ライフサイエンスコーパス: M. avium

1 M. avium complex infection was identified by use of the

2 M. avium entry resulted in the phosphorylation of N-WASp

3 M. avium express glycopeptidolipids (GPLs) as a major ce

4 M. avium infects macrophages and actively interfere with

5 M. avium is commonly acquired by ingestion, and a large

6 M. avium isolates were significantly more likely to be a

7 M. avium mmpL4 proteins were found to bind to VDAC-1 pro

8 M. avium or M. tuberculosis infection was markedly incre

9 M. avium subsp. hominissuis biofilm triggered robust tum

10 M. avium subsp. paratuberculosis also has been reported

11 M. avium subsp. paratuberculosis exposed to milk entered

12 M. avium subsp. paratuberculosis infection of the bovine

13 M. avium subsp. paratuberculosis isolates from bovine fe

14 M. avium subsp. paratuberculosis was also shown to inter

15 M. avium subsp. paratuberculosis was capable of invading

16 M. avium subsp. silvaticum isolates were observed to hav

17 M. avium was isolated in 62 (0.83%) of 7,472 patients an

18 M. avium was recovered more frequently from sterile site

19 to examine the genetic conservation among 10 M. avium subsp. paratuberculosis isolates, two isolates

20 We determined the subspecies of 257 M. avium strains isolated from patients at the M.D. Ande

21 On the transcriptional level, over 300 M. avium subsp. paratuberculosis genes were significantl

22 monstrate that the loss of mtfD results in a M. avium 104 strain, which preferentially activates macr

23 cterial uptake by macrophages, we screened a M. avium transposon mutant library for the inability to

24 on of inflammatory cytokines by host-adapted M. avium strains.

25 to detect the presence of antibodies against M. avium subsp. paratuberculosis in host serum.

26 nM against P. carinii DHFR, 0.57 nM against M. avium DHFR, and 55 nM against rat DHFR.

27 IFN-gamma and can confer protection against M. avium infection in immunocompromised mice.

28 irst study to demonstrate protection against M. avium subsp. paratuberculosis infection with expressi

29 wever 13 was no more potent than PTX against M. avium DHFR, and its SI was no better than that of TMP

30 his, TNF-alpha has a protective role against M. avium.

31 (22), was both potent and selective against M. avium DHFR (IC(50) = 0.47 nM, SI = 1300) but was not

32 During initial colonization of the airways, M. avium subsp. hominissuis forms microaggregates compos

33 sp. avium serotype 1 and serotype 2, 3 (also M. avium subsp. silvaticum); and the ruminant type, M. a

34 Although M. avium is known for its genetic plasticity, these obse

35 identify large sequence polymorphisms among M. avium subspecies obtained from a variety of host anim

36 Total lipids from an M. avium subsp. paratuberculosis (Map) ovine strain (S-t

37 We interrogated an M. avium subsp. paratuberculosis DeltasigL mutant agains

38 led the global gene expression pattern of an M. avium subsp. avium isolate, and they significantly up

39 We have utilized an M. avium subsp. paratuberculosis whole-genome microarray

40 To determine whether an M. avium subsp. paratuberculosis protein delivered to th

41 M. abscessus (34%) and M. avium complex (83%) were the most commonly isolated n

42 compared to both the wild-type M. avium and M. avium containing the vector alone.

43 I values of >100 against both P. carinii and M. avium DHFR relative to rat DHFR.

44 the most potent against P. carinii DHFR and M. avium DHFR was the 2'-(5-carboxy-1-butynyl)dibenz[b,f

45 o no seroreactivity against M. kansasii- and M. avium subsp. paratuberculosis-infected animals.

46 f Mycobacterium tuberculosis, M. leprae, and M. avium complex infections.

47 obacterium avium subsp. paratuberculosis and M. avium subsp. avium, respectively.

48 s of M. avium sub0:36 PMparatuberculosis and M. avium sub0:36 PMavium, as well as DNA from M. fortuit

49 lonized the six SDSs, but L. pneumophila and M. avium were not detected.

50 ., M. intracellulare, Acanthamoeba spp., and M. avium peaked during the dry season.

51 acrophages infected with M. tuberculosis and M. avium or with avirulent M. smegmatis.

52 cells (which have been shown to induce anti-M. avium subsp. hominissuis activity when added to THP-1

53 , patients whose isolates were identified as M. avium (adjusted odds ratio [AOR], 2.14; 95% confidenc

54 sferase recognition in the tissue-associated M. avium subsp. paratuberculosis isolates.

