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1 M. leprae DNA can be detected in soil near human and ani
2 M. leprae DNA was identified in 16.0% of soil from house
3 M. leprae infection success was also dependent of the gl
4 M. leprae invasion of Schwann cells leads to the neurolo
5 M. leprae recovered from recipient mice fed control diet
6 M. leprae recovered from target Mphi incubated with norm
7 M. leprae recovered from target Mphi possessed high meta
8 M. leprae retained 56% viability in Schwann cells for 3
9 M. leprae sigE was found to be capable of complementing
10 M. leprae was detected in crude cell lysates of skin bio
11 M. leprae-mediated OASL expression was dependent on cyto
12 M. leprae-sonicate-induced IFN-gamma was similar for all
13 The HD-DDS-ML assay detected as few as 100 M. leprae organisms present in homogenates of human skin
15 erent VNTR loci and examined a battery of 12 M. leprae strains derived from patients in different reg
16 detection for the RLEP and RLPM assays is 30 M. leprae per specimen (0.76 bacilli per reaction; coeff
17 detection for the RLEP and RLPM assays is 30 M. leprae per specimen (0.76 bacilli per reaction; CV%:
19 nase inhibitor PKI-166 effectively abrogates M. leprae-induced myelin damage in in vitro and in vivo
28 berculosis, induces cross-protection against M. leprae that is comparable or potentially superior to
30 assay relies on the PCR amplification of an M. leprae-specific 231-bp fragment of folP1 containing c
31 ll as against intracellular M. abscessus and M. leprae, indicating their potential as the basis for a
35 sults thus indicate that M. lepromatosis and M. leprae diverged approximately 10 million years ago.
36 ibed above indicate that M. lepromatosis and M. leprae diverged from a common ancestor after the mass
37 ncestor (MRCA), and both M. lepromatosis and M. leprae have since accumulated new pseudogenes or acqu
38 nt of these genes placed M. lepromatosis and M. leprae in a tight cluster with long terminal branches
41 els from England, Ireland, and Scotland, and M. leprae in squirrels from Brownsea Island, England.
43 rative genomic analysis of these strains and M. leprae strains from Asia and Brazil identified 51 sin
47 heat shock chaperone, of M. tuberculosis and M. leprae, while that of Ndk shows significant identity
50 d for miRNAs, including acting on apoptosis, M. leprae recognition and engulfment, Schwann cell (SC)
53 al nerve may involve adhesion events between M. leprae (or M. leprae-parasitized macrophages) and the
57 e determined cytokines/chemokines induced by M. leprae proteins in blood of leprosy patients and ende
58 axonal damage are not directly initiated by M. leprae but by infected macrophages that patrol axons;
59 kin-10 (IL-10), were induced in monocytes by M. leprae in vitro and preferentially expressed in disse
61 ta suggest that T cell activation in situ by M. leprae in tuberculoid leprosy leads to local up-regul
62 ed by real-time PCR after the stimulation by M. leprae antigens in the PBMC (peripheral blood mononuc
64 differential PCR revealed that 221 contained M. leprae whereas only six, all from Mexico, harbored M.
65 atosis; 2 LL and 2 Lucio reactions contained M. leprae; and 1 LL reaction contained both species.
67 ith SNP type 3I-1, ancestral to contemporary M. leprae isolates found in southern states of America a
70 e possess compensatory mechanisms to control M. leprae growth and feature elements resembling mid-bor
71 gh in itself a weak stimulator of cytokines, M. leprae primed the cells for increased production of t
72 Based on these mutations, a heteroduplex DDS M. leprae (HD-DDS-ML) assay was developed for the simult
73 ermine their suitability for differentiating M. leprae, we developed PCR systems to amplify 5 differe
74 claimed that their macrophages cannot digest M. leprae in vitro; such a defect could explain both lep
77 over a promycobacterial role for OASL during M. leprae infection that directs the host immune respons
78 understanding of the immune response during M. leprae infection and the identification or testing of
79 ouse T-cell hybridomas raised against either M. leprae or M. tuberculosis CFP-10 displayed a cross-re
81 may greatly increase the risk of endoneurial M. leprae bacteremia, and also enhance the risk of ische
83 amino acid mismatches between the equivalent M. leprae and M. tuberculosis sequences; of these, eight
88 titative polymerase chain reaction assay for M. leprae, were validated as clinical diagnostic assays
91 matosis, 19 of 47 (40.43%) were positive for M. leprae, and 2 of 47 (4.26%) contained both organisms.
