ライフサイエンスコーパス: S. typhimurium

1 S. typhimurium A1 is auxotrophic (Leu/Arg-dependent) but

2 S. typhimurium accesses fucose and sialic acid within th

3 S. typhimurium Deltaxth and Deltaxth/nfo were significan

4 S. typhimurium expressing PA-PhoQ protein were attenuate

5 S. typhimurium grown in tissue culture medium synthesize

6 S. typhimurium has recently been shown to synthesize its

7 S. typhimurium has two T3SS: Salmonella pathogenicity is

8 S. typhimurium localized predominantly in granulocytes.

9 S. typhimurium mntH mutants showed only a slight attenua

10 S. typhimurium PhoQ (ST-PhoQ) is repressed by millimolar

11 S. typhimurium was able to colonize mmp-3(-/-) mice, alb

12 S. typhimurium-immune and -nonimmune mice were fed 1 of

13 S. typhimurium-mediated germ-line cell death is not obse

14 S. typhimurium-stimulated cytotoxic T lymphocytes recogn

15 By day 15, S. typhimurium A1 was undetectable in the liver, lung, s

16 A S. typhimurium fis mutant demonstrates a two- to threefo

17 t cations, and can functionally complement a S. typhimurium phoQ-null mutant.

18 Furthermore, the virulence of a S. typhimurium fis mutant is attenuated 100-fold when ad

19 Apically added S. typhimurium promoted the translocation of ARF6 and it

20 In addition, S. typhimurium infection-induced autophagy was blocked b

21 B- mutants assembled into fibers on adjacent S. typhimurium that presented CsgB on its surfaces.

22 crete IL-1beta in response to P. aeruginosa, S. typhimurium, and Listeria monocytogenes infection, as

23 s were still able to produce IFN-gamma after S. typhimurium infection.

24 3 and NLRC4 in innate immune defense against S. typhimurium, mice lacking both NLRs were markedly mor

25 ficile infection, could also protect against S. typhimurium disease.

26 Although S. typhimurium can enter intestinal epithelial cells, ba

27 Although S. typhimurium is a promising delivery vehicle because o

28 An S. typhimurium strain carrying a mutation in sseJ was mi

29 flagellin secretion, flagellar assembly, and S. typhimurium-induced proinflammatory responses through

30 flagellar promoters in both V. cholerae and S. typhimurium identified sigma28-, sigma54-, FlrA- and

31 the nucleotide sequences of the E. coli and S. typhimurium genomes.

32 the rate constants to IICBGlc in E. coli and S. typhimurium membranes.

33 Inactivation of lpxM in both E. coli and S. typhimurium resulted in the loss of l-Ara4N addition,

34 ration of lipid A's derived from E. coli and S. typhimurium.

35 tracellular matrix production by E. coli and S. typhimurium.

36 e ribose transporter of Escherichia coli and S. typhimurium.

37 ed in mixed colony biofilms with E. coli and S. typhimurium.

38 city to inhibit growth of S. enteritidis and S. typhimurium in bacterial cultures; this was the resul

39 unds of selection to live S. enteritidis and S. typhimurium were performed, alternating with a negati

40 specific DNA aptamers to S. enteritidis and S. typhimurium.

41 hance the entry of wild-type S. flexneri and S. typhimurium into cultured cells; (ii) interact with p

42 sms were used to isolate E. coli O157:H7 and S. typhimurium separately from a cocktail of bacteria an

43 Weight loss, serum cytokine levels, and S. typhimurium splenic translocation were measured.

44 sp. D7, E. coli O157:H7, K. pneumoniae, and S. typhimurium were cloned and expressed in E. coli DH5a

45 s were conducted using S. flexneri SF621 and S. typhimurium SB220, neither of which is capable of inv

46 despite the presence of high levels of anti-S. typhimurium antibody.