55 Mycobacterium avium (M. avium) subspecies vary widely in both pathogenicity a

56 ii (T. gondii, tg), and Mycobacterium avium (M. avium, ma) are the principal causes of morbidity and

57 Because M. avium subsp. paratuberculosis can be delivered to the

58 fied to the species level by MycoID as being M. avium (n = 98; 61.1%), M. intracellulare (n = 57; 35.

59 he concentration of several elements between M. avium and M. tuberculosis vacuoles were also observed

60 ative levels of protein expression from both M. avium subsp. paratuberculosis strains were measured b

61 pneumophila from recolonizing biofilms, but M. avium gene numbers increased by 0.14-0.76 logs in the

62 en and mesenteric lymph node colonization by M. avium subsp. paratuberculosis.

63 munization with a novel PE gene expressed by M. avium (MaPE) showed that a dominant T-cell immune res

64 iking of a negative fecal sample followed by M. avium sub0:36 PMparatuberculosis DNA extraction resul

65 be most common (n = 238, 92.6%), followed by M. avium subsp. avium serotype 1 (n = 12, 4.7%) and sero

66 nderlying thymic atrophy during infection by M. avium with the participation of locally produced NO,

67 The invasion of the intestinal mucosa by M. avium subsp. paratuberculosis and Mycobacterium avium

68 vention of the cell communication pathway by M. avium subsp. paratuberculosis, which loosens the inte

69 acterizes a pathogenic mechanism utilized by M. avium subsp. hominissuis to bind and invade the host

70 Once inside the cell, M. avium subsp. paratuberculosis is known to survive har

71 In comparison, M. avium was recovered from 141 water/biofilm samples.

72 88 suggesting that released exosomes contain M. avium-expressed TLR ligands.

73 M. avium subsp. hominissuis is the dominant M. avium subspecies clinically, that the two bird-type s

74 l a novel signaling pathway activated during M. avium subsp. paratuberculosis entry that links the pr

75 a are required for granuloma assembly during M. avium infections in mice.

76 ordination of immune responses occurs during M. avium subsp. paratuberculosis infection, with these r

77 ng-term repopulating HSCs proliferate during M. avium infection, and that this response requires inte

78 n in murine macrophages infected with either M. avium or M. smegmatis.

79 ttle (n = 3) and cattle infected with either M. avium subsp. avium and Mycobacterium bovis were expos

80 clear phagocytes cocultured with established M. avium subsp. hominissuis biofilm and surveyed various

81 For this evaluation, M. avium subsp. paratuberculosis subtyping was based on

82 ation scheme (tissue-associated versus fecal M. avium subsp. paratuberculosis isolates).

83 d from the environment, but risk factors for M. avium complex infection and disease are poorly unders

84 sting that MBP-1 expression is important for M. avium subsp. hominissuis adherence to the host cell.

85 H (sigH) that was shown to be important for M. avium subsp. paratuberculosis survival inside gamma i

86 intestinal mucosa is important in order for M. avium subsp. paratuberculosis to establish infection.

87 esults indicate that soil is a reservoir for M. avium complex associated with human infection and tha

88 ergoing standard macrolide-based therapy for M. avium complex lung disease were monitored at standard

89 The region is unique for M. avium and is not present in M. tuberculosis or M. par

90 ile very similar to yet distinguishable from M. avium subsp. avium.

91 d MAC mycobacteria can be distinguished from M. avium subsp. paratuberculosis by multiple clusters of

92 e was competitively hybridized with DNA from M. avium subsp. paratuberculosis K10, and open reading f

93 Interestingly, exosomes isolated from M. avium-infected but not from uninfected macrophages ca

94 study we isolated different GPL species from M. avium, and using mass spectrometry and NMR analyses,

95 on, and a large number of AIDS patients have M. avium in their intestinal tracts.

96 neous colitis displayed significantly higher M. avium subsp. paratuberculosis-specific immunoglobulin

97 The reasoning behind how M. avium subsp. hominissuis biofilm is allowed to establ

98 To identify M. avium genes and host cell pathways involved in the ba

99 To identify M. avium subsp. paratuberculosis genes associated with t

100 Genome diversity in M. avium subspecies appears to be mediated by large sequ

101 better decipher the role of sigma factors in M. avium subsp. paratuberculosis pathogenesis, we target

102 Together our data support a role for GPLs in M. avium pathogenesis.

103 associated with the HLA-DRalpha promoter in M. avium-infected THP-1 cells stimulated with IFN-gamma.

