection by L. monocytogenes.

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

50 this phosphatase modulates cell invasion by L. monocytogenes.

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

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

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

54 represent the initial point of entry used by L. monocytogenes for infection, the innate immune respon

55 L/6 (L. monocytogenes-resistant) and BALB/c (L. monocytogenes-susceptible) mice with adenoviral vecto

56 cation within the cytosol of infected cells, L. monocytogenes utilizes two multidrug efflux pumps, Md

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

58 4-deficient (Irf4(-/-)) mice could not clear L. monocytogenes infection and generated decreased numbe

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

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

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

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

63 host tissues and showed that each decreases L. monocytogenes systemic dissemination in orally inocul

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

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

66 OCRL promotes actin depolymerization during L. monocytogenes infection; in agreement with this hypot

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

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

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

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

71 The emerging L. monocytogenes genotype ST6 was identified as the main

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

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

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

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

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

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

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

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

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

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

82 ted the importance of aerobic metabolism for L. monocytogenes infection, these findings provide furth

83 ce of menaquinone and aerobic metabolism for L. monocytogenes pathogenesis.

84 a productive intracellular growth niche for L. monocytogenes.

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

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

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

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

89 ins protected primary human macrophages from L. monocytogenes-induced apoptosis.

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

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

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

93 ithelium and macrophages and have identified L. monocytogenes as a source of ligand for the orphan re

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

95 ) and high-throughput microscopy to identify L. monocytogenes mutants defective in optimal intracellu

96 unctive dexamethasone may be discontinued if L. monocytogenes is identified, as there is no proven be

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

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

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

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

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

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

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

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

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

106 ing the potential regulatory role of LbrA in L. monocytogenes.

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

108 ticular that induced by the weak Ag, p60, in L. monocytogenes-susceptible BALB/c mice.

109 ctors responsible for lysozyme resistance in L. monocytogenes.

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

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

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

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

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

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

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

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

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

119 Here we demonstrate that, during infection, L. monocytogenes triggers the cellular redistribution of

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

121 ected target cells and inhibit intracellular L. monocytogenes bacteria.

122 nzyme) decreases the levels of intracellular L. monocytogenes and of actin associated with invading b

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

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

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

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

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

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

129 monocytogenes infection could directly lyse L. monocytogenes-infected target cells and inhibit intra

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

131 motion, mimicking the orientation of motile L. monocytogenes.

132 ice with adenoviral vectors encoding natural L. monocytogenes-derived soluble Ags (listeriolysin O an

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

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

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

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

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

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

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

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

141 used 20 signature-tagged wild-type clones of L. monocytogenes in guinea pigs in combination with exte

142 A microarray comparison of L. monocytogenes between the transcriptome of the strong

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

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

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

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

147 anti-IL-6 mAb displayed impaired control of L. monocytogenes infection accompanied by alterations in

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

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

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

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

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

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

154 rate that mice infected with lethal doses of L. monocytogenes produce higher levels of fibrin and dis

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

156 wild-type mice challenged with high doses of L. monocytogenes.

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

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

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

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

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

162 e escape and initial intracellular growth of L. monocytogenes in epithelial cells and macrophages but

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

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

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

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

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

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

169 y, Toso(-/-) mice succumbed to infections of L. monocytogenes, whereas WT mice successfully eliminate

170 Renitence and inhibition of L. monocytogenes escape were partially attributable to h

171 multiple laboratory and clinical isolates of L. monocytogenes to stimulate host production of IFN-bet

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

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

174 er, these data reveal that the modulation of L. monocytogenes infection by treatment with lactobacill

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

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

177 infection and generated decreased numbers of L. monocytogenes-specific CD8(+) T cells with impaired e

178 icate that the characteristic orientation of L. monocytogenes must be due to polarized ActA rather th

179 d contribution of LLO to the pathogenesis of L. monocytogenes, we developed a screen that combined sa

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

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

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

183 ntrolling the intracellular proliferation of L. monocytogenes.

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

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

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

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

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

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

190 miR regulation, and a dramatic reshaping of L. monocytogenes transcriptome.

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

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

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

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

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

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

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

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

199 The outbreak strain of L. monocytogenes was isolated from chicken salad and its

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

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

202 nscriptome and up-regulated transcription of L. monocytogenes genes encoding enzymes allowing utiliza

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

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

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

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

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

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

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

210 of TLR10 resulted in increased viability of L. monocytogenes in both HT-29 and THP-1 cells.

211 fect of treatment with each Lactobacillus on L. monocytogenes counts in host tissues and showed that

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

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

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

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

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

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

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

219 Adhesion forces between pathogenic L. monocytogenes EGDe and silicon nitride (Si(3)N(4)) we

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

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

222 While type I interferons may promote L. monocytogenes virulence, this study demonstrates that

223 ron (IFN-beta), which, surprisingly, promote L. monocytogenes virulence.

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

225 otection in C57BL/6 mice against recombinant L. monocytogenes expressing an immunodominant epitope of

226 ugh its phosphatase activity, OCRL restricts L. monocytogenes invasion by modulating actin dynamics a

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

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

229 amma2Vdelta2 T effector cells in subclinical L. monocytogenes infection could directly lyse L. monocy

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

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

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

233 y, we demonstrated that subclinical systemic L. monocytogenes infection of rhesus macaques via parent

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

235 We demonstrate that L. monocytogenes infection causes profound systemic IL-6

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

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

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

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

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

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

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

243 We show that L. monocytogenes colonized the liver in all asymptomatic

244 The L. monocytogenes intracellular life cycle is critical fo

245 The L. monocytogenes PrsA2 chaperone thus appears evolutiona

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

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

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

249 ach Lactobacillus significantly reshaped the L. monocytogenes transcriptome and up-regulated transcri

250 ape, and subsequent cell-to-cell spread, the L. monocytogenes factors required for rapid replication

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

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

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

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

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

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

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

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

259 increased bacterial growth and mortality to L. monocytogenes.

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

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

262 involved in mediating the immune response to L. monocytogenes in IECs.

263 for infection, the innate immune response to L. monocytogenes in these cells has been poorly characte

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

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

266 that the impaired CD8(+) T cell response to L. monocytogenes is T cell intrinsic.

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

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

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

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

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

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

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

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

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

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

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

278 ins undergoing tyrosine phosphorylation upon L. monocytogenes infection.

279 ivated and showed initial proliferation upon L. monocytogenes infection.

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

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

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

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

284 in epithelia, and activation required viable L. monocytogenes.

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

286 ts support a novel dissemination model where L. monocytogenes replicates in intestinal villi, is shed

287 Whereas L. monocytogenes (Lm)ClpP2 is both structurally and func

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

289 ptake systems may offer a mechanism by which L. monocytogenes can respond to zinc deficiency within a

290 esulted in contamination of cantaloupes with L. monocytogenes.

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

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

293 egression analysis identified infection with L. monocytogenes ST6 as the sole predictor of unfavorabl

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

295 ) T cell lines in mice during infection with L. monocytogenes.

296 ant milk formula, previously inoculated with L. monocytogenes, inhibited the growth of bacteria 1.5 l

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