Herpesvirus-encoded microRNAs detected in human gingiva alter host cell transcriptome and regulate viral infection

Naqvi, Afsar Raza; Seal, Alexandra; Shango, Jennifer; Brambila, Maria F.; Martínez, Gloria; Chapa, Gabriela; Hasan, Shirin; Yadavalli, Tejabhiram; Jaishankar, Dinesh; Shukla, Deepak; Nares, Salvador

doi:10.1016/j.bbagrm.2018.03.001

Cited by 24 publications

(39 citation statements)

References 77 publications

(95 reference statements)

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“…However, there are other novel, but less well‐characterized, mechanisms of herpesvirus‐bacteria synergy that remain to be explored. For example, several studies have identified herpesvirus‐encoded microRNAs in inflammatory gingival and pulpal tissues . These microRNAs may serve as master regulators of host genes/pathways that may influence the clinical course of periodontal infections.…”

Section: Discussionmentioning

confidence: 99%

Herpesvirus‐bacteria synergistic interaction in periodontitis

Chen

Feng

Slots

2019

Periodontology 2000

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The etiopathogenesis of severe periodontitis includes herpesvirus‐bacteria coinfection. This article evaluates the pathogenicity of herpesviruses (cytomegalovirus and Epstein‐Barr virus) and periodontopathic bacteria (Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis) and coinfection of these infectious agents in the initiation and progression of periodontitis. Cytomegalovirus and A. actinomycetemcomitans/P. gingivalis exercise synergistic pathogenicity in the development of localized (“aggressive”) juvenile periodontitis. Cytomegalovirus and Epstein‐Barr virus are associated with P. gingivalis in adult types of periodontitis. Periodontal herpesviruses that enter the general circulation may also contribute to disease development in various organ systems. A 2‐way interaction is likely to occur between periodontal herpesviruses and periodontopathic bacteria, with herpesviruses promoting bacterial upgrowth, and bacterial factors reactivating latent herpesviruses. Bacterial‐induced gingivitis may facilitate herpesvirus colonization of the periodontium, and herpesvirus infections may impede the antibacterial host defense and alter periodontal cells to predispose for bacterial adherence and invasion. Herpesvirus‐bacteria synergistic interactions, are likely to comprise an important pathogenic determinant of aggressive periodontitis. However, mechanistic investigations into the molecular and cellular interaction between periodontal herpesviruses and bacteria are still scarce. Herpesvirus‐bacteria coinfection studies may yield significant new discoveries of pathogenic determinants, and drug and vaccine targets to minimize or prevent periodontitis and periodontitis‐related systemic diseases.

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Section: Discussionmentioning

confidence: 99%

Herpesvirus‐bacteria synergistic interaction in periodontitis

Chen

Feng

Slots

2019

Periodontology 2000

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“…However, the presence of the viral genome and its contribution to disease manifestation remains unanswered. To understand the biological relevance of these findings in periodontitis, we examined the expression of four previously identified viral miRNAs reported in our previous studies (Naqvi, Seal, Shango, Brambila, et al, 2018;Zhong, Naqvi, Bair, Nares, & Khan, 2017). In biopsy samples derived from obese periodontally healthy and diseased subjects, quantification of v-miRs revealed higher levels of herpesviral miR-NAs in diseased tissues compared with their healthy counterparts.…”

Section: Studies From Various Groups Including Ours Have Demonstratedmentioning

confidence: 94%

“…We selected 10 different algorithms tools to identify potential targets. or control mimics were purchased (Qiagen), and transfection was performed using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA) in HEK293 and human oral keratinocytes as previously described (Naqvi, Seal, Shango, Brambila, et al, 2018).…”

Section: Mirna-targeted Pathway and Gene Prediction Analysismentioning

confidence: 99%

“…For instance, Porphyromonas gingivalis (Pg) derived virulence factor peptidylarginine deiminase (PPAD) can impair biological activity of epidermal growth factor (EGF) by citrullination of C-terminal arginine (Pyrc et al, 2013). The presence of herpesviruses is increasingly acknowledged to exacerbate pathogenesis of oral inflammatory diseases including periodontitis (Naqvi, Seal, Shango, Brambila, et al, 2018;Parra & Slots 1996;. However, the presence of the viral genome and its contribution to disease manifestation remains unanswered.…”