47 uNPs nanocomposite was then attached to anti-S. typhimurium antibody (MWCNTs/AuNPs/Ab(1)) and used as

48 train to deliver the NY-ESO-1 tumor antigen (S. typhimurium-NY-ESO-1) through a type III protein secr

49 at lead to IkappaBalpha degradation, such as S. typhimurium-induced epithelial Ca(2+) mobilization or

50 Unlike control bacteria, attenuated S. typhimurium expressing LIGHT inhibited growth of prim

51 A strain of attenuated S. typhimurium previously evaluated in human volunteers

52 Both S. typhimurium and E. coli MntH also transport 55Fe2+ ho

53 t dispensable for inflammasome activation by S. typhimurium.

54 Subversion of NADPH oxidase assembly by S. typhimurium was accompanied by increased bacterial re

55 t immune defenses that could be exploited by S. typhimurium to persist and survive in the host.

56 ques, the gene expression profile induced by S. typhimurium in ligated ileal loops was dominated by T

57 paB activation and IL-8 secretion induced by S. typhimurium, but not by TNF-alpha, was preceded by an

58 ; however, compared with potent induction by S. typhimurium flagellin, H. pylori FlaA-dependent p38 a

59 ot result in resistance to oral infection by S. typhimurium, but rather, leads to increased susceptib

60 mice and preweaned pups to oral infection by S. typhimurium.

61 Similarly, CsgA was secreted by S. typhimurium csgB- mutants formed curli on CsgB-presen

62 ently shown that SipA, a protein secreted by S. typhimurium, is necessary and sufficient to drive PMN

63 ucing PMNs, which may act primarily to clear S. typhimurium infection, but in the process also induce

64 ium by both exogenous indole added to clonal S. typhimurium populations and indole produced by E. col

65 es synthetic ecosystem comprised of E. coli, S. typhimurium, and V. harveyi we discovered both cross-

66 Additionally, under these conditions S. typhimurium-induced IL-1 release occurred independent

67 induced proinflammatory response, we created S. typhimurium Tn-10 transposon mutants and identified a

68 support of this finding, flagellin-deficient S. typhimurium mutants did not secrete detectable levels

69 lagellar hierarchy and the sigma28-dependent S. typhimurium peritrichous flagellar hierarchy.

70 To directly detect S. typhimurium after IMS, a sandwich immunoassay was imp

71 immunosensor was able to specifically detect S. typhimurium in spiked water and juice samples with a

72 highly selective and can successfully detect S. typhimurium down to 600 CFU mL(-1) (equivalent to 18

73 ionally confirmed by capturing and detecting S. typhimurium in ground chicken and ground beef.

74 , and the ribose/galactose receptor directed S. typhimurium toward necrosis.

75 hat the aptamer biosensor could discriminate S. typhimurium from 6 other model bacteria strains.

76 CL3 and CCL4 in mouse macrophages and during S. typhimurium oral infection.

77 ation contributes to macrophage death during S. typhimurium infection.

78 tions have been shown to divide labor during S. typhimurium infections.

79 did not assemble inflammasome specks during S. typhimurium infection, so phosphorylation of NLRC4 S5

80 complemented with the mlrA gene from either S. typhimurium or E. coli present on a low-copy-number p

81 Silencing of host IDO significantly enhances S. typhimurium colonization, suggesting that IDO express

82 chitecture and cellular trafficking enhances S. typhimurium virulence and could represent a mechanism

83 s epithelia, subsequent to apical epithelial-S. typhimurium interaction, is likely a major means of a

84 Immediately after injection, few S. typhimurium (<4 in 10,000) adhered to tumor vasculatu

85 Finally, S. typhimurium, but not TNF-alpha, induced a Ca(2+)-depe

86 For S. typhimurium MntH, the Km for 54Mn2+ ( approximately 0

87 ad a detection limit of 10(2) CFU mL(-1) for S. typhimurium, providing an instrument-free quantitativ

88 3% (v/v) MEO formulated films was 21.98 for S. typhimurium and 10.15mm(2) for P. aeruginosa.

