Evidence map›Paper›PMID 30835734›Full record

ArticlePLoS neglected tropical diseases2019

The unique tropism of Mycobacterium leprae to the nasal epithelial cells can be explained by the mammalian cell entry protein 1A.

Viesta Beby Fadlitha, Fuki Yamamoto, Irfan Idris, Haslindah Dahlan, Naoya Sato, Vienza Beby Aftitah, Andini Febriyanda, Takao Fujimura, Hiroaki Takimoto

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PLoS neglected tropical diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Leprosy.Nature reviews. Disease primers · 2024
    Review
  4. Review
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Viesta Beby FadlithaDepartment of Dermatology, Kitasato University Graduate School of Medical Science, Sagamihara, Kanagawa, Japan.
Fuki YamamotoDepartment of Dermatology, Kitasato University Graduate School of Medical Science, Sagamihara, Kanagawa, Japan.
Irfan IdrisHasanuddin University Medical Research Centre, Makassar, South Sulawesi, Indonesia.
Haslindah DahlanHasanuddin University Medical Research Centre, Makassar, South Sulawesi, Indonesia.
Naoya SatoDepartment of Dermatology, Toshiba Rinkan Hospital, Sagamihara, Kanagawa, Japan.
Vienza Beby AftitahDepartment of Cellular Immunology, Kitasato University Graduate School of Medical Science, Sagamihara, Kanagawa, Japan.
Andini FebriyandaHasanuddin University Medical Research Centre, Makassar, South Sulawesi, Indonesia.
Takao FujimuraDepartment of Dermatology, Kitasato University Graduate School of Medical Science, Sagamihara, Kanagawa, Japan.ORCID 0000-0003-4243-5822
Hiroaki TakimotoDepartment of Bioscience, Kitasato University School of Science, Sagamihara, Kanagawa, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leprosy is a chronic infection where the skin and peripheral nervous system is invaded by Mycobacterium leprae. The infection mechanism remains unknown in part because culture methods have not been established yet for M. leprae. Mce1A protein (442 aa) is coded by mce1A (1326 bp) of M. leprae. The Mce1A homolog in Mycobacterium tuberculosis is known to be associated with M. tuberculosis epithelial cell entry, and survival and multiplication within macrophages. Studies using recombinant proteins have indicated that Mce1A of M. leprae is also associated with epithelial cell entry. This study is aimed at identifying particular sequences within Mce1A associated with M. leprae epithelial cell entry. Recombinant proteins having N-terminus and C-terminus truncations of the Mce1A region of M. leprae were created in Escherichia coli. Entry activity of latex beads, coated with these truncated proteins (r-lep37 kDa and r-lep27 kDa), into HeLa cells was observed by electron microscopy. The entry activity was preserved even when 315 bp (105 aa) and 922 bp (308 aa) was truncated from the N-terminus and C-terminus, respectively. This 316-921 bp region was divided into three sub-regions: 316-531 bp (InvX), 532-753 bp (InvY), and 754-921 bp (InvZ). Each sub-region was cloned into an AIDA vector and expressed on the surface of E. coli. Entry of these E. coli into monolayer-cultured HeLa and RPMI2650 cells was observed by electron microscopy. Only E. coli harboring the InvX sub-region exhibited cell entry. InvX was further divided into 4 domains, InvXa-InvXd, containing sequences 1-24 aa, 25-46 aa, 47-57 aa, and 58-72 aa, respectively. Recombinant E. coli, expressing each of InvXa-InvXd on the surface, were treated with antibodies against these domains, then added to monolayer cultured RPMI cells. The effectiveness of these antibodies in preventing cell entry was studied by colony counting. Entry activity was suppressed by antibodies against InvXa, InvXb, and InvXd. This suggests that these three InvX domains of Mce1A are important for M. leprae invasion into nasal epithelial cells.

Indexed as

Bacterial ProteinsCell LineColony Count, MicrobialDNA, BacterialEscherichia coliGenetic VectorsHeLa CellsHumansLeprosyMicrospheresMycobacterium lepraeNasal SeptumRecombinant ProteinsBacterial ProteinsDNA, BacterialMce1A protein, Mycobacterium lepraeRecombinant Proteins

Identifiers

PMID30835734
PMCPMC6420055

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.