ライフサイエンスコーパス: Mtb

1 Mtb and related species may be able to combat this harsh

2 Mtb exhibits a unique capacity to co-metabolize differen

3 Mtb grew as a clump in dead cells, and macrophages which

4 Mtb RNA polymerase (RNAP) is the target of the first-lin

5 Mtb-antigen processing and presentation are key events i

6 Quantitative expression analysis of 2,068 Mtb genes from the predicted first operons identified th

7 NA) miR-33 and its passenger strand miR-33*, Mtb inhibited integrated pathways involved in autophagy,

8 berculosis (Mtb) growth and Mtb Antigen 85C (Mtb Ag85C) activity.

9 cial for host defense, little is known about Mtb-infected necrotic neutrophils.

10 macrophages and dendritic cells to activate Mtb antigen-specific CD4(+) T cells.

11 ned that V-58 rapidly and directly activates Mtb AC Rv1625c to produce high levels of cAMP regardless

12 NanoDisk-MS diagnosed active Mtb cases with high sensitivity and specificity in a cas

13 splays acceptable antituberculosis activity (Mtb IC50 = 525 nM, Mtb Wayne IC50 = 76 nM, and MDR Mtb p

14 In addition, Mtb-infected DCs triggered a significant release of the

15 levels were analyzed in healthy adolescents, Mtb-unexposed control subjects, and patients with pulmon

16 After Mtb infection, TNF-alpha is also downregulated in Ipr1-e

17 ession signatures in macrophages early after Mtb infection.

18 n addition, MSCs secreted nitric oxide after Mtb infection, and inhibition of NO by N(G)-monomethyl-L

19 oncentration of 1.7 muM (0.6 mug/mL) against Mtb in biotin-free medium.

20 ompounds that have increased potency against Mtb and the ability to overcome resistance.

21 on of their antitubercular potential against Mtb.

22 ry concentration (MIC) of 12.5 mug/mL and an Mtb Ag85C apparent IC50 of 8.8 muM.

23 tricted CD8(+) T cell clone isolated from an Mtb latently infected individual as a peptide from the M

24 We identified an Mtb protein (PPE15) that showed weak amino acid sequence

25 The results identify an Mtb-specific structural module of Mtb RNAP and establish

26 a loss of fitness caused by drug action and Mtb's sensitivity to host-derived stresses.

27 Optimal capreomycin binding and Mtb ribosome inhibition requires ribosomal RNA methylati

28 Mycobacterium tuberculosis (Mtb) growth and Mtb Antigen 85C (Mtb Ag85C) activity.

29 otently and selectively inhibit Mtb RNAP and Mtb growth, and we report crystal structures of Mtb RNAP

30 cally diverse populations and quickly assess Mtb treatment responses for emerging drug-resistant stra

31 gamma from co-cultures of DCs and autologous Mtb antigen-specific CD4(+) T cells.

32 l, the hedgehog pathway was downregulated by Mtb-stimulation, but Shh levels in astrocytes were uncha

33 TJP breakdown was driven by Mtb-dependent secretion of matrix metalloproteinase (MMP

34 Chemical stimulation of cAMP production by Mtb within macrophages also caused down regulation of TN

35 ata define a mammalian miRNA circuit used by Mtb to coordinately inhibit autophagy and reprogram host

36 tablish PPM1A as a checkpoint target used by Mtb to suppress macrophage apoptosis.

37 to recognize infected macrophages and clear Mtb.

38 rom this series were active against clinical Mtb strains, while no cross-resistance to conventional a

39 ompared to wild type and esat-6 complemented Mtb strains.

40 e Mtb 50S ribosomal subunit and the complete Mtb 70S ribosome, solved by cryo-electron microscopy.

41 preserve Mtb phagosome integrity and control Mtb replication.

42 ore the capability of macrophages to control Mtb growth, thereby identifying a potential host-directe

43 ability of each T cell population to control Mtb in the lungs of mice was restricted for opposite rea

44 SMURF1 controls Mtb replication in human macrophages and associates with

45 inactivating mutations in the corresponding Mtb gene tlyA, which cause resistance to capreomycin, ou

46 le method of producing cultures of >/=90% DD Mtb in starved cells.