89 ree impedimetric aptamer-based biosensor for S. typhimurium detection.

90 ptotic and proinflammatory, is essential for S. typhimurium to efficiently colonize the cecum and PP

91 t published paper-based detection method for S. typhimurium in bird feces and whole milk.

92 . pneumophila and three CFU per reaction for S. typhimurium and S. aureus.

93 cation, and functional analysis of ArnT from S. typhimurium.

94 has 93% sequence identity to the enzyme from S. typhimurium.

95 he first two domains of full-length NAT from S. typhimurium and to investigate the role of the C term

96 o acids), the truncation mutants of NAT from S. typhimurium are toxic when overexpressed intracellula

97 de controls hydrolysis of Ac-CoA by NAT from S. typhimurium.

98 ble periplasmic globular domain of PbgA from S. typhimurium and E. coli, which revealed that the glob

99 ent of the T3SS apparatus (rod protein) from S. typhimurium (PrgJ), Burkholderia pseudomallei (BsaK),

100 of Mg (2+); the structure of the RhamD from S. typhimurium was also obtained in the presence of 3-de

101 ere we show that the bacterial E3 SspH2 from S. typhimurium selectively binds the human UbcH5 ~ Ub co

102 To address this issue, we grew S. typhimurium inside RAW264.7 cells in the presence of

103 LOD was under 5 CFU/mL for E. coli O157:H7, S. typhimurium and L. monocytogenes.

104 e seven protofilaments rather than the 11 in S. typhimurium.

105 to investigate the role of Rac1 and Cdc42 in S. typhimurium-induced pro-inflammatory responses in the

106 te that all eight of the native cysteines in S. typhimurium ArnT are in the reduced form and not invo

107 hical control of fimbrial gene expression in S. typhimurium.

108 abolishes S-2-hydroxymyristate formation in S. typhimurium.

109 h the exception of the 2-hydroxymyristate in S. typhimurium.

110 An mlrA homologue was identified in S. typhimurium.

111 eased antibiotic tolerance can be induced in S. typhimurium by both exogenous indole added to clonal

112 equence identity, are not interchangeable in S. typhimurium and S. flexneri.

113 ir of oxidatively damaged DNA is involved in S. typhimurium intramacrophage proliferation, null mutan

114 er, mice lacking additional TLRs involved in S. typhimurium recognition were less susceptible to infe

115 enotoxicity in CHO cells and mutagenicity in S. typhimurium, the Salmonella assay was far more sensit

116 as independent of PhoP/PhoQ and PmrA/PmrB in S. typhimurium.

117 ron of seven genes (designated pmrHFIJKLM in S. typhimurium), which is regulated by the PmrA transcri

118 e N-terminal AhpC-reducing domain present in S. typhimurium AhpF.

119 This structure is not present in S. typhimurium SgrS, which explains its higher level of

120 (TNF-alpha or carbachol) but was present in S. typhimurium supernatants, indicating PIF is of bacter

121 tion, and thus type 1 fimbrial production in S. typhimurium.

122 ArnT, consists of 548 amino acid residues in S. typhimurium with 12 possible membrane-spanning region

123 We have investigated the role in S. typhimurium virulence of the putative SPI-2 effector

124 ous structures of lipid A precursors seen in S. typhimurium mutants defective in 3-deoxy-d-manno-octu

125 r data show that indole-induced tolerance in S. typhimurium is mediated primarily by the oxidative st

126 ine-glutaraldehyde chemistry and inactivated S. typhimurium were captured from various samples and de

127 it from other Salmonella species, including S. typhimurium and S. choleraesuis.

128 ve stress, elevated hmp expression increases S. typhimurium susceptibility to hydrogen peroxide.

