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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 to detect the presence of antibodies against M. avium subsp. paratuberculosis in host serum.
25  nM against P. carinii DHFR, 0.57 nM against M. avium DHFR, and 55 nM against rat DHFR.
26  IFN-gamma and can confer protection against M. avium infection in immunocompromised mice.
27 irst study to demonstrate protection against M. avium subsp. paratuberculosis infection with expressi
28 wever 13 was no more potent than PTX against M. avium DHFR, and its SI was no better than that of TMP
29  (22), was both potent and selective against M. avium DHFR (IC(50) = 0.47 nM, SI = 1300) but was not
30  During initial colonization of the airways, M. avium subsp. hominissuis forms microaggregates compos
31 sp. avium serotype 1 and serotype 2, 3 (also M. avium subsp. silvaticum); and the ruminant type, M. a
32                                     Although M. avium is known for its genetic plasticity, these obse
33  identify large sequence polymorphisms among M. avium subspecies obtained from a variety of host anim
34                         Total lipids from an M. avium subsp. paratuberculosis (Map) ovine strain (S-t
35                           We interrogated an M. avium subsp. paratuberculosis DeltasigL mutant agains
36                  Through the screening of an M. avium genomic library in Mycobacterium smegmatis, we
37 led the global gene expression pattern of an M. avium subsp. avium isolate, and they significantly up
38                          We have utilized an M. avium subsp. paratuberculosis whole-genome microarray
39                      To determine whether an M. avium subsp. paratuberculosis protein delivered to th
40  compared to both the wild-type M. avium and M. avium containing the vector alone.
41 I values of >100 against both P. carinii and M. avium DHFR relative to rat DHFR.
42  the most potent against P. carinii DHFR and M. avium DHFR was the 2'-(5-carboxy-1-butynyl)dibenz[b,f
43 o no seroreactivity against M. kansasii- and M. avium subsp. paratuberculosis-infected animals.
44 f Mycobacterium tuberculosis, M. leprae, and M. avium complex infections.
45 obacterium avium subsp. paratuberculosis and M. avium subsp. avium, respectively.
46 s of M. avium sub0:36 PMparatuberculosis and M. avium sub0:36 PMavium, as well as DNA from M. fortuit
47 lonized the six SDSs, but L. pneumophila and M. avium were not detected.
48 ., M. intracellulare, Acanthamoeba spp., and M. avium peaked during the dry season.
49 acrophages infected with M. tuberculosis and M. avium or with avirulent M. smegmatis.
50  cells (which have been shown to induce anti-M. avium subsp. hominissuis activity when added to THP-1
51 , patients whose isolates were identified as M. avium (adjusted odds ratio [AOR], 2.14; 95% confidenc
52 sferase recognition in the tissue-associated M. avium subsp. paratuberculosis isolates.
53                         Mycobacterium avium (M. avium) subspecies vary widely in both pathogenicity a
54 ii (T. gondii, tg), and Mycobacterium avium (M. avium, ma) are the principal causes of morbidity and
55                                      Because M. avium subsp. paratuberculosis can be delivered to the
56 fied to the species level by MycoID as being M. avium (n = 98; 61.1%), M. intracellulare (n = 57; 35.
57 he concentration of several elements between M. avium and M. tuberculosis vacuoles were also observed
58 ative levels of protein expression from both M. avium subsp. paratuberculosis strains were measured b
59  pneumophila from recolonizing biofilms, but M. avium gene numbers increased by 0.14-0.76 logs in the
60 en and mesenteric lymph node colonization by M. avium subsp. paratuberculosis.
61 munization with a novel PE gene expressed by M. avium (MaPE) showed that a dominant T-cell immune res
62 iking of a negative fecal sample followed by M. avium sub0:36 PMparatuberculosis DNA extraction resul
63 be most common (n = 238, 92.6%), followed by M. avium subsp. avium serotype 1 (n = 12, 4.7%) and sero
64 nderlying thymic atrophy during infection by M. avium with the participation of locally produced NO,
65     The invasion of the intestinal mucosa by M. avium subsp. paratuberculosis and Mycobacterium avium
66 vention of the cell communication pathway by M. avium subsp. paratuberculosis, which loosens the inte
67 acterizes a pathogenic mechanism utilized by M. avium subsp. hominissuis to bind and invade the host
68                        Once inside the cell, M. avium subsp. paratuberculosis is known to survive har
69                               In comparison, M. avium was recovered from 141 water/biofilm samples.
70 88 suggesting that released exosomes contain M. avium-expressed TLR ligands.
