A luciferase-based assay for rapid assessment of drug activity against Mycobacterium tuberculosis including monitoring of macrophage viability

Larsson, Marie; Lerm, Maria; Ängeby, Kristian; Nordvall, Michaela Jonsson; Juréen, Pontus; Schӧn, Thomas

doi:10.1016/j.mimet.2014.08.015

Cited by 14 publications

(8 citation statements)

References 22 publications

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“…Relevant to our data, earlier studies have demonstrated that INH can either induce or inhibit the cytochrome P450 system which may result in the alterations of 25-OHase and 1-OHase [43], [44]. Furthermore, rifampicin can increase CYP3A4-dependent 25(OH)D 3 metabolism in liver but not CYP24A1 [25], [45]. There are no available data on the impact of ethambutol and pyrazinamide on vitamin D metabolism or the effect of the 4-drug standard regimen studied in this report.…”

Section: Discussionsupporting

confidence: 83%

“…One possible explanation was the first-line anti-tuberculosis drugs might directly or indirectly interfere the enzymes in the vitamin D metabolism pathway such as CYP27A1 or CYP24A1 which may interfere with the activation of the vitamin D receptor in macrophages. Another limitation is the concentrations of the anti-TBs were based on the minimal inhibitory concentration (MIC) from published in vitro THP-1 cell culture and TB experiments in the literature [25], [26], [27], [28]. Also our THP-1 cells were not infected by Mtb .…”

Section: Discussionmentioning

confidence: 99%

“…The concentrations of each drug were examined over a range of doses known to inhibit Mtb growth from previously published studies [24], [25], [26], [27], [28], [29] at a final concentration of 1.0 µg/mL, 5.0 µg/mL and 10.0 µg/mL. THP-1 cells were then incubated in 37 °C, 5% CO 2 for 6 hours, following which cell suspensions were centrifuged and supernatants removed.…”

Section: Methodsmentioning

confidence: 99%

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The effects of first-line anti-tuberculosis drugs on the actions of vitamin D in human macrophages

Chesdachai

Zughaier

et al. 2016

Journal of Clinical & Translational Endocrinology

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Tuberculosis (TB) is a major global health problem. Patients with TB have a high rate of vitamin D deficiency, both at diagnosis and during the course of treatment with anti-tuberculosis drugs. Although data on the efficacy of vitamin D supplementation on Mycobacterium tuberculosis (Mtb) clearance is uncertain from randomized controlled trials (RCTs), vitamin D enhances the expression of the anti-microbial peptide human cathelicidin (hCAP18) in cultured macrophages in vitro. One possible explanation for the mixed (primarily negative) results of RCTs examining vitamin D treatment in TB infection is that anti-TB drugs given to enrolled subjects may impact actions of vitamin D to enhance cathelicidin in macrophages. To address this hypothesis, human macrophage-like monocytic (THP-1) cells were treated with varying doses of first-line anti-tuberculosis drugs in the presence of the active form of vitamin D, 1N1,25-dihydroxyvitamin D3 (1,25(OH)2D3). The expression of hCAP18 was determined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). 1,25(OH)2D3 strongly induced expression of hCAP18 mRNA in THP-1 cells (fold-change from control). The combination of the standard 4-drug TB therapy (isoniazid, rifampicin, pyrazinamide and ethambutol) in the cultured THP-1 cells demonstrated a significant decrease of hCAP18 mRNA at the dosage of 10 ug/mL. In 31 subjects with newly diagnosed drug-sensitive TB randomized to either high-dose vitamin D3 (1.2 million IU over 8 weeks, n=13) versus placebo (n=18), there was no change from baseline to week 8 in hCAP18 mRNA levels in peripheral blood mononuclear cells or in plasma concentrations of LL-37, the protein product of hCAP18.These data suggest that first-line anti-TB drugs may alter the vitamin D-dependent increase in hCAP18 and LL-37 human macrophages.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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The effects of first-line anti-tuberculosis drugs on the actions of vitamin D in human macrophages

Chesdachai

Zughaier

et al. 2016

Journal of Clinical & Translational Endocrinology

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“…To discern the susceptibility of the rCSF‐1‐ and rIL‐34‐derived Mϕs to Mm , we challenged frog bone marrow‐derived CSF‐1‐ and IL‐34‐Mϕs with fluorescently labeled (calcein; does not affect Mm viability) Mm . The CSF‐1‐Mϕs were significantly more susceptible to Mm infection than the IL‐34‐Mϕs (Fig.…”

Section: Resultsmentioning

confidence: 99%

Colony-stimulating factor-1- and interleukin-34-derived macrophages differ in their susceptibility to Mycobacterium marinum

Popović

Yaparla

Paquin‐Proulx

et al. 2019

Journal of Leukocyte Biology

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Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), remains the leading global cause of death from an infectious agent. Mycobacteria thrive within their host M s and presently, there is no animal model that permits combined in vitro and in vivo study of mycobacteria-host M interactions. Mycobacterium marinum (Mm), which causes TB in aquatic vertebrates, has become a promising model for TB research, owing to its close genetic relatedness to Mtb and the availability of alternative, natural host aquatic animal models. Here, we adopted the Xenopus laevis frog-Mm surrogate infection model to study host M susceptibility and resistance to mycobacteria. M differentiation is regulated though the CSF-1 receptor (CSF-1R), which is activated by CSF-1 and the unrelated IL-34 cytokines. Using combined in vitro and in vivo approaches, we demonstrated that CSF-1-M s exacerbate Mm infections, are more susceptible to mycobacterial entry and are less effective at killing this pathogen. By contrast, IL-34-M s confer anti-Mm resistance in vivo, are less susceptible to Mm entry and more effectively eliminate internalized mycobacteria. Moreover, we showed that the human CSF-1-and IL-34-M s are likewise, respectively, susceptible and resistant to mycobacteria, and that both frog and human CSF-1-M s are more prone to the spread of mycobacteria and to being infected by Mm-laden M s than the respective IL-34-M subsets. This work marks the first report describing the roles of these M subsets in mycobacterial disease and may well lead to the development of more targeted anti-Mtb approaches.

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“…Еще одно перспективное направление, появившееся в последнее время, -детекция бактерий и действия на них антибиотиков в моделях природных систем патоген-хозяин. Пока эти исследования ограничены детекцией бактерий и наблюдением за их гибелью, вызванной антибиотиками [29,30], но в дальнейшем, безусловно, возможным станет и наблюдение за индукцией стрессовых генов бактерии, вызванной антибиотиком, в сложных системах.…”

Section: изменение экспрессии генов бактерии в ответ на воздействие аunclassified

Application of reporter strains for new antibiotic screening

Osterman

et al. 2016

BIOMED KHIM

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Screening for new antibiotics remains an important area of biology and medical science. Indispensable for this type of research is early identification of antibiotic mechanism of action. Preferentially, it should be studied quickly and cost-effectively, on the stage of primary screening. In this review we describe an application of reporter strains for rapid classification of antibiotics by its target, without prior purification of an active compound and determination of chemical structure

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A luciferase-based assay for rapid assessment of drug activity against Mycobacterium tuberculosis including monitoring of macrophage viability

Cited by 14 publications

References 22 publications

The effects of first-line anti-tuberculosis drugs on the actions of vitamin D in human macrophages

The effects of first-line anti-tuberculosis drugs on the actions of vitamin D in human macrophages

Colony-stimulating factor-1- and interleukin-34-derived macrophages differ in their susceptibility to Mycobacterium marinum

Application of reporter strains for new antibiotic screening

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