104 iological significance of such regulators in M. avium subsp. paratuberculosis rremains elusive.

105 suggest that GPLs play an important role in M. avium pathogenesis.

106 rental strain, suggesting a role for sigH in M. avium subsp. paratuberculosis virulence.

107 ies suggested a substantial role for sigL in M. avium subsp. paratuberculosis virulence, as indicated

108 for the control of inflammatory signaling in M. avium-infected human primary macrophages.

109 cidity, and oxidative stress were similar in M. avium subsp. paratuberculosis and Mycobacterium tuber

110 e sequence polymorphisms present uniquely in M. avium subsp. paratuberculosis.

111 a 16S rRNA gene A1408G mutation and included M. avium, Mycobacterium intracellulare, and Mycobacteriu

112 subsp. hominissuis; the bird type, including M. avium subsp. avium serotype 1 and serotype 2, 3 (also

113 ected Rag2(-/-)gammac(-/-) animals increased M. avium growth in the liver.

114 siRNA-mediated knockdown of Keap1 increased M. avium-induced expression of inflammatory cytokines an

115 cked down for MR expression showed increased M. avium phagosome-lysosome fusion relative to control c

116 Upon translocation, dendritic cells ingest M. avium subsp. paratuberculosis, but this process does

117 MBP-1 immune serum significantly inhibited M. avium subsp. hominissuis infection throughout the res

118 avium-M. intracellulare complex strains into M. avium and M. intracellulare may provide a tool to bet

119 Microarray analysis of intracellular M. avium subsp. paratuberculosis RNA indicates the incre

120 l isolates with the sequenced bovine isolate M. avium subsp. paratuberculosis (MAP) K-10.

121 o included were previously reported or known M. avium subsp. paratuberculosis antigens to serve as a

122 ould be facilitated growth of pathogens like M. avium inside macrophages.

123 noculated with 10(2) to 10(8) CFU/ml of live M. avium subsp. paratuberculosis organisms.

124 Monitoring cellular markers, only live M. avium subsp. paratuberculosis bacilli were able to pr

125 r the vehicle containing heat-killed or live M. avium subsp. paratuberculosis.

126 M. intracellulare (n = 57; 35.8%), and mixed M. avium and M. intracellulare (n = 2; 1.3%).

127 oculation of a wild-type strain and a mutant M. avium subsp. paratuberculosis strain (with an inactiv

128 e 333 participants with positive or negative M. avium sensitin skin tests, age-adjusted independent p

129 To examine the ability of M. avium subsp. paratuberculosis to infect bovine epithe

130 in a significant reduction in the amount of M. avium subsp. paratuberculosis recovered from mouse ti

131 ons, we performed a global scale analysis of M. avium subsp. paratuberculosis isolates that were repr

132 tification of previously unknown antigens of M. avium subsp. paratuberculosis.

133 Shedding levels (CFU of M. avium subsp. paratuberculosis/g of feces) for the ani

134 ch is that it enables a direct comparison of M. avium subsp. paratuberculosis proteins to each other

135 nels (VDAC) were identified as components of M. avium vacuoles in macrophages.

136 otocols to ensure that low concentrations of M. avium subsp. paratuberculosis can be detected.

137 ans or siRNA lead to significant decrease of M. avium survival.

138 or months following intestinal deposition of M. avium subsp. paratuberculosis despite a lack of fecal

139 onstrated a sensitivity for the detection of M. avium sub0:36 PMparatuberculosis DNA by use of the IS

140 ployed for the systematic differentiation of M. avium subsp. paratuberculosis strains to understand t

141 apoptosis but did not lead to elimination of M. avium subsp. hominissuis.

142 e for studying the molecular epidemiology of M. avium subsp. paratuberculosis.

143 tudy revealed the rapid genetic evolution of M. avium in chronically infected patients, accompanied b

144 e been infected by environmental exposure of M. avium subsp. paratuberculosis.

145 observed that the constitutive expression of M. avium proteins has a modest impact on the ability to

146 Therefore, the sequenced genome of M. avium strain 104 has been associated with disease in

147 ted consistency among infecting genotypes of M. avium subsp. paratuberculosis isolated from diverse h

148 cells) in response to different genotypes of M. avium subsp. paratuberculosis isolates recovered from

149 data analysis revealed unique gene groups of M. avium subsp. paratuberculosis that were regulated und

150 ributed to decreased intracellular growth of M. avium in primary human macrophages that was reconstit

151 ture media determined differential growth of M. avium subsp. paratuberculosis strains and that this s

152 s and lead to a discrepancy in the growth of M. avium subsp. paratuberculosis strains.