71  M. avium subsp. hominissuis is the dominant M. avium subspecies clinically, that the two bird-type s
72 l a novel signaling pathway activated during M. avium subsp. paratuberculosis entry that links the pr
73 ng-term repopulating HSCs proliferate during M. avium infection, and that this response requires inte
74 n in murine macrophages infected with either M. avium or M. smegmatis.
75 ttle (n = 3) and cattle infected with either M. avium subsp. avium and Mycobacterium bovis were expos
76 clear phagocytes cocultured with established M. avium subsp. hominissuis biofilm and surveyed various
77                         For this evaluation, M. avium subsp. paratuberculosis subtyping was based on
78 ation scheme (tissue-associated versus fecal M. avium subsp. paratuberculosis isolates).
79 d from the environment, but risk factors for M. avium complex infection and disease are poorly unders
80 sting that MBP-1 expression is important for M. avium subsp. hominissuis adherence to the host cell.
81  H (sigH) that was shown to be important for M. avium subsp. paratuberculosis survival inside gamma i
82  intestinal mucosa is important in order for M. avium subsp. paratuberculosis to establish infection.
83 esults indicate that soil is a reservoir for M. avium complex associated with human infection and tha
84 ergoing standard macrolide-based therapy for M. avium complex lung disease were monitored at standard
85                     The region is unique for M. avium and is not present in M. tuberculosis or M. par
86 ile very similar to yet distinguishable from M. avium subsp. avium.
87 d MAC mycobacteria can be distinguished from M. avium subsp. paratuberculosis by multiple clusters of
88 e was competitively hybridized with DNA from M. avium subsp. paratuberculosis K10, and open reading f
89        Interestingly, exosomes isolated from M. avium-infected but not from uninfected macrophages ca
90 study we isolated different GPL species from M. avium, and using mass spectrometry and NMR analyses,
91 on, and a large number of AIDS patients have M. avium in their intestinal tracts.
92 neous colitis displayed significantly higher M. avium subsp. paratuberculosis-specific immunoglobulin
93                     The reasoning behind how M. avium subsp. hominissuis biofilm is allowed to establ
94                                  To identify M. avium genes and host cell pathways involved in the ba
95                                  To identify M. avium subsp. paratuberculosis genes associated with t
96                          Genome diversity in M. avium subspecies appears to be mediated by large sequ
97 better decipher the role of sigma factors in M. avium subsp. paratuberculosis pathogenesis, we target
98 Together our data support a role for GPLs in M. avium pathogenesis.
99  associated with the HLA-DRalpha promoter in M. avium-infected THP-1 cells stimulated with IFN-gamma.
100 iological significance of such regulators in M. avium subsp. paratuberculosis rremains elusive.
101  Interestingly, the loss of mtfD resulted in M. avium 104 containing only the non-serotype specific G
102  suggest that GPLs play an important role in M. avium pathogenesis.
103 rental strain, suggesting a role for sigH in M. avium subsp. paratuberculosis virulence.
104 ies suggested a substantial role for sigL in M. avium subsp. paratuberculosis virulence, as indicated
105 for the control of inflammatory signaling in M. avium-infected human primary macrophages.
106 cidity, and oxidative stress were similar in M. avium subsp. paratuberculosis and Mycobacterium tuber
107 e sequence polymorphisms present uniquely in M. avium subsp. paratuberculosis.
108 a 16S rRNA gene A1408G mutation and included M. avium, Mycobacterium intracellulare, and Mycobacteriu
109 subsp. hominissuis; the bird type, including M. avium subsp. avium serotype 1 and serotype 2, 3 (also
110 ected Rag2(-/-)gammac(-/-) animals increased M. avium growth in the liver.