47 n contrast, thioridazine did not generate DD Mtb from starved cells but killed those generated by rif

48 ther they contribute to the generation of DD Mtb or kill them.

49 Of the agents tested, rifamycins led to DD Mtb generation, an effect lacking in a rifampin-resistan

50 rating such "differentially detectable" (DD) Mtb in vitro would aid studies of the biology and drug s

51 bolomic profiling revealed that MS-deficient Mtb cultured on fatty acids accumulated high levels of t

52 bitor of ICL restored growth of MS-deficient Mtb, despite inhibiting entry of carbon into the glyoxyl

53 cAMP signaling might be leveraged to disrupt Mtb pathogenesis.

54 te that the macrophage environment dominates Mtb's response to drug pressure and suggest novel routes

55 tory network activated in macrophages during Mtb infection.

56 f cAMP signaling in Mtb, particularly during Mtb's interactions with macrophages.

57 severe necrotic lung lesions, more efficient Mtb growth control in the lungs, and longer survival.

58 own of autophagy initiator beclin-1 enhanced Mtb survival, whereas rapamycin-induced autophagy increa

59 these values are consistent with established Mtb infection.

60 ethods to identify IVE-TB (in-vivo expressed Mtb) antigens expressed in the lung.

61 killing alongside conventional extracellular Mtb killing data, generates the biphasic responses typic

62 compartment on days 0, 7, 14, 21, and 28 for Mtb quantification, and compared the slope of microbial

63 for a novel diagnostic platform (TB-DzT) for Mtb detection and the identification of drug resistant m

64 in growing cells, may also be essential for Mtb's survival in acidic conditions.

65 tiality of the periplasmic protease MarP for Mtb to survive in acidified phagosomes and establish and

66 inst Mycobacterium marinum (Mm) (a model for Mtb), Pseudomonas aeruginosa (Pa), Legionella pneumophil

67 Two IS samples were obtained for Mtb culture from children enrolled as cases in the Pneum

68 iated structures and are more permissive for Mtb growth.

69 Neutrophil necrosis was required for Mtb growth after uptake of infected neutrophils by human

70 dren investigated with IS and GA samples for Mtb.

71 re, the protein composition of exosomes from Mtb-infected and uninfected THP-1-derived macrophages wa

72 significantly more abundant in exosomes from Mtb-infected cells; 63% of these were predicted to be me

73 r amino acid biosynthetic pathways as future Mtb drug targets.

74 tal structures of near full-length hexameric Mtb Mpa in apo and ADP-bound forms.

75 However, the mechanistic aspects of how Mtb responds to beta-lactams such as Amoxicillin in comb

76 We have identified Mtb-specific peptide fragments and developed a method to

77 lysis of in silico blood measures identifies Mtb-specific frequencies of effector T cell phenotypes a

78 el antigen discovery approach in identifying Mtb antigens, including those that induce unconventional

79 In Mtb 70S, bridge B9 is mostly maintained, leading to corr

80 responsible for the import of fatty acids in Mtb were previously unknown.

81 ng TB vaccine antigens, ESAT-6 and Ag85B, in Mtb-infected mice and in vaccinated humans with and with

82 hages, indicating a complex role for cAMP in Mtb pathogenesis.

83 of drug-tolerant and drug-resistant cells in Mtb cultures.

84 ung hemodynamics and pathological changes in Mtb infected cells can be used for the selective targeti

85 ition by V-58 was carbon source dependent in Mtb and did not occur in Mycobacterium smegmatis, sugges

86 Deletion of Pat and DAc genes in Mtb revealed distinct phenotypes for strains lacking one

87 YP) enzymes, many of which are implicated in Mtb survival and pathogenicity in the human host.

88 t were recognized at 10-fold-lower levels in Mtb-infected individuals with a history of TB disease le

89 sterol assimilation are inexorably linked in Mtb and reveals a key function for Rv3723/LucA in in coo

90 (e.g. beta-lactamase) and redox potential in Mtb.