153 Growth of M. avium subsp. paratuberculosis within MAC-T cells also

154 rRNA gene target for rapid identification of M. avium complex (MAC) and a region of the heat shock pr

155 of sigL in the pathogenesis and immunity of M. avium subsp. paratuberculosis infection, a potential

156 re is growing evidence that the incidence of M. avium and related nontuberculous species is increasin

157 k, it was investigated whether incubation of M. avium subsp. paratuberculosis with milk has an effect

158 did not affect the isolation or infection of M. avium.

159 ed by reinfection with a separate isolate of M. avium.

160 by PCR of the DNA extracted from isolates of M. avium sub0:36 PMparatuberculosis and M. avium sub0:36

161 THP-1 cells infected with sheep isolates of M. avium subsp. paratuberculosis or the M. avium subsp.

162 The cattle and human isolates of M. avium subsp. paratuberculosis, regardless of their sh

163 Subspecies and host adapted isolates of M. avium were distinguishable by the presence or absence

164 of the three evaluated for the isolation of M. avium subsp. paratuberculosis from milk, as it achiev

165 e an optimized protocol for the isolation of M. avium subsp. paratuberculosis in milk.

166 Several mutants of M. avium subsp. paratuberculosis were identified which i

167 The ingestion of small numbers of M. avium cells induces a protective immune response in t

168 ove our understanding of the pathogenesis of M. avium subsp. paratuberculosis.

169 ests, age-adjusted independent predictors of M. avium complex infection in a multivariate model inclu

170 rom Ohio farms were assessed for presence of M. avium subsp. paratuberculosis using four different pr

171 xt steps to further elucidate the process of M. avium subsp. paratuberculosis invasion.

172 haracterizing the gene expression profile of M. avium subsp. paratuberculosis exposed to different st

173 characterize the surface-exposed proteome of M. avium subsp. hominissuis.

174 fadD2 is a regulator of M. avium invasion, and its effect is through Cdc42.

175 In this report, the stress response of M. avium subsp. paratuberculosis on a genome-wide level

176 associated with transcriptional responses of M. avium subsp. paratuberculosis during macrophage infec

177 The results of M. avium subsp. paratuberculosis strain typing and obser

178 onged soil exposure are at increased risk of M. avium complex infection.

179 n of Cdc42 probably follows the secretion of M. avium proteins.

180 (n=597), suggesting the high sensitivity of M. avium subsp. paratuberculosis to acidic environments.

181 the wild-type strain and a mutant strain of M. avium subsp. paratuberculosis deficient in tissue col

182 d infection with a highly virulent strain of M. avium, but not with a low-virulence strain, led to a

183 technique, we found 15 different strains of M. avium subsp. paratuberculosis from a total of 142 iso

184 To our surprise, strains of M. avium subsp. paratuberculosis were able to traverse t

185 No strains of M. avium subsp. paratuberculosis were found.

186 stages of infection by different strains of M. avium subsp. paratuberculosis, a first step in unders

187 nd cytosol were prepared from two strains of M. avium subsp. paratuberculosis, i.e., laboratory-adapt

188 proteins exposed at the bacterial surface of M. avium subsp. hominissuis.

189 mon of which was nearly identical to that of M. avium strains.

190 of HDAC activity, were added at the time of M. avium or M. tuberculosis infection or TLR2 stimulatio

191 ohne's disease, allowing the transmission of M. avium subsp. paratuberculosis between animals.

192 The understanding of M. avium pathogenesis has been hampered by the inability

193 ile facilitates an improved understanding of M. avium subsp. hominissuis and how it establishes infec

194 ols for developing a better understanding of M. avium subsp. paratuberculosis infection in the host a

195 To improve our understanding of M. avium subsp. paratuberculosis pathogenesis, we examin

196 0.5 to 2.0% did not affect the viability of M. avium subsp. paratuberculosis.

197 ce time-to-diagnosis (from 16 to 8 weeks) of M. avium subsp. paratuberculosis infection and can also

198 t in natural infection but are modified once M. avium subsp. paratuberculosis is adapted to laborator

199 Only M. avium sub0:36 PMparatuberculosis DNA was detectable a

200 Sera from noninfected, M. bovis-infected, or M. avium subsp. paratuberculosis-infected (by natural an

201 (L5P), yet both lipids are present in other M. avium subspecies.