111  siRNA-mediated knockdown of Keap1 increased M. avium-induced expression of inflammatory cytokines an
112 cked down for MR expression showed increased M. avium phagosome-lysosome fusion relative to control c
113   Upon translocation, dendritic cells ingest M. avium subsp. paratuberculosis, but this process does
114   MBP-1 immune serum significantly inhibited M. avium subsp. hominissuis infection throughout the res
115 avium-M. intracellulare complex strains into M. avium and M. intracellulare may provide a tool to bet
116         Microarray analysis of intracellular M. avium subsp. paratuberculosis RNA indicates the incre
117 l isolates with the sequenced bovine isolate M. avium subsp. paratuberculosis (MAP) K-10.
118 o included were previously reported or known M. avium subsp. paratuberculosis antigens to serve as a
119 ould be facilitated growth of pathogens like M. avium inside macrophages.
120 noculated with 10(2) to 10(8) CFU/ml of live M. avium subsp. paratuberculosis organisms.
121       Monitoring cellular markers, only live M. avium subsp. paratuberculosis bacilli were able to pr
122 r the vehicle containing heat-killed or live M. avium subsp. paratuberculosis.
123 M. intracellulare (n = 57; 35.8%), and mixed M. avium and M. intracellulare (n = 2; 1.3%).
124 oculation of a wild-type strain and a mutant M. avium subsp. paratuberculosis strain (with an inactiv
125 e 333 participants with positive or negative M. avium sensitin skin tests, age-adjusted independent p
126                    To examine the ability of M. avium subsp. paratuberculosis to infect bovine epithe
127  in a significant reduction in the amount of M. avium subsp. paratuberculosis recovered from mouse ti
128 ons, we performed a global scale analysis of M. avium subsp. paratuberculosis isolates that were repr
129 tification of previously unknown antigens of M. avium subsp. paratuberculosis.
130                      Shedding levels (CFU of M. avium subsp. paratuberculosis/g of feces) for the ani
131 ch is that it enables a direct comparison of M. avium subsp. paratuberculosis proteins to each other
132 nels (VDAC) were identified as components of M. avium vacuoles in macrophages.
133 (-/-) knockout mice to low concentrations of M. avium strain 101 given orally, followed by treatment
134 otocols to ensure that low concentrations of M. avium subsp. paratuberculosis can be detected.
135 ans or siRNA lead to significant decrease of M. avium survival.
136 or months following intestinal deposition of M. avium subsp. paratuberculosis despite a lack of fecal
137 onstrated a sensitivity for the detection of M. avium sub0:36 PMparatuberculosis DNA by use of the IS
138 ployed for the systematic differentiation of M. avium subsp. paratuberculosis strains to understand t
139 apoptosis but did not lead to elimination of M. avium subsp. hominissuis.
140 e for studying the molecular epidemiology of M. avium subsp. paratuberculosis.
141 e been infected by environmental exposure of M. avium subsp. paratuberculosis.
142 observed that the constitutive expression of M. avium proteins has a modest impact on the ability to
143           Therefore, the sequenced genome of M. avium strain 104 has been associated with disease in
144 ted consistency among infecting genotypes of M. avium subsp. paratuberculosis isolated from diverse h
145 cells) in response to different genotypes of M. avium subsp. paratuberculosis isolates recovered from
146 data analysis revealed unique gene groups of M. avium subsp. paratuberculosis that were regulated und
147 ributed to decreased intracellular growth of M. avium in primary human macrophages that was reconstit
148 ture media determined differential growth of M. avium subsp. paratuberculosis strains and that this s
149 s and lead to a discrepancy in the growth of M. avium subsp. paratuberculosis strains.
150                                    Growth of M. avium subsp. paratuberculosis within MAC-T cells also
151 rRNA gene target for rapid identification of M. avium complex (MAC) and a region of the heat shock pr
152  of sigL in the pathogenesis and immunity of M. avium subsp. paratuberculosis infection, a potential
153 re is growing evidence that the incidence of M. avium and related nontuberculous species is increasin
154 k, it was investigated whether incubation of M. avium subsp. paratuberculosis with milk has an effect
155 did not affect the isolation or infection of M. avium.