129 ind that indole signaling by E. coli induces S. typhimurium antibiotic tolerance in a Caenorhabditis

130 eserving tight junctions, thereby inhibiting S. typhimurium from gaining access to the systemic circu

131 The number of viable internalized S. typhimurium in Caco2 cells stably transfected with CA

132 enteritidis fimU mutant was transduced into S. typhimurium, and this strain was analysed for the exp

133 negative selection step against heat killed S. typhimurium and a mixture of related pathogens, inclu

134 oxlyated lipid A isolated from (32)P-labeled S. typhimurium cells.

135 In normal mice S. typhimurium stimulated production of the CXC chemokin

136 ial adhesion, approximately 10,000-fold more S. typhimurium accumulated in tumors than any other orga

137 ed ROS in phagosomes containing SPI-2 mutant S. typhimurium.

138 response to TLR plus ATP stimulation but not S. typhimurium.

139 tions of endosomes, we found that lipid A of S. typhimurium grown in an acidic, low-Mg2+ medium close

140 Furthermore, the ability of S. typhimurium mutants to induce IkappaB-alpha degradati

141 Piperidine did not affect the ability of S. typhimurium to elicit interleukin-8 secretion by epit

142 Oral administration of S. typhimurium-NY-ESO-1 to mice resulted in the regressi

143 E mutant resulted in increased attachment of S. typhimurium to human colonic epithelial cell lines (T

144 ered caspase-11, which enhanced clearance of S. typhimurium sifA in vivo.

145 oposed platform was applied for detection of S. typhimurium in inoculated Starling bird fecal samples

146 id (less than 1h) and sensitive detection of S. typhimurium in real samples.

147 strated its suitability for the detection of S. typhimurium in spiked (1 x 10(2), 1 x 10(4) and 1 x 1

148 Using this system, the limit of detection of S. typhimurium was found to be 10(2) CFU mL(-1) in cultu

149 sensitive and specific for the detection of S. typhimurium.

150 e showed increased systemic dissemination of S. typhimurium from the gut, suggesting that IL-17 defic

151 this study was to investigate the effect of S. typhimurium on inflammasomes in primary human monocyt

152 This study shows that exposure of S. typhimurium to sublethal concentrations of CAMP activ

153 eviously that fimU affects the expression of S. typhimurium type 1 fimbriae, and that fimU is functio

154 We further demonstrate that growth of S. typhimurium in low doses of the alpha-helical peptide

155 Growth of S. typhimurium in the presence of CAMP also leads to Rpo

156 Cation hexaammines also inhibited growth of S. typhimurium strains dependent on CorA for Mg(2+) upta

157 rophages to suppress intracellular growth of S. typhimurium was impaired.

158 The 352 gene homologues of S. typhimurium LT2 confined to subspecies I of S. enteri

159 The distribution of close homologues of S. typhimurium LT2 genes in eight related enterobacteria

160 After systemic injection of S. typhimurium into tumor-bearing mice, we used intravit

161 eus and casein, but not to i.p. injection of S. typhimurium or Salmonella LPS.

162 Intratumoral inoculation of S. typhimurium-NY-ESO-1 to NY-ESO-1-negative tumors resu

163 ntrast to P. aeruginosa, a small inoculum of S. typhimurium can proliferate in the C. elegans intesti

164 When C. elegans is placed on a lawn of S. typhimurium, the bacteria accumulate in the lumen of

165 spleen and liver and decreased maturation of S. typhimurium granulomas.

166 three unsequenced genomes to a microarray of S. typhimurium LT2 genes.

167 , feeding for 5 hours on a 1:1000 mixture of S. typhimurium and E. coli followed by transfer to 100%

168 and is consistent with the emerging model of S. typhimurium flagellin-induced inflammation.

169 extracted from a PhoP-constitutive mutant of S. typhimurium grown in the presence or absence of O(2).

170 The DeltahilA isogenic mutant of S. typhimurium lacks this butyrate-regulated locus and s

171 PmrA null mutants of S. typhimurium produce lipid A species without any pEtN

172 b) chromosome and 94-kb virulence plasmid of S. typhimurium strain LT2.