94 , and our previously developed RLEP qPCR for M. leprae, were validated as clinical diagnostic assays
95 Armadillos are a large natural reservoir for M. leprae, and leprosy may be a zoonosis in the region.
97 A systematic, population-based search for M. leprae resistance in suspected leprosy relapse cases
101 S values were 14 to 28% of the dS values for M. leprae and Mycobacterium tuberculosis, a more diverge
102 genates from eight leprosy patients and from M. leprae-infected mouse or armadillo tissues infected w
103 use the reductase portion of the enzyme from M. leprae shows significant primary structure similarity
104 ide further fine structural data on LAM from M. leprae (LepLAM) and a tuberculosis clinical isolate,
105 cterium leprae infection, which results from M. leprae invasion of the Schwann cell of the peripheral
107 v (RvLAM), LepLAM derived from in vivo grown M. leprae is apparently simpler in its arabinan architec
112 ced Stat4 phosphorylation and DNA binding in M. leprae-activated T cells from tuberculoid but not fro
113 e concluded that the massive genome decay in M. leprae does not markedly affect the peptidoglycan bio
117 genes analyzed that were also pseudogenes in M. leprae showed nearly neutral evolution, and their rel
118 n with 10 variable-number tandem repeats, in M. leprae strains obtained from 33 wild armadillos from
121 identical, or almost identical, sequences in M. leprae and M. tuberculosis and would not be suitable
122 tion and was also shown to be upregulated in M. leprae-infected human macrophage cell lineages, prima
123 in other pathogenic mycobacteria, including M. leprae and M. bovis, suggesting that a core of basic
125 The crystal structures of the inhibited M. leprae and M. tuberculosis InhA complexes provide the
126 humanized ErbB2-specific antibody, inhibits M. leprae binding to and activation of ErbB2 and Erk1/2
127 ence and immunoelectron microscopy on intact M. leprae with mAbs against recombinant (r) ML-LBP21 rev
130 of leprosy, we identified that intracellular M. leprae activated Erk1/2 directly by lymphoid cell kin
131 ion-based systematic approach to investigate M. leprae resistance in a unique population revealed an
132 acrophages infected with live and irradiated M. leprae, as a function of multiplicity of infection un
134 erodimers mediated cell activation by killed M. leprae, indicating the presence of triacylated lipopr
135 iffer in their ability to digest heat-killed M. leprae in vitro, or in their ability to sustain the v
136 ligate intracellular bacterial pathogen like M. leprae subverts nervous system signaling to propagate
138 cells, murine macrophages infected with live M. leprae demonstrated little, if any, apoptosis, even w
140 t a subset of the presumptively mannosylated M. leprae glycoproteins act as ligands for langerin and
142 ularly ML2478, as biomarker tools to measure M. leprae exposure using IFN-gamma or IFN-inducible prot
145 rin antibody attenuated rLN-alpha2G-mediated M. leprae adherence, suggesting that M. leprae interacts
149 s viruses and for the virulent mycobacterium M. leprae, may be a novel mechanism that this pathogen u
152 results suggest that the reduced ability of M. leprae to survive at elevated temperatures results fr
157 uctures of the AG were also found; the AG of M. leprae is smaller than that of M. tuberculosis, altho
158 dia has historically impaired assessments of M. leprae resistance, a parameter only recently detectab
159 ector Mphi was necessary for augmentation of M. leprae metabolism by normal effector Mphi as well as
160 d a long-term line, have a higher binding of M. leprae compared to CD209-negative Schwann cells.
