Comparative whole-genome sequence analysis of Mycobacterium tuberculosis isolated from tuberculous meningitis and pulmonary tuberculosis patients

Faksri, Kiatichai; Xia, Eryu; Ong, Rick Twee‐Hee; Tan, Jun; Nonghanphithak, Ditthawat; Makhao, Nampueng; Thamnongdee, Nongnard; Thanormchat, Arirat; Phurattanakornkul, Arisa; Rattanarangsee, Somcharn; Ratanajaraya, Chate; Suriyaphol, Prapat; Prammananan, Therdsak; Teo, Yik-Ying; Chaiprasert, Angkana

doi:10.1038/s41598-018-23337-y

Cited by 30 publications

(25 citation statements)

References 33 publications

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“…Nevertheless, we have shown that glibenclamide enhances IL-10 levels in vitro . In Thailand, East Asian (w/Beijing) strains predominated in both TB meningitis and pulmonary TB disease ( 56 ). However, our study used only Mtb H37Rv, the most studied strain of TB in research laboratories ( 57 ), and BCG, with which most Thai people have been vaccinated ( 58 ).…”

Section: Discussionmentioning

confidence: 99%

Glibenclamide Reduces Primary Human Monocyte Functions Against Tuberculosis Infection by Enhancing M2 Polarization

Kewcharoenwong¹,

Prabowo

Bancroft

et al. 2018

Front. Immunol.

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Tuberculosis (TB) is a global public health problem, which is caused by Mycobacterium tuberculosis (Mtb). Type 2 diabetes mellitus (T2DM) is one of the leading predisposing factors for development of TB after HIV/AIDS. Glibenclamide is a widely used anti-diabetic drug in low and middle-income countries where the incidence of TB is very high. In a human macrophage cell line, glibenclamide, a K+ATP-channel blocker, promoted alternative activation of macrophages by enhancing expression of the M2 marker CD206 during M2 polarization. M2 macrophages are considered poorly microbicidal and associated with TB susceptibility. Here, we investigated the effect of glibenclamide on M1 and M2 phenotypes of primary human monocytes and further determined whether specific drug treatment for T2DM individuals influences the antibacterial function of monocytes in response to mycobacterial infection. We found that glibenclamide significantly reduced M1 (HLA-DR+ and CD86+) surface markers and TNF-α production on primary human monocytes against mycobacterial infection. In contrast, M2 (CD163+ and CD206+) surface markers and IL-10 production were enhanced by pretreatment with glibenclamide. Additionally, reduction of bactericidal activity also occurred when primary human monocytes from T2DM individuals who were being treated with glibenclamide were infected with Mtb in vitro, consistent with the cytokine responses. We conclude that glibenclamide reduces M1 and promotes M2 polarization leading to impaired bactericidal ability of primary human monocytes of T2DM individuals in response to Mtb and may lead to increased susceptibility of T2DM individuals to TB and other bacterial infectious diseases.

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Section: Discussionmentioning

confidence: 99%

Glibenclamide Reduces Primary Human Monocyte Functions Against Tuberculosis Infection by Enhancing M2 Polarization

Kewcharoenwong¹,

Prabowo

Bancroft

et al. 2018

Front. Immunol.

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“…The intersecting SNPs were used for further analysis. Criteria for single nucleotide variant filtering was used to meet high-confidence variants, according to the study of Faksri et al 52 ; mapping quality >50, base Genomic sequence data availability. Whole genome sequence data used in this study were deposited at European Nucleotide Archive (ENA) of EMBL-EBI under the accession numbers ERP006738.…”

Section: Methodsmentioning

confidence: 99%

Homoplastic single nucleotide polymorphisms contributed to phenotypic diversity in Mycobacterium tuberculosis

Tantivitayakul

Ruangchai

Juthayothin

et al. 2020

Sci Rep

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Homoplastic mutations are mutations independently occurring in different clades of an organism. The homoplastic changes may be a result of convergence evolution due to selective pressures. Reports on the analysis of homoplastic mutations in Mycobacterium tuberculosis have been limited. Here we characterized the distribution of homoplastic single nucleotide polymorphisms (SNPs) among genomes of 1,170 clinical M. tuberculosis isolates. They were present in all functional categories of genes, with pe/ppe gene family having the highest ratio of homoplastic SNPs compared to the total SNPs identified in the same functional category. Among the pe/ppe genes, the homoplastic Snps were common in a relatively small number of homologous genes, including ppe18, the protein of which is a component of a promising candidate vaccine, M72/AS01E. The homoplastic SNPs in ppe18 were particularly common among M. tuberculosis Lineage 1 isolates, suggesting the need for caution in extrapolating the results of the vaccine trial to the population where L1 is endemic in Asia. As expected, homoplastic SNPs strongly associated with drug resistance. Most of these mutations are already well known. However, a number of novel mutations associated with streptomycin resistance were identified, which warrants further investigation. A SNP in the intergenic region upstream of Rv0079 (DATIN) was experimentally shown to increase transcriptional activity of the downstream gene, suggesting that intergenic homoplastic SNPs should have effects on the physiology of the bacterial cells. Our study highlights the potential of homoplastic mutations to produce phenotypic changes. Under selective pressure and during interaction with the host, homoplastic mutations may confer advantages to M. tuberculosis and deserve further characterization. Mycobacterium tuberculosis (Mtb) is a successful human-adapted species that has undergone long-term coevolution with its human host 1. Previous studies 2,3 revealed the clonal expansion of Mtb, indicating a very low possibility of horizontal gene transfer between strains. Therefore, genetic variations in Mtb appear to be primarily derived from nucleotide substitutions, insertions, and deletions 4,5. The global population of M. tuberculosis sensu stricto is grouped into five phylogenetic lineages, including L1 (Indo-Oceanic family); L2 (East Asian family); L3 (East-African Indian family); L4 (Euro-American); and L7 6,7. In the past decade, several studies have demonstrated associations between Mtb lineages with demographic profiles, geographic distribution, transmission capacity, pathogenesis, cytokine induction, and drug resistance 6,8-10 .Once a strong association has been established, it may be explained through the identification of genotype-specific mutations, in coding or intergenic regions 11-13. Some phenotypes, such as drug resistance, usually occur in several phylogenetic lineages. Mutations that promote drug resistance can be identified by correlating

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“…The majority of the tuberculosis burden and deaths are concentrated in middle-income countries. There are few studies making attempts to relate extrapulmonary forms of the disease to a specific genetic variant of M. tuberculosis on a genome-wide scale ( 2 – 4 ). In order to continue efforts to identify a genetic variant that could impact disease severity and tissue tropism, more genome sequences of extrapulmonary strains from different geographic regions need to be analyzed.…”

Section: Genome Announcementmentioning

confidence: 99%

Sequencing and Annotation of the Genome of Mycobacterium tuberculosis MYC004, a Strain Causing Meningitis in Mexico

et al. 2018

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Comparative whole-genome sequence analysis of Mycobacterium tuberculosis isolated from tuberculous meningitis and pulmonary tuberculosis patients

Cited by 30 publications

References 33 publications

Glibenclamide Reduces Primary Human Monocyte Functions Against Tuberculosis Infection by Enhancing M2 Polarization

Glibenclamide Reduces Primary Human Monocyte Functions Against Tuberculosis Infection by Enhancing M2 Polarization

Homoplastic single nucleotide polymorphisms contributed to phenotypic diversity in Mycobacterium tuberculosis

Sequencing and Annotation of the Genome of Mycobacterium tuberculosis MYC004, a Strain Causing Meningitis in Mexico

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