173 A104, and 89.2% and 82.9% in the presence of S. typhimurium TA102), than their monomers.

174 A104, and 79.7% and 68.9% in the presence of S. typhimurium TA102, than were their monomers.

175 pectively 82.4% and 79.3% in the presence of S. typhimurium TA104, and 89.2% and 82.9% in the presenc

176 Also, during intracellular replication of S. typhimurium in BMDMs, IFN-gamma and NOS2 repressed CC

177 d are necessary for continued replication of S. typhimurium in the liver and spleen of susceptible mi

178 elopment of a genetically modified strain of S. typhimurium, selected for prostate tumor targeting an

179 Mice were gavaged with 2 isogenic strains of S. typhimurium after administration of streptomycin.

180 type (WT) or several SPI-2 mutant strains of S. typhimurium.

181 A subset of S. typhimurium lipid A modifications were induced by low

182 correlated with an increase in the titer of S. typhimurium in the C. elegans lumen, which reached 10

183 injected weekly to determine the toxicity of S. typhimurium A1-R.

184 rary of random internal deletion variants of S. typhimurium flagellin was constructed and screened fo

185 echanism of this suppression is dependent on S. typhimurium LPS (sLPS).

186 nists were uncovered in either V. harveyi or S. typhimurium assay, whereas weak to moderate antagonis

187 ipid A, E. coli lipopolysaccharide (LPS), or S. typhimurium LPS activate caspase-11 independently of

188 The experiments described here compare oral S. typhimurium or Y. enterocolitica infection in stromel

189 se, designated lpxR, by screening an ordered S. typhimurium genomic DNA library, harbored in Escheric

190 enteriae, Salmonella enterica, S. paratyphi, S. typhimurium, S. bongori, and S. diarizonae.

191 growth of pathogenic bacteria, particularly S. typhimurium, during turkey escalope storage at 4 degr

192 results suggest that the intestinal pathogen S. typhimurium can intercept indole signaling from the c

193 ential role in the control of the persistent S. typhimurium infection in mice.

194 morphology in an upregulated curli producing S. typhimurium derivative containing a temperature- and

195 that it increased mouse survival and reduced S. typhimurium translocation into and colonization of va

196 ght junction protein expression, and reduced S. typhimurium translocation to the spleen.

197 Mutations in the lsr operon render S. typhimurium unable to eliminate AI-2 from the extrace

198 The resulting S. typhimurium fimU mutant was found to be non-fimbriate

199 r membrane, as judged by assays of separated S. typhimurium membranes and by SDS-polyacrylamide gel a

200 s host-pathogen interaction requires several S. typhimurium genes.

201 Compared with E. coli SgrS, S. typhimurium SgrS produces more SgrT and this rescues

202 In this study, S. typhimurium BER mutants are characterized for the fir

203 esized that individual chemoreceptors target S. typhimurium to specific tumor microenvironments.

204 Therefore, the sites of long-term S. typhimurium persistence in the mouse are not known no

205 The strain, termed S. typhimurium A1, selectively grew in prostate tumors i

206 We therefore conclude that S. typhimurium fliE is essential for flagellin secretion

207 Here, we demonstrate that S. typhimurium induces formation of focal adhesion-like

208 We demonstrate that S. typhimurium manipulates the migratory properties of i

209 ere, for the first time, we demonstrate that S. typhimurium-induced PMN transmigration across Madin-D

210 sly unknown metabolite, we demonstrated that S. typhimurium LT2 can utilize l-talarate as carbon sour

211 model of long-term infection, we found that S. typhimurium preferentially associates with anti-infla