161 e is attributable to the specific binding of M. leprae to the laminin-alpha2 (LN-alpha2) chain on Sch
162 n configuration of the peptide side chain of M. leprae did not affect recognition by NOD2 or cytokine
163 The un-cross-linked peptide side chains of M. leprae consist of tetra- and tripeptides, some of whi
164 , MLVA was applied to a global collection of M. leprae isolates derived from leprosy patients and pro
165 ponses accompanied by an apparent deficit of M. leprae-specific antibodies to strong humoral response
166 IFN-gamma could indicate distinct degrees of M. leprae exposure, and thereby the risk of infection an
167 a new tool for the simultaneous detection of M. leprae and of its susceptibility to DDS from a single
169 d diagnostic test for the early detection of M. leprae infection and epidemiological surveys of the i
173 have begun to elucidate the early events of M. leprae infection of Schwann cells on a molecular leve
175 ranuloma Mphi harvested from the footpads of M. leprae-infected athymic nu/nu mice, were cocultured w
176 d the glycosylation of a recombinant form of M. leprae SodC (rSodC) produced in Mycobacterium smegmat
178 sults demonstrate that the RuvA homologue of M. leprae is a functional branch-migration subunit.Where
179 cimens we corroborated the identification of M. leprae with detection of mycolic acids specific to th
183 Since the genome sequence of an isolate of M. leprae has become available, multiple-locus variable-
184 s greater discrimination between isolates of M. leprae and enhances the potential of this technique t
185 Two genetic loci in several isolates of M. leprae have previously been demonstrated to contain v
186 21, and 27 bp from four clinical isolates of M. leprae propagated in armadillo hosts were screened by
187 (UDP-N-acetyl-muramate:L-alanine ligase) of M. leprae showed K(m) and V(max) for L-alanine and glyci
188 , specific mechanisms in the localization of M. leprae to peripheral nerve may involve adhesion event
190 cobacterial species, whereas the majority of M. leprae-reactive MHC-restricted T cells were species s
193 digan et al. (2017) use a zebrafish model of M. leprae infection to show that infected macrophages pa
198 d M. smegmatis, the muramic acid residues of M. leprae peptidoglycan are exclusively N acetylated.
200 Immunohistochemical staining of sections of M. leprae-infected nude mouse footpads resulted in stron
203 ent study, we have analyzed the structure of M. leprae peptidoglycan in detail by combined liquid chr
204 e exceedingly passive obligate life style of M. leprae with a degraded genome and host cell dependenc
206 d based on humoral reactivity to a subset of M. leprae protein antigens produced in recombinant form.
207 ling is identified as a downstream target of M. leprae-induced ErbB2 activation that mediates demyeli
208 ptor alpha-dystroglycan as neural targets of M. leprae has not only opened up a new area of scientifi
209 their relative ages were similar to those of M. leprae pseudogenes, suggesting that they were pseudog
212 d to allow monitoring of the transmission of M. leprae in different countries where leprosy is endemi
213 sue macrophages and to mediate the uptake of M. leprae, was present on Schwann cells, colocalizing wi
214 in their ability to sustain the viability of M. leprae in tissue culture; that monocytes, macrophages
215 anuloma may markedly affect the viability of M. leprae residing in Mphi in the lepromatous lesion.
216 n was associated with decreased viability of M. leprae that was concomitant with upregulation of eith
218 lly, it was determined that the cell wall of M. leprae contained significantly more mycolic acids att
220 nvolve adhesion events between M. leprae (or M. leprae-parasitized macrophages) and the endothelial c
221 ion of mice with purified M. tuberculosis or M. leprae antigen 85B also induced protection against M.