156 ed by reinfection with a separate isolate of M. avium.
157 by PCR of the DNA extracted from isolates of M. avium sub0:36 PMparatuberculosis and M. avium sub0:36
158  THP-1 cells infected with sheep isolates of M. avium subsp. paratuberculosis or the M. avium subsp.
159             The cattle and human isolates of M. avium subsp. paratuberculosis, regardless of their sh
160      Subspecies and host adapted isolates of M. avium were distinguishable by the presence or absence
161  of the three evaluated for the isolation of M. avium subsp. paratuberculosis from milk, as it achiev
162 e an optimized protocol for the isolation of M. avium subsp. paratuberculosis in milk.
163                           Several mutants of M. avium subsp. paratuberculosis were identified which i
164 um smegmatis, we have identified a number of M. avium genes that are associated with increased invasi
165            The ingestion of small numbers of M. avium cells induces a protective immune response in t
166 ove our understanding of the pathogenesis of M. avium subsp. paratuberculosis.
167 ests, age-adjusted independent predictors of M. avium complex infection in a multivariate model inclu
168 rom Ohio farms were assessed for presence of M. avium subsp. paratuberculosis using four different pr
169 xt steps to further elucidate the process of M. avium subsp. paratuberculosis invasion.
170 haracterizing the gene expression profile of M. avium subsp. paratuberculosis exposed to different st
171 characterize the surface-exposed proteome of M. avium subsp. hominissuis.
172                      fadD2 is a regulator of M. avium invasion, and its effect is through Cdc42.
173       In this report, the stress response of M. avium subsp. paratuberculosis on a genome-wide level
174 associated with transcriptional responses of M. avium subsp. paratuberculosis during macrophage infec
175                               The results of M. avium subsp. paratuberculosis strain typing and obser
176 onged soil exposure are at increased risk of M. avium complex infection.
177 n of Cdc42 probably follows the secretion of M. avium proteins.
178  (n=597), suggesting the high sensitivity of M. avium subsp. paratuberculosis to acidic environments.
179  the wild-type strain and a mutant strain of M. avium subsp. paratuberculosis deficient in tissue col
180 d infection with a highly virulent strain of M. avium, but not with a low-virulence strain, led to a
181  technique, we found 15 different strains of M. avium subsp. paratuberculosis from a total of 142 iso
182                  To our surprise, strains of M. avium subsp. paratuberculosis were able to traverse t
183                                No strains of M. avium subsp. paratuberculosis were found.
184  stages of infection by different strains of M. avium subsp. paratuberculosis, a first step in unders
185 nd cytosol were prepared from two strains of M. avium subsp. paratuberculosis, i.e., laboratory-adapt
186 proteins exposed at the bacterial surface of M. avium subsp. hominissuis.
187 mon of which was nearly identical to that of M. avium strains.
188  of HDAC activity, were added at the time of M. avium or M. tuberculosis infection or TLR2 stimulatio
189 ohne's disease, allowing the transmission of M. avium subsp. paratuberculosis between animals.
190                         The understanding of M. avium pathogenesis has been hampered by the inability
191 ile facilitates an improved understanding of M. avium subsp. hominissuis and how it establishes infec
192 ols for developing a better understanding of M. avium subsp. paratuberculosis infection in the host a
193              To improve our understanding of M. avium subsp. paratuberculosis pathogenesis, we examin
194  0.5 to 2.0% did not affect the viability of M. avium subsp. paratuberculosis.
195 ce time-to-diagnosis (from 16 to 8 weeks) of M. avium subsp. paratuberculosis infection and can also
196 t in natural infection but are modified once M. avium subsp. paratuberculosis is adapted to laborator
197                                         Only M. avium sub0:36 PMparatuberculosis DNA was detectable a
198 Sera from noninfected, M. bovis-infected, or M. avium subsp. paratuberculosis-infected (by natural an
199  (L5P), yet both lipids are present in other M. avium subspecies.
200             Isolates of non-paratuberculosis M. avium from 207 other patients in Southern California
201 h is not seen until much later in planktonic M. avium subsp. hominissuis infection.