212 The function of PagL is unknown, given that S. typhimurium mutants lacking pagL display no obvious p

213 This survival implies that S. typhimurium avoids or withstands bactericidal events

214 Our results indicate that S. typhimurium requires cues from the innate immune syst

215 Here, we show that S. typhimurium can persist for as long as 1 yr in the me

216 Our findings show that S. typhimurium contains versatile enzymes capable of mod

217 We now show that S. typhimurium releases ammonium into the medium when gr

218 Our results suggest that S. typhimurium activates a protein kinase C-dependent si

219 These findings suggest that S. typhimurium enhances invasion efficiency by promoting

220 Together, these results suggest that S. typhimurium has limited ability to adhere to tumor va

221 Recent evidence suggests that S. typhimurium alters ROS production by murine macrophag

222 The S. typhimurium A1 strain grew throughout the tumor, incl

223 The S. typhimurium A1-R mutant, which is auxotrophic for leu

224 The S. typhimurium lpxO gene encodes a polypeptide of 302 am

225 The S. typhimurium virulence gene product PhoP/PhoQ signals

226 The S. typhimurium-NY-ESO-1 construct elicited NY-ESO-1-spec

227 ored by introducing a plasmid containing the S. typhimurium fis gene or a plasmid containing hilD, a

228 We have identified the gene encoding the S. typhimurium lipid A 3'-O-deacylase, designated lpxR,

229 of expression of the malEfimY fusion in the S. typhimurium fimU mutant and parental strain confirmed

230 Most of these clones are present in the S. typhimurium genome and are also expressed in murine m

231 y, we measured the antitumor efficacy of the S. typhimurium A1-R mutant, which is auxotrophic for leu

232 l as that found in a recent structure of the S. typhimurium enzyme, combined with the closure of the

233 ructuring protein nucleation function of the S. typhimurium gene silencer AT8 for the leuO gene silen

234 ansfer of genes is frequent, with 11% of the S. typhimurium LT2 genes missing from S. enterica serova

235 A gene located near minute 51 on the S. typhimurium and E. coli chromosomes (previously terme

236 i identified through a motif search over the S. typhimurium genome.

237 ons demonstrated that piperidine reduced the S. typhimurium-induced polymorphonuclear leukocyte trans

238 We propose that antigen delivery through the S. typhimurium type III secretion system is a promising

239 tolerance in response to indole, even though S. typhimurium does not natively produce indole.

240 Thus, S. typhimurium flagellin is the major molecular trigger

241 n of either chemokines (E. coli LPS) or TNF (S. typhimurium LPS) synthesis by anti-IL-18 treatment ma

242 ponse of adult IFN-gamma-knockout animals to S. typhimurium infection resembled that of the wild-type

243 ereby impairing mucosal barrier functions to S. typhimurium dissemination.

244 ed-3 and ced-4 mutants are hypersensitive to S. typhimurium-mediated killing.

245 in abrogated the impairment of resistance to S. typhimurium by hemolysis.

246 -3(-/-) mice were markedly more resistant to S. typhimurium infection than the control mice.

247 RP12-deficient mice were highly resistant to S. typhimurium infection.

248 N-gamma-deficient mice were not resistant to S. typhimurium LPS, suggesting an IFN-gamma-independent

249 scriptional changes occurring in response to S. typhimurium and Y. enterocolitica colonization of PP

250 and IFN-gamma-regulated genes in response to S. typhimurium but not Y. enterocolitica.

251 ing an early and lethal cytokine response to S. typhimurium colonization.

252 However, the response to S. typhimurium in primary human monocytes has not been s

253 ncrease mucosal levels of 5HT in response to S. typhimurium infection, and succumbed to the infection

254 embled Nlrc4(-/-) BMDMs in their response to S. typhimurium or flagellin.

255 vate caspase-1 and pyroptosis in response to S. typhimurium, indicating that S533 phosphorylation is

256 in the tumor controls the immune response to S. typhimurium.

257 -1beta secretion specifically in response to S. typhimurium.

258 from primary human monocytes in response to S. typhimurium.