91 r targeted stimulation of cAMP production in Mtb, and provide new insights into the myriad roles of c

92 macrophages and stimulate cAMP production in Mtb.

93 be exploited to diminish drug-resistance in Mtb through redox-based interventions.

94 vidence that the alphaCTD may play a role in Mtb transcription regulation.

95 s into the myriad roles of cAMP signaling in Mtb, particularly during Mtb's interactions with macroph

96 of ESAT-6, IL-6 and phosphorylated-STAT3 in Mtb-infected mouse lungs.

97 structural basis for studying translation in Mtb as well as developing new tuberculosis drugs.

98 ce1 functions as a fatty acid transporter in Mtb and determine that facilitating cholesterol and fatt

99 mammalian perilipin-1 and was upregulated in Mtb dormancy.

100 tegrate cholesterol and fatty acid uptake in Mtb.

101 (AAPs)-that potently and selectively inhibit Mtb RNAP and Mtb growth, and we report crystal structure

102 the small molecule V-58 was shown to inhibit Mtb replication within macrophages and stimulate cAMP pr

103 Rather, it led to accelerated intracellular Mtb growth regardless of prior activation or macrophage

104 re insufficient to act against intracellular Mtb, providing proof of principle for the efficacy of a

105 Transcriptional analysis of intracellular Mtb exposed to drugs identified a set of genes common to

106 Integrated modelling of intracellular Mtb killing alongside conventional extracellular Mtb kil

107 rtantly, macrophage killing of intracellular Mtb.

108 inths and those induced by the intracellular Mtb are often mutually antagonistic and, as a consequenc

109 at the killing dynamics of the intracellular Mtb sub-population is critical to predicting clinical TB

110 lease enabled rifampicin to effectively kill Mtb at concentrations that were insufficient to act agai

111 Individuals with no known Mtb exposure had IFN-gamma values less than 0.2 IU/ml.

112 ized by T cells from individuals with latent Mtb infection differs as a function of previous diagnosi

113 lidated in an independent cohort of latently Mtb-infected individuals.

114 nd mechanisms that contribute to maintaining Mtb phagosome integrity have not been investigated.

115 icking pathway in macrophages that maintains Mtb in spacious proteolytic phagolysosomes.

116 The exposure associated with maximal Mtb kill was an AUC0-24/MIC of 23.37 +/- 1.16.

117 50 = 525 nM, Mtb Wayne IC50 = 76 nM, and MDR Mtb patient isolates IC50 = 140 nM) and favorable pharma

118 effective against multi drug resistant (MDR) Mtb.

119 ue of the ETC as a drug target, by measuring Mtb's respiration using extracellular flux technology.

120 scription of a post-translationally modified Mtb-derived protein antigen presented in the context of

121 ntituberculosis activity (Mtb IC50 = 525 nM, Mtb Wayne IC50 = 76 nM, and MDR Mtb patient isolates IC5

122 d 6.62 muM against active and nonreplicating Mtb, respectively.

123 ion, in the setting of repeated occupational Mtb exposure.

124 resent structural and functional analyses of Mtb TlyA interaction with its obligatory co-substrate fo

125 rproduction of PPM1A suppressed apoptosis of Mtb-infected macrophages by a mechanism that involves in

126 est that drug-induced selective apoptosis of Mtb-infected macrophages is achievable.

127 ivation, resulting in increased apoptosis of Mtb-infected macrophages.

128 murf1 is required for selective autophagy of Mtb and host defense against tuberculosis infection.

129 rophage death did not result in clearance of Mtb.

130 8(+) T cells are important to the control of Mtb infection.

131 assay, we demonstrated accurate detection of Mtb and 5 mutations associated with resistance to three

132 Detection of Mtb is enhanced by combining 2 IS with GA sample collect

133 dentified as scaffold for the development of Mtb-ThyX inhibitors.