Section: Studies From Various Groups Including Ours Have Demonstratedmentioning

confidence: 99%

“…Additionally, similar to cellular miRNAs, viral miRNAs can also posttranscriptionally regulate numerous host genes. We recently showed that viral miRNAs can alter expression of both host mRNAs and miR-NAs in v-miR expressing oral keratinocytes and myeloid cells (macrophages) (Naqvi, Seal, Shango, Brambila, et al, 2018;Naqvi, Seal, Shango, Shukla, et al, 2018;Naqvi, Shango, Seal, Shukla, & Nares, 2018a). These widespread v-miR-mediated transcriptome changes can affect numerous cellular functions including immune responses, phagocytosis and cell migration.…”

Section: Studies From Various Groups Including Ours Have Demonstratedmentioning

confidence: 99%

See 2 more Smart Citations

Dysregulation of human miRNAs and increased prevalence of HHV miRNAs in obese periodontitis subjects

Naqvi

Brambila

Martínez

et al. 2019

J Clinic Periodontology

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Aim: To evaluate human and herpesvirus-encoded microRNA (miRNA) expression in healthy and diseased gingiva of obese and non-obese subjects and compare the impact of localized and systemic inflammation on human miRNA profiles. Material and methods: Healthy and inflamed gingival biopsies were collected from obese and non-obese subjects. Human and herpesvirus miRNA expression was quantified using quantitative PCR. Predicted targets of dysregulated miRNAs were identified using bioinformatics analysis, validated by dual luciferase assays and their expression assessed in healthy and diseased tissues. Results: Our results show differential expression of miRNAs in both diseased groups compared to healthy counterparts. MMP-16 is identified as a novel target of miRNAs altered in disease. Expression analysis of genes predicted as target of differentially expressed miRNAs show significant changes in disease compared with healthy tissues. Finally, quantitation of four herpesvirus derived viral miRNAs show that expression and prevalence of herpesvirus miRNAs in diseased gingiva of obese subjects. Conclusion: Our findings show that miRNA (both cellular and virus) expression are differentially responsive to local and systemic inflammation. Some of these miRNAs can modulate key cellular genes with direct consequences on inflammatory pathways suggesting their impact on oral tissue transcriptome and functions.

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Non‐coding RNA LINC01010 regulates macrophage polarization and innate immune functions by modulating NFκB signaling pathway

Valverde,

Naqvi,

Naqvi

2024

Journal Cellular Physiology

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Innate immune response is regulated by tissue resident or infiltrating immune cells such as macrophages (Mφ) that play critical role in tissue development, homeostasis, and repair of damaged tissue. However, the epigenetic mechanisms that regulate Mφ plasticity and innate immune functions are not well understood. Long non‐coding RNA (lncRNA) are among the most abundant class of transcriptome but their function in myeloid cell biology is less explored. In this study, we deciphered the regulatory role of previously uncharacterized lncRNAs in Mφ polarization and innate immune responses. Two lncRNAs showed notable changes in their levels during M1 and M2 Mφ differentiation. Our findings indicate that LINC01010 expression increased and AC007032 expression decreased significantly. LINC01010 exhibit myeloid cell‐specificity, while AC007032.1 is ubiquitous and expressed in both myeloid and lymphoid (T cells, B cells and NK cells) cells. Expression of these lncRNAs is dysregulated in periodontal disease (PD), a microbial biofilm‐induced immune disease, and responsive to lipopolysaccharide (LPS) from different oral and non‐oral bacteria. Knockdown of LINC01010 but not AC007032.1 reduced the surface expression of Mφ differentiation markers CD206 and CD68, and M1Mφ polarization markers MHCII and CD32. Furthermore, LINC01010 RNAi attenuated bacterial phagocytosis, antigen processing and cytokine secretion suggesting its key function in innate immunity. Mechanistically, LINC01010 knockdown Mφ treated with Escherichia coli LPS exhibit significantly reduced expression of multiple nuclear factor kappa B pathway genes. Together, our data highlight functional role of a PD‐associated lncRNA LINC01010 in shaping macrophage differentiation, polarization, and innate immune activation.

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Herpesvirus-encoded microRNAs detected in human gingiva alter host cell transcriptome and regulate viral infection

Cited by 24 publications

References 77 publications

Herpesvirus‐bacteria synergistic interaction in periodontitis

Herpesvirus‐bacteria synergistic interaction in periodontitis

Dysregulation of human miRNAs and increased prevalence of HHV miRNAs in obese periodontitis subjects

Non‐coding RNA LINC01010 regulates macrophage polarization and innate immune functions by modulating NFκB signaling pathway

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