202 dded to THP-1 cells infected with planktonic M. avium subsp. hominissuis).
203          In an effort to identify protective M. avium subsp. paratuberculosis sequences, a genomic DN
204                                    Recently, M. avium subsp. paratuberculosis isolates recovered from
205 ice were challenged with kanamycin-resistant M. avium 104.
206  channels in the transport of known secreted M. avium proteins, we demonstrated that the porin channe
207 paratuberculosis than are passively shedding M. avium subsp. paratuberculosis.
208                               Results showed M. avium subsp. hominissuis to be most common (n = 238,
209                              Sequence of six M. avium clones identified one gene involved in glycopep
210 bsequently, we analyzed the virulence of six M. avium subsp. paratuberculosis mutants with inactivati
211 re repeatedly positive for NTMs, the species M. avium, M. mucogenicum, and Mycobacterium abscessus we
212 MAC probe but negative with species-specific M. avium and M. intracellulare probes), and 3 (7%) were
213                      In a prospective study, M. avium subspecies paratuberculosis detection in early
214                                  In summary, M. avium subsp. paratuberculosis interacts with the inte
215 icantly less efficient at dissemination than M. avium subsp. hominissuis.
216 pithelial cells with greater efficiency than M. avium subsp. paratuberculosis exposed to broth medium
217 bspecies do cause human infections, and that M. avium infects mainly postmenopausal women.
218                   We therefore conclude that M. avium subsp. hominissuis is the dominant M. avium sub
219 yer's patches, were used to demonstrate that M. avium subsp. paratuberculosis enters the intestinal m
220 cell monolayers, it was also determined that M. avium subsp. paratuberculosis crosses apical and baso
221                                We found that M. avium-infected macrophages release exosomes containin
222                         We hypothesized that M. avium subsp. paratuberculosis harnesses host response
223          Our data collectively indicate that M. avium subsp. hominissuis biofilm induces TNF-alpha-dr
224      In addition, the results indicated that M. avium subsp. paratuberculosis had equal abilities to
225                             We now know that M. avium subsp. paratuberculosis activates the epithelia
226                                 We show that M. avium subsp. paratuberculosis infection led to phagos
227            In the present study we show that M. avium-infected macrophages release GPLs, which are tr
228  mammary tissue and milk, and we showed that M. avium subsp. paratuberculosis infects bovine mammary
229 or this important receptor, and suggest that M. avium could potentially modify its GPL structure to l
230      A number of studies have suggested that M. avium subsp. paratuberculosis interacts with M cells
231 th cells was highly similar, suggesting that M. avium might have evolved mechanisms that are used to
232                                          The M. avium subsp. avium isolates showed limited diversity.
233                                          The M. avium subsp. paratuberculosis isolates could be diffe
234                                          The M. avium subsp. paratuberculosis isolates were obtained
235                             In addition, the M. avium 104 mtfD mutant exhibits decreased ability to s
236 e Mycobacterium tuberculosis complex and the M. avium-M. intracellulare complex, as well as rapid- an
237  this activation is regulated in part by the M. avium fadD2 gene.
238 874 membrane and cytosolic proteins from the M. avium subsp. paratuberculosis proteome.
239 es with 58% of G+C content versus 69% in the M. avium genome.
240 ne was deleted by allelic replacement in the M. avium strain 104.
241 ycobacterium tuberculosis complex (MTC), the M. avium complex (MAC), the M. chelonae-M. abscessus gro
242    These results suggest that members of the M. avium complex have a novel mechanism for activating c
243 mplex infection was identified by use of the M. avium sensitin skin test.
244                                  None of the M. avium subsp. paratuberculosis isolates had ORFs class
245  glycolipids found in copious amounts on the M. avium cell surface.
246 s of M. avium subsp. paratuberculosis or the M. avium subsp. avium isolate.
247  were identified as mycobacteria outside the M. avium-M. intracellulare complex.