134 , we examined the spatiotemporal dynamics of Mtb-containing phagosomes and identified an interferon-g

135 tion as an essential physiologic function of Mtb malate synthase and advances its validation as a tar

136 iR-155 promotes the survival and function of Mtb-specific T cells, enabling an effective adaptive imm

137 (2-VIC) as a mechanism-based inactivator of Mtb ICL1 and ICL2.

138 roduct analogues are nanomolar inhibitors of Mtb phospho-MurNAc-pentapeptide translocase, the enzyme

139 mportant tools to reveal the interactions of Mtb with mammalian hosts and facilitate the determinatio

140 Internalization of Mtb aggregates caused macrophage death, and phagocytosis

141 and compared the slope of microbial kill of Mtb by these regimens to the standard regimen of isoniaz

142 oniazid treatment potentiated the killing of Mtb Furthermore, we demonstrate that the addition of sma

143 mycin induced selective apoptotic killing of Mtb-infected human macrophages, which was completely blo

144 Finally, selective killing of Mtb-infected macrophages and subsequent bacterial releas

145 autophagy increased intracellular killing of Mtb.

146 e ETC can be exploited to enhance killing of Mtb.

147 hway of defense that promotes maintenance of Mtb within intact membrane-bound compartments for effici

148 Where studied, the majority of Mtb in the sputum of most untreated subjects with active

149 roven activity in an in vivo murine model of Mtb infection.

150 ng cell-based approaches and mouse models of Mtb infection, we characterized the function(s) of SP110

151 dentify an Mtb-specific structural module of Mtb RNAP and establish that Rif functions by a steric-oc

152 An isocitrate lyase-deficient mutant of Mtb (Deltaicl1) exhibited a delayed growth phenotype in

153 e generated a ppe15 gene-disrupted mutant of Mtb and examined its ability to metabolically incorporat

154 gle IS sample underestimated the presence of Mtb in children hospitalized with severe or very severe

155 ontaining DNA expressing a fusion protein of Mtb antigens 85A, 85B and TB10.4.

156 highly effective, leading to a reduction of Mtb to undetectable levels in a mouse model of infection

157 We hypothesized that the repertoire of Mtb-derived epitopes recognized by T cells from individu

158 ing antigens expressed at distinct stages of Mtb infection.

159 depletion of MS resulted in sterilization of Mtb in both the acute and chronic phases of mouse infect

160 ence 150 in hypervirulent Beijing strains of Mtb, is important for TB pathogenesis.

161 OR gate would function during the stress of Mtb infection.

162 s onto a low-resolution crystal structure of Mtb tryptophan synthase showed they locate to the interf

163 growth, and we report crystal structures of Mtb RNAP in complex with AAPs.

164 We report crystal structures of Mtb RNAP, alone and in complex with Rif, at 3.8-4.4 A re

165 citrate lyase (ICL), may mediate survival of Mtb during the acute and chronic phases of infection in

166 ssential for in vitro growth and survival of Mtb on even-chain fatty acids, in part, for a previously

167 one hand, miR-155 maintains the survival of Mtb-infected macrophages, thereby providing a niche favo

168 involved in the pathogenesis and survival of Mtb.

169 -arginine enhanced intracellular survival of Mtb.

170 that the intrinsically low susceptibility of Mtb to fluoroquinolones correlates with a reduction in c

171 Using genome-wide transcriptomics of Mtb infected lungs we developed data sets and methods to

172 emergence of resistance and transmission of Mtb in the largest outbreak of multidrug-resistant TB in

173 e receptor was not involved in the uptake of Mtb.

174 s or siRNA knockdown decreased the uptake of Mtb.

175 to the heat-shock response and virulence of Mtb Here, we show that PafE subunits formed four-helix b

176 AAPs bind to a different site on Mtb RNAP than Rif, exhibit no cross-resistance with Rif,

177 um as well as BioA under- and overexpressing Mtb strains.

178 infected necrotic cells by other phagocytes, Mtb growth therein, and sustained infection.