222 ated to other clinically relevant organisms: M. leprae, P. aeruginosa and S. aureus, despite weak seq
224 quisition and uptake mechanism in pathogenic M. leprae, as the siderophores from this organism are ve
225 n efficiently transport iron into pathogenic M. leprae, which is responsible for leprosy, in addition
227 aised in mice or rabbits against recombinant M. leprae and M. tuberculosis CFP-10 proteins reacted on
230 withstanding these discriminatory responses, M. leprae proteins did not distinguish patients from EC
231 Importantly, and in contrast to subcutaneous M. leprae footpad infection, systemic M. leprae-specific
232 aneous M. leprae footpad infection, systemic M. leprae-specific gamma interferon and antibody respons
233 indicate that M. lepromatosis is closer than M. leprae to the MRCA, and a Bayesian dating analysis su
234 d from 14 species of mycobacteria other than M. leprae and four bacterial species known to colonize h
235 stinctive properties among the hsp, and that M. leprae hsp may have a potential therapeutic role in t
241 additional cytokines/chemokines showed that M. leprae and ML2478 induced significantly higher concen
243 Taken together, our results suggest that M. leprae plays an active role to control the release of
245 ning in extracellular areas, suggesting that M. leprae CFP-10, like its homologue in M. tuberculosis,
246 ediated M. leprae adherence, suggesting that M. leprae interacts with cells by binding to beta4 integ
249 ant fragments of LN-alpha2 (rLN-alpha2), the M. leprae-binding site was localized to the G domain.
252 ides were synthesized based on data from the M. leprae genome, each peptide containing three or more
253 ns as a probe, a major 28-kDa protein in the M. leprae cell wall fraction that binds alpha2 laminins
255 superoxide dismutase C (SodC) protein of the M. leprae cell wall was identified as a langerin-reactiv
257 ion resulting from direct interaction of the M. leprae-specific phenolic glycolipid 1 (PGL-1) with my
260 ncestor around 27,000 years ago, whereas the M. leprae strain is closest to one that circulated in Me
261 eotide 3'-phosphodiesterase), along with the M. leprae antigen PGL-1 in the peripheral nerve biopsy s
266 cells and subsequent Schwann cell binding to M. leprae, whereas Th1 cytokines did not induce CD209 ex
268 ers of adaptive immune responses, exposed to M. leprae, Mycobacterium tuberculosis (Mtb), and Mycobac
269 ich could be used to distinguish exposure to M. leprae from exposure to Mycobacterium tuberculosis or
273 rrelated directly with effective immunity to M. leprae, as assessed by the clinical course of infecti
274 licate the response of innate macrophages to M. leprae PGL-1 in initiating nerve damage in leprosy.
275 Myelinated Schwann cells were resistant to M. leprae invasion but undergo demyelination upon bacter
279 In mice, TNF-alpha production in response to M. leprae was essentially absent in TLR2-deficient macro
281 enic mycobacteria including M. tuberculosis, M. leprae, and M. avium but not by nonpathogenic mycobac
284 espite the general assumption that untreated M. leprae infected humans represent the major source of
285 hwann cells and macrophages bind and take up M. leprae, contributing to the pathogenesis of leprosy.
292 read to growth-permissive macrophages, while M. leprae PGL-1 induces macrophages to cause nerve demye
293 CD3-CD56+ (NK) subset, rIL-15 combined with M. leprae induced the expansion of CD3+CD56+ T cells.
294 nized mice were experimentally infected with M. leprae, both cellular infiltration into the local lym
295 n monocyte-derived macrophages infected with M. leprae, entered the infected cell, colocalized with t
296 se, finding that infection of monocytes with M. leprae induces IL-32 and DC differentiation in a NOD2
297 imulation of TOLLIP-deficient monocytes with M. leprae produced significantly less IL-1Ra (P < .001),
298 he level of matching of these sequences with M. leprae sequences was 90.9%, which substantiated the s
299 CE (caspase-1), in monocytes stimulated with M. leprae compared with Mycobacterium bovis BCG stimulat