248  conserved membrane protein homologue to the M. avium subsp. paratuberculosis MAP2446c gene and four
249 osis, 15 were identified as belonging to the M. avium-M. intracellulare complex (but not M. paratuber
250 trated a degree of cross-reactivity with the M. avium subsp. avium proteins that was higher than the
251 ling) assay determined that contact with the M. avium subsp. hominissuis biofilm led to early, widesp
252 vestigated whether it is possible that these M. avium subsp. paratuberculosis-infected animals could
253 t L. casei, M. tuberculosis H37Ra, and three M. avium strains and for cytotoxic activity against seve
254                                        Thus, M. avium subsp. paratuberculosis is an opportunist that
255 itutive expression of these genes confers to M. avium the ability to invade HT-29 intestinal epitheli
256 dney (MDBK) epithelial cells were exposed to M. avium subsp. paratuberculosis.
257 d in the cytoplasm of HEp-2 cells exposed to M. avium, the recombinant protein was shown to be potent
258          Hematological tumors predisposed to M. avium colonization but not infection.
259  50 years of age or older were more prone to M. avium infection than younger women or men of all ages
260 igated macrophage recruitment in response to M. avium subsp. paratuberculosis using a MAC-T bovine ma
261 ata suggest that the macrophage responses to M. avium subsp. paratuberculosis isolates from cattle an
262 is no efficient approach to prevent or treat M. avium subsp. hominissuis infection in the lungs.
263 rs) were culture positive, indicating a true M. avium subsp. paratuberculosis infection.
264  by molecular assays for the presence of two M. avium subsp. paratuberculosis-specific targets.
265                                      The two M. avium subsp. avium isolates had 210 and 135 divergent
266 ad 210 and 135 divergent ORFs, while the two M. avium subsp. silvaticum isolates examined had 77 and
267 lly detect either M. intracellulare, the two M. avium subspecies associated with human disease, or al
268 in efficiency compared to both the wild-type M. avium and M. avium containing the vector alone.
269 s of three types: the human or porcine type, M. avium subsp. hominissuis; the bird type, including M.
270 m subsp. silvaticum); and the ruminant type, M. avium subsp. paratuberculosis.
271                                To understand M. avium interaction with two evolutionarily distinct ho
272 aOH resulted in a greater recovery of viable M. avium subsp. paratuberculosis cells from milk than fr
273 H treatment decreased the recovery of viable M. avium subsp. paratuberculosis cells more than treatme
274                             Counts of viable M. avium subsp. paratuberculosis cells ranging from 1 to
275 ery and challenging them with live, virulent M. avium subsp. paratuberculosis.
276 tes from the 448 included patients, 54% were M. avium, 18% were M. intracellulare, and 28% were M. ch
277 d M. intracellulare probes), and 3 (7%) were M. avium; none were M. intracellulare.
278                       To investigate whether M. avium needs to attach to the internal surface of the
279 el of experimentally inducible IRIS in which M. avium-infected T cell-deficient mice undergo a fatal
280 ery early stages of infection of calves with M. avium subsp. paratuberculosis.
281 ges infected with M. smegmatis compared with M. avium, we observed enhanced secretion of TNF-alpha, I
282 ges infected with M. smegmatis compared with M. avium.
283 We determined that macrophages infected with M. avium compared to M. smegmatis showed diminished TNF-
284  well as cattle experimentally infected with M. avium subsp. paratuberculosis (n = 3) were used to pr
285 he low-shedding cows are truly infected with M. avium subsp. paratuberculosis than are passively shed
286 re passively shedding or truly infected with M. avium subsp. paratuberculosis.
287   The inability of macrophages infected with M. avium to sustain MAPK activation and to produce high
288         Patients treated for infections with M. avium (AOR, 5.64; 95% CI, 1.51-21.10) and M. chimaera
289  immunocompetent mice challenged orally with M. avium can develop protection against the infection, a
290        Two hundred twenty-nine patients with M. avium complex lung disease, 55% women and 53% with no
291 lly, only 10 of the 62 (16.2%) patients with M. avium had probable to definite evidence of infection,
292                     Of the 238 patients with M. avium subsp. hominissuis, 65 (27.3%) showed evidence
293 y, especially in the elderly population with M. avium complex lung disease.
294                                 Studies with M. avium have shown that cytoskeletal rearrangement via
295 fection, a level much higher than those with M. avium (P < 0.001).
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.

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