Genomic plasticity between human and mycobacterial DNA: A review

Danjuma, Lawal; Ling, Mok Pooi; Hamat, Rukman Awang; Higuchi, Akon; Alarfaj, Abdullah A.; Marlina, Marlina; Benelli, Giovanni; Arulselvan, Palanisamy; Rajan, Mariappan; Subbiah, Suresh Kumar

doi:10.1016/j.tube.2017.03.006

Cited by 10 publications

(8 citation statements)

References 124 publications

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“…It has been well established that various bacterial infections can significantly influence the host cells' transcriptional profile, thus changing the disease susceptibility. 3 Several complex processes are involved in the various stages of infection that may benefit the survival of bacteria.…”

Section: Introductionmentioning

confidence: 99%

Comparative transcriptomic analysis of THP‐1‐derived macrophages infected with Mycobacterium tuberculosis H37Rv, H37Ra and BCG

Zhao

Wazir

et al. 2021

J Cellular Molecular Medi

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Section: Introductionmentioning

confidence: 99%

Comparative transcriptomic analysis of THP‐1‐derived macrophages infected with Mycobacterium tuberculosis H37Rv, H37Ra and BCG

Zhao

Wazir

et al. 2021

J Cellular Molecular Medi

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“…MBD2, as a reader of DNA methylation, might contribute to interpret DNA methylation patterns into different functional output, including immune system function (Wood and Zhou, 2016). Although the role of MBD2 in tuberculosis is undefined, previous study reported that mycobacterial proteins could modify gene methylation in mammalian host tissues (Danjuma et al, 2017). For example, BCG-induced epigenetic reprogramming of immune cell function could enhance anti-mycobacterial immunity in macrophages (Verma et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

A Two-Way Proteome Microarray Strategy to Identify Novel Mycobacterium tuberculosis-Human Interactors

Cao¹,

Lyu²,

Jia³

et al. 2019

Front. Cell. Infect. Microbiol.

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Tuberculosis (TB) is still a serious threat to human health which is caused by mycobacterium tuberculosis ( Mtb ). The main reason for failure to eliminate TB is lack of clearly understanding the molecular mechanism of Mtb pathogenesis. Determining human Mtb -interacting proteins enables us to characterize the mechanism and identify potential molecular targets for TB diagnosis and treatment. However, experimentally systematic Mtb interactors are not readily available. In this study, we performed an unbiased, comprehensive two-way proteome microarray based approach to systematically screen global human Mtb interactors and determine the binding partners of Mtb effectors. Our results, for the first time, screened 84 potential human Mtb interactors. Bioinformatic analysis further highlighted these protein candidates might engage in a wide range of cellular functions such as activation of DNA endogenous promoters, transcription of DNA/RNA and necrosis, as well as immune-related signaling pathways. Then, using Mtb proteome microarray followed His tagged pull-down assay and Co-IP, we identified one interacting partner (Rv0577) for the protein candidate NRF1 and three binding partners (Rv0577, Rv2117, Rv2423) for SMAD2, respectively. This study gives new insights into the profile of global Mtb interactors potentially involved in Mtb pathogenesis and demonstrates a powerful strategy in the discovery of Mtb effectors.

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“…In there, they resident and persist by a variety of immune evasion strategies, including hiding from PRR recognition [2], preventing T cell responses by down-regulating MHC molecules [3], as well as evading macrophage killing systems [3] and so on. In addition, the genomic plasticity might also be partially responsible for the antigenic variations of diverse Mtb stains and the variable protective efficacies of diverse BCG strains [4].…”

Section: Introductionmentioning

confidence: 99%

“…Actually, some important comparative analyses have showed us the panoramic views of genome variations among BCG vaccine strains [4,5].…”

Section: Introductionmentioning

confidence: 99%

Mycobacteria tuberculosisPPE36 modulates host inflammation by promoting E3 ligase Smurf1-mediated MyD88 degradation

Peng

Yan

Xiong

2021

Preprint

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Mycobacterium tuberculosis (Mtb) PPE36, a cell-wall associated protein is highly specific and conserved for the Mtb complex group. Although it has been proven essential for iron utilization, little is known about the role of PPE36 in regulating host immune responses. Here we exhibited that PPE36 preferentially enriched in Mtb virulent strains, and could efficiently inhibit host inflammatory responses and increase bacterial loads both in mycobacterium-infected macrophages and mice. In exploring the underlying mechanisms, we found that PPE36 could robustly inhibit the activation of inflammatory NF-κB and MAPK (ERK, p38 and JNK) pathways by promoting E3 ligase Smurf1-mediated ubiquitination and proteasomal degradation of MyD88 protein. Our research revealed a previously unknown function of PPE36 on modulating host immune responses, and provided some clues to the development of novel tuberculosis treatment strategies based on immune regulation.Author SummaryMycobacterium tuberculosis (Mtb) has developed diverse immune evasion strategies to successfully establish infection in host. Identifying the important Mtb immune regulatory proteins and elucidating the underlying mechanisms are critical for tuberculosis control. Here we demonstrated that PPE36, a Mtb cell-wall associated protein, was predominantly enriched in virulent mycobacterial strains, and obviously inhibited inflammatory responses and facilitated bacterial survival in infected macrophages. Compared with the wild-type BCG, BCG lacking PPE36 (BCGΔPPE36) induced more inflammation, lower bacterial loads as well as the improved histopathological changes in the lungs of infected mice. We further found that PPE36 significantly reduced host MyD88 abundance, and inhibited the activation of subsequunt inflammatory NF-κB and MAPK pathways. In addition, this direct inhibition effect of PPE36 on MyD88 was mediated by the promoted E3 ligase Smurf1 ubiquitin -protesome pathway. This study identified PPE36 as a immune regulatory protein of Mtb, and showed it played an important role in the Mtb immune evasion.

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Genomic plasticity between human and mycobacterial DNA: A review

Cited by 10 publications

References 124 publications

Comparative transcriptomic analysis of THP‐1‐derived macrophages infected with Mycobacterium tuberculosis H37Rv, H37Ra and BCG

Comparative transcriptomic analysis of THP‐1‐derived macrophages infected with Mycobacterium tuberculosis H37Rv, H37Ra and BCG

A Two-Way Proteome Microarray Strategy to Identify Novel Mycobacterium tuberculosis-Human Interactors

Mycobacteria tuberculosisPPE36 modulates host inflammation by promoting E3 ligase Smurf1-mediated MyD88 degradation

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