202 Isolates of non-paratuberculosis M. avium from 207 other patients in Southern California

203 h is not seen until much later in planktonic M. avium subsp. hominissuis infection.

204 dded to THP-1 cells infected with planktonic M. avium subsp. hominissuis).

205 In an effort to identify protective M. avium subsp. paratuberculosis sequences, a genomic DN

206 Recently, M. avium subsp. paratuberculosis isolates recovered from

207 ice were challenged with kanamycin-resistant M. avium 104.

208 channels in the transport of known secreted M. avium proteins, we demonstrated that the porin channe

209 paratuberculosis than are passively shedding M. avium subsp. paratuberculosis.

210 Results showed M. avium subsp. hominissuis to be most common (n = 238,

211 Sequence of six M. avium clones identified one gene involved in glycopep

212 bsequently, we analyzed the virulence of six M. avium subsp. paratuberculosis mutants with inactivati

213 re repeatedly positive for NTMs, the species M. avium, M. mucogenicum, and Mycobacterium abscessus we

214 MAC probe but negative with species-specific M. avium and M. intracellulare probes), and 3 (7%) were

215 In a prospective study, M. avium subspecies paratuberculosis detection in early

216 In summary, M. avium subsp. paratuberculosis interacts with the inte

217 icantly less efficient at dissemination than M. avium subsp. hominissuis.

218 pithelial cells with greater efficiency than M. avium subsp. paratuberculosis exposed to broth medium

219 bspecies do cause human infections, and that M. avium infects mainly postmenopausal women.

220 We therefore conclude that M. avium subsp. hominissuis is the dominant M. avium sub

221 yer's patches, were used to demonstrate that M. avium subsp. paratuberculosis enters the intestinal m

222 cell monolayers, it was also determined that M. avium subsp. paratuberculosis crosses apical and baso

223 We found that M. avium-infected macrophages release exosomes containin

224 We hypothesized that M. avium subsp. paratuberculosis harnesses host response

225 Our data collectively indicate that M. avium subsp. hominissuis biofilm induces TNF-alpha-dr

226 In addition, the results indicated that M. avium subsp. paratuberculosis had equal abilities to

227 We now know that M. avium subsp. paratuberculosis activates the epithelia

228 We show that M. avium subsp. paratuberculosis infection led to phagos

229 In the present study we show that M. avium-infected macrophages release GPLs, which are tr

230 mammary tissue and milk, and we showed that M. avium subsp. paratuberculosis infects bovine mammary

231 or this important receptor, and suggest that M. avium could potentially modify its GPL structure to l

232 A number of studies have suggested that M. avium subsp. paratuberculosis interacts with M cells

233 eotide polymorphisms (SNPs), suggesting that M. avium accumulates mutations at higher rates during pe

234 th cells was highly similar, suggesting that M. avium might have evolved mechanisms that are used to

235 The M. avium subsp. avium isolates showed limited diversity.

236 The M. avium subsp. paratuberculosis isolates could be diffe

237 The M. avium subsp. paratuberculosis isolates were obtained

238 In addition, the M. avium 104 mtfD mutant exhibits decreased ability to s

239 e Mycobacterium tuberculosis complex and the M. avium-M. intracellulare complex, as well as rapid- an

240 this activation is regulated in part by the M. avium fadD2 gene.

241 874 membrane and cytosolic proteins from the M. avium subsp. paratuberculosis proteome.

242 es with 58% of G+C content versus 69% in the M. avium genome.

243 ne was deleted by allelic replacement in the M. avium strain 104.

244 ycobacterium tuberculosis complex (MTC), the M. avium complex (MAC), the M. chelonae-M. abscessus gro

245 These results suggest that members of the M. avium complex have a novel mechanism for activating c

246 mplex infection was identified by use of the M. avium sensitin skin test.

247 None of the M. avium subsp. paratuberculosis isolates had ORFs class

248 glycolipids found in copious amounts on the M. avium cell surface.

249 s of M. avium subsp. paratuberculosis or the M. avium subsp. avium isolate.