179 Phagocytosed Mtb did not replicate within MSCs, thus suggesting an in

180 ive sampling for linezolid pharmacokinetics, Mtb intracellular burden, viable monocyte count, and RNA

181 ulate ICDH activity through phosphorylation, Mtb is capable of regulating ICDH activity by acetylatio

182 A blood polyfunctional, Mtb DosR latency antigen specific, regulatory, central m

183 ted macrophages, and is required to preserve Mtb phagosome integrity and control Mtb replication.

184 d that mutations in the gene rv2170 promoted Mtb replication under these conditions and rescued the g

185 s the pro-inflammatory response to pulmonary Mtb, leading to poorly formed granulomas, more severe lu

186 The purified Mtb ClpB/DnaK system reactivated a heat-denatured model

187 ld allow more definitive detection of recent Mtb infection and potentially improve identification of

188 s where cytokine-mediated activation renders Mtb tolerant to four frontline drugs.

189 n of a minority population of drug resistant Mtb, a clinically relevant scenario referred to as heter

190 tentiates AG activity against drug-resistant Mtb.

191 ular drug used to combat multidrug-resistant Mtb strains.

192 Absolute quantification of serum Mtb antigen concentration was informative in assessing r

193 In both species, Mtb infection drove ESAT-6-specific T cells to be more d

194 ibition is due to interference with specific Mtb metabolic pathways rather than a generalized cAMP to

195 lance toward a reduced state that stimulates Mtb respiration and converts persister cells to metaboli

196 Subsequent Mtb screening of the complete in-house quinolone library

197 ADEP antibiotics also target Mtb, with the assumption that uncontrolled ADEP-activate

198 We recently described that Mtb infection upregulated expression of the host phospha

199 Intriguingly, we find that Mtb in myeloid cells isolated from the lungs of experime

200 We find that Mtb's ETC rapidly reroutes around inhibition by these dr

201 We found that Mtb induces necrosis of human neutrophils in an ESX-1-de

202 The Mtb Rv2170 protein shows lysine acetyltransferase activi

203 We compared the Mtb yield of 2 IS samples to that of 1 IS sample and GA

204 ly infected individual as a peptide from the Mtb protein, MPT32.

205 Importantly, metabolome profiling in the Mtb surrogate, Mycobacterium bovis BCG, reveals signific

206 umulation, and greater lung pathology in the Mtb-co-infected lung.

207 eability and increased TJP expression in the Mtb-stimulated BBB co-cultures.

208 and translocates protein substrates into the Mtb proteasome core particle for degradation.

209 nits, a 100-nt long expansion segment of the Mtb 23S rRNA, named H54a or the 'handle', switches inter

210 we present the near-atomic structures of the Mtb 50S ribosomal subunit and the complete Mtb 70S ribos

211 Here, we reconstituted the activities of the Mtb ClpB/DnaK bichaperone system with the cofactors DnaJ

212 ere, we present the crystal structure of the Mtb DnaE1 polymerase.

213 ors bedaquiline, Q203 and clofazimine on the Mtb ETC, and the value of the ETC as a drug target, by m

214 ells induced by vaccination to recognize the Mtb-infected cell.

215 instances these cells did not recognize the Mtb-infected cell.

216 ies between Mycobacterium tuberculosis ThyX (Mtb-ThyX) and Tm-ThyX, our crystal structure paves the w

217 ill provide insight into natural immunity to Mtb and will guide development of novel vaccine strategi

218 een shown to control host innate immunity to Mtb infection.