259 ques, resulting in blunted TH17 responses to S. typhimurium infection and increased bacterial dissemi

260 ethod was confirmed to be highly specific to S. typhimurium without interference from other pathogeni

261 as the highest antimutagenic activity toward S. typhimurium TA98 and TA100.

262 t than l-Ara4N containing forms in wild type S. typhimurium grown in broth but accumulate to high lev

263 lipid A subtypes (St1 to St6) from wild type S. typhimurium.

264 layers' ability to respond to both wild-type S. typhimurium and purified flagellin but had no affect

265 Gel filtration chromatography of wild-type S. typhimurium cell extracts identified stable pools of

266 estored all defects and produced a wild-type S. typhimurium phenotype.

267 mlrA mutants of wild-type S. typhimurium SL1344 or SR-11 no longer produced curli

268 Unlike wild-type S. typhimurium, the fliE-deficient mutant did not activa

269 effect on inducing apoptosis than wild-type S. typhimurium.

270 s to flagellins from Salmonella typhimurium (S. typhimurium) and Bacillus subtilis (B. subtilis) were

271 he Salmonella enterica serotype Typhimurium (S. typhimurium) genome contains a large repertoire of pu

272 ns, Salmonella enterica serovar Typhimurium (S. typhimurium) and Clostridium difficile, use a common

273 Salmonella enterica serovar Typhimurium (S. typhimurium) and Yersinia enterocolitica are enteric

274 of Salmonella enterica serovar Typhimurium (S. typhimurium) infection in the mouse model of typhoid

275 Salmonella enterica serovar Typhimurium (S. typhimurium) infects a wide variety of mammalian host

276 Salmonella enterica serovar Typhimurium (S. typhimurium) is a leading cause of food poisoning wor

277 and Salmonella enterica serovar Typhimurium (S. typhimurium) is associated with extracellular matrix

278 of Salmonella enterica serovar typhimurium (S. typhimurium) to the production of type I fimbriae enc

279 gen Salmonella enterica serovar Typhimurium (S. typhimurium), but the individual contributions of cas

280 enterica subspecies I, serovar Typhimurium (S. typhimurium), is a leading cause of human gastroenter

281 In Salmonella enterica serovar Typhimurium (S. typhimurium), most SPI-1 genes are arranged in operon

282 ses a positive selection step against viable S. typhimurium and a negative selection step against hea

283 d a reduced ability to compete with virulent S. typhimurium for colonization of murine organs, while

284 n 30 min at both species (E. coli O157:H7 vs S. typhimurium ) and strain (E. coli O157:H7 vs E. coli

285 e active with E. coli TrxR and Trx1 than was S. typhimurium AhpC, demonstrating the specialized catal

286 To gain insights into the mechanism by which S. typhimurium inhibits intraphagosomal ROS production,

287 While S. typhimurium strains lacking the SPI-1-encoded type II

288 For example, while S. typhimurium is primarily an intracellular pathogen, Y

289 re decreased in treated mice challenged with S. typhimurium.

290 eceiving MET-1 or control, then gavaged with S. typhimurium.

291 d increased susceptibility to infection with S. typhimurium compared with wild-type mice, the kinetic

292 ificantly more susceptible to infection with S. typhimurium than mice lacking both pro-inflammatory c

293 y to colitis and sepsis after infection with S. typhimurium, partly because of reduced induction of 5

294 ortality during severe CLP or infection with S. typhimurium.

295 d were infected orally or intravenously with S. typhimurium.

296 ection of Nos2(-/-) macrophages or mice with S. typhimurium, the increased iron accumulation was para

297 revealed during oral infection of mice with S. typhimurium, wherein endogenous IFN-gamma and NOS2 en

298 (C57BL/6, Ifn-gamma(-/), and Nos2(-/-)) with S. typhimurium were used to gain an understanding of the

299 e PC-3 tumors that were injected weekly with S. typhimurium A1-R, 7 were alive and well at the time t

300 t strains, suggesting that the ability of WT S. typhimurium to prevent NADPH oxidase assembly at the