250 conserved membrane protein homologue to the M. avium subsp. paratuberculosis MAP2446c gene and four

251 trated a degree of cross-reactivity with the M. avium subsp. avium proteins that was higher than the

252 ling) assay determined that contact with the M. avium subsp. hominissuis biofilm led to early, widesp

253 vestigated whether it is possible that these M. avium subsp. paratuberculosis-infected animals could

254 t L. casei, M. tuberculosis H37Ra, and three M. avium strains and for cytotoxic activity against seve

255 Thus, M. avium subsp. paratuberculosis is an opportunist that

256 itutive expression of these genes confers to M. avium the ability to invade HT-29 intestinal epitheli

257 dney (MDBK) epithelial cells were exposed to M. avium subsp. paratuberculosis.

258 d in the cytoplasm of HEp-2 cells exposed to M. avium, the recombinant protein was shown to be potent

259 Hematological tumors predisposed to M. avium colonization but not infection.

260 50 years of age or older were more prone to M. avium infection than younger women or men of all ages

261 igated macrophage recruitment in response to M. avium subsp. paratuberculosis using a MAC-T bovine ma

262 ata suggest that the macrophage responses to M. avium subsp. paratuberculosis isolates from cattle an

263 is no efficient approach to prevent or treat M. avium subsp. hominissuis infection in the lungs.

264 rs) were culture positive, indicating a true M. avium subsp. paratuberculosis infection.

265 by molecular assays for the presence of two M. avium subsp. paratuberculosis-specific targets.

266 The two M. avium subsp. avium isolates had 210 and 135 divergent

267 ad 210 and 135 divergent ORFs, while the two M. avium subsp. silvaticum isolates examined had 77 and

268 lly detect either M. intracellulare, the two M. avium subspecies associated with human disease, or al

269 in efficiency compared to both the wild-type M. avium and M. avium containing the vector alone.

270 s of three types: the human or porcine type, M. avium subsp. hominissuis; the bird type, including M.

271 m subsp. silvaticum); and the ruminant type, M. avium subsp. paratuberculosis.

272 To understand M. avium interaction with two evolutionarily distinct ho

273 aOH resulted in a greater recovery of viable M. avium subsp. paratuberculosis cells from milk than fr

274 H treatment decreased the recovery of viable M. avium subsp. paratuberculosis cells more than treatme

275 Counts of viable M. avium subsp. paratuberculosis cells ranging from 1 to

276 ery and challenging them with live, virulent M. avium subsp. paratuberculosis.

277 tes from the 448 included patients, 54% were M. avium, 18% were M. intracellulare, and 28% were M. ch

278 d M. intracellulare probes), and 3 (7%) were M. avium; none were M. intracellulare.

279 To investigate whether M. avium needs to attach to the internal surface of the

280 el of experimentally inducible IRIS in which M. avium-infected T cell-deficient mice undergo a fatal

281 ery early stages of infection of calves with M. avium subsp. paratuberculosis.

282 ges infected with M. smegmatis compared with M. avium, we observed enhanced secretion of TNF-alpha, I

283 ges infected with M. smegmatis compared with M. avium.

284 We determined that macrophages infected with M. avium compared to M. smegmatis showed diminished TNF-

285 well as cattle experimentally infected with M. avium subsp. paratuberculosis (n = 3) were used to pr

286 he low-shedding cows are truly infected with M. avium subsp. paratuberculosis than are passively shed

287 re passively shedding or truly infected with M. avium subsp. paratuberculosis.

288 Patients treated for infections with M. avium (AOR, 5.64; 95% CI, 1.51-21.10) and M. chimaera

289 Two hundred twenty-nine patients with M. avium complex lung disease, 55% women and 53% with no

290 lly, only 10 of the 62 (16.2%) patients with M. avium had probable to definite evidence of infection,

291 Of the 238 patients with M. avium subsp. hominissuis, 65 (27.3%) showed evidence

292 y, especially in the elderly population with M. avium complex lung disease.

293 Studies with M. avium have shown that cytoskeletal rearrangement via

294 fection, a level much higher than those with M. avium (P < 0.001).

295 d to characterize the genomic changes within M. avium isolates collected from single patients over ti

296 Invasion by wt M. avium led to the recruitment of neuronal Wiskott-Aldr

297 Supernatant obtained from wt M. avium incubated with HEp2 epithelial cells rescued th

298 and Western blot analysis indicated that wt M. avium subsp. paratuberculosis activates Cdc42 and Rho

299 ted with the Cdc42 of cells infected with wt M. avium subsp. paratuberculosis but not with the deltaO

300 l cells less efficiently than wild-type (wt) M. avium subsp. paratuberculosis.