219 otein LC3, and the lysosomal marker LAMP1 to Mtb-associated structures and are more permissive for Mt

220 To determine factors leading to Mtb proliferation and host cell death, we used live cell

221 Preferential loss of T-cell reactivity to Mtb epitopes that are homologous to bacteria in the micr

222 dependent IFN-gamma secretion in response to Mtb with critical implications for future intervention s

223 tral memory CD4 T-cell responses specific to Mtb dormancy related (DosR) latency, but not classical i

224 nstrate that the addition of small thiols to Mtb drug treatment shifted the menaquinol/menaquinone ba

225 ll death, we used live cell imaging to track Mtb infection outcomes in individual primary human macro

226 apoptosis is essential for M. tuberculosis (Mtb) to replicate intracellularly while protecting it fr

227 le the removal of apoptotic M. tuberculosis (Mtb)-infected cells, or efferocytosis, is considered ben

228 sis of biotin in Mycobacterium tuberculosis (Mtb) and is an essential enzyme for bacterial survival a

229 for virulence of Mycobacterium tuberculosis (Mtb) and plays an essential role in phagosome rupture an

230 TB) is caused by Mycobacterium tuberculosis (Mtb) and provided original proof that an infectious agen

231 aureus (SA) and Mycobacterium tuberculosis (Mtb) are appreciably sensitive to changes in the intrace

232 Mycobacterium tuberculosis (Mtb) can persist in the human host in a latent state for

233 demonstrate that Mycobacterium tuberculosis (Mtb) causes breakdown of type IV collagen and decreases

234 Mycobacterium tuberculosis (Mtb) causes latent tuberculosis infection in one-third o

235 entially growing Mycobacterium tuberculosis (Mtb) cells, but the remaining cells are persisters, cell

236 Mycobacterium tuberculosis (Mtb) characteristically causes an asymptomatic infection

237 Mycobacterium tuberculosis (Mtb) contributes to the pathogenesis of childhood acute

238 ns of avidin and Mycobacterium tuberculosis (Mtb) CYP142A1 were assessed through collision-induced di

239 Mycobacterium tuberculosis (Mtb) displays a high degree of metabolic plasticity to a

240 Mycobacterium tuberculosis (Mtb) DprE1, an essential isomerase for the biosynthesis

241 activity against Mycobacterium tuberculosis (Mtb) due to mechanism-based inhibition of BioA, a pyrido

242 tial pathway for Mycobacterium tuberculosis (Mtb) during the persistent phase of human TB infection.

243 The Mycobacterium tuberculosis (Mtb) electron transport chain (ETC) has received signifi

244 Mycobacterium tuberculosis (Mtb) encounters stresses during the pathogenesis and tre

245 Mycobacterium tuberculosis (Mtb) enters the host in aerosol droplets deposited in lu

246 Mycobacterium tuberculosis (Mtb) expresses a broad-spectrum beta-lactamase (BlaC) th

247 or inhibition of Mycobacterium tuberculosis (Mtb) growth and Mtb Antigen 85C (Mtb Ag85C) activity.

248 ese may restrict Mycobacterium tuberculosis (Mtb) growth, or progress to central necrosis and cavitat

249 Mycobacterium tuberculosis (Mtb) has a proteasome system that is essential for its a

250 of a vaccine for Mycobacterium tuberculosis (Mtb) has been impeded by the absence of correlates of pr

251 nst the pathogen Mycobacterium tuberculosis (Mtb) have been advanced through phenotypic screens of ex

252 nostic tools for Mycobacterium tuberculosis (Mtb) have many disadvantages including low sensitivity,

253 screened against Mycobacterium tuberculosis (Mtb) in order to identify novel hits with antitubercular

254 at high risk of Mycobacterium tuberculosis (Mtb) infection and tuberculosis disease, but also play a

255 c factors affect Mycobacterium tuberculosis (Mtb) infection outcomes remains largely unknown.

256 However, in Mycobacterium tuberculosis (Mtb) infection, a discriminatory or protective role for

257 ferent stages of Mycobacterium tuberculosis (Mtb) infection, in particular early secreted versus dorm

258 is indicative of Mycobacterium tuberculosis (Mtb) infection, which predisposes individuals to tubercu

259 to detect active Mycobacterium tuberculosis (Mtb) infections in clinically diverse populations and qu

260 he metabolism of Mycobacterium tuberculosis (Mtb) inside its host cell is heavily dependent on choles

261 kDa (ESAT-6) of Mycobacterium tuberculosis (Mtb) is an essential virulence factor and macrophages ar

262 ulosis, in which Mycobacterium tuberculosis (Mtb) is predominantly intracellular.

263 Mycobacterium tuberculosis (Mtb) is the causative agent of tuberculosis, which kills

264 Mycobacterium tuberculosis (Mtb) kills more humans than any other infection and is c

265 ellular pathogen Mycobacterium tuberculosis (Mtb) lives within phagosomes and also disrupts these org

266 ls infected with Mycobacterium tuberculosis (Mtb) may develop symptoms and signs of disease (tubercul

267 , infection with Mycobacterium tuberculosis (Mtb) occurs in over a third of the world's population, o

268 Ribosomes from Mycobacterium tuberculosis (Mtb) possess species-specific ribosomal RNA (rRNA) expan

269 ic evidence that Mycobacterium tuberculosis (Mtb) PYK uses AMP and glucose-6-phosphate (G6P) as syner

270 st intracellular Mycobacterium tuberculosis (Mtb) residing inside macrophages.

271 Mycobacterium tuberculosis (Mtb) scavenges lipids (cholesterol and fatty acids) to m

272 human infection, Mycobacterium tuberculosis (Mtb) survives the normally bacteriocidal phagosome of ma

273 hA expression in Mycobacterium tuberculosis (Mtb) that reduces the efficacy of ethionamide, a second-

274 MSCs phagocytose Mycobacterium tuberculosis (Mtb) through two types of scavenger receptors (SRs; MARC

275 Mycobacterium tuberculosis (Mtb) uses a complex 3', 5'-cyclic AMP (cAMP) signaling n

276 e major pathogen Mycobacterium tuberculosis (Mtb) uses its intrinsic PHP-exonuclease that is distinct

277 n the surface of Mycobacterium tuberculosis (Mtb), is actively involved in the pathogenesis and survi

278 losis, caused by Mycobacterium tuberculosis (Mtb), is the infectious disease responsible for the high

279 Infection with Mycobacterium tuberculosis (Mtb), the bacterium that causes tuberculosis, remains a

280 immunity against Mycobacterium tuberculosis (Mtb), the cause of tuberculosis (TB).

281 Mycobacterium tuberculosis (Mtb), the etiologic agent of TB, usually resides in the

282 of exosomes from Mycobacterium tuberculosis (Mtb)-infected cells have not been described, can contrib

283 ductase (Ndh) of Mycobacterium tuberculosis (Mtb).

284 e target to kill Mycobacterium tuberculosis (Mtb).

285 immunity against Mycobacterium tuberculosis (Mtb).

286 tidrug-resistant Mycobacterium tuberculosis (Mtb).

287 of intracellular Mycobacterium tuberculosis (Mtb).

288 e human pathogen Mycobacterium tuberculosis (Mtb).

289 n persistence of Mycobacterium tuberculosis (Mtb).

290 ClpC1 and ClpX, inMycobacterium tuberculosis(Mtb) are essential and, therefore, promising drug target

291 accinated humans with and without underlying Mtb infection.

292 e recognition and modification that underpin Mtb sensitivity to capreomycin.

293 d IL-18, sensing of mycobacterial viability, Mtb protein 6-kDa early secretory antigenic target-media

294 The virulent Mtb H37Rv strain encodes 20 cytochrome P450 (CYP) enzyme

295 ings reveal another important scenario where Mtb could be influencing changes in host cells that unve

296 taken up into MSC endosomes colocalized with Mtb phagosomes, thus suggesting that the latter were fus

297 nfected human-derived THP-1 macrophages with Mtb and inoculated hollow fiber systems.

298 Infection of BMDM and human macrophages with Mtb with esat-6 deletion induced diminished STAT3 activa

299 ompound was evaluated against wild-type (WT) Mtb in biotin-free and -containing medium as well as Bio

300 t (MDR) and extensively drug resistant (XDR) Mtb strains that emerge globally as a public health thre