Enhancement of immune response to a DNA vaccine against Mycobacterium tuberculosis Ag85B by incorporation of an autophagy inducing system

Meerak, Jomkhwan; Wanichwecharungruang, Supason; Palaga, Tanapat

doi:10.1016/j.vaccine.2012.11.075

Cited by 42 publications

(32 citation statements)

References 31 publications

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“…In other studies, for evaluation of autophagy induction as an immunostimulatory model in the development of an efficient candidate DNA vaccine against Mycobacterium tuberculosis (MTB), coadministration of a plasmid containing MTB antigen 85B with a plasmid encoding the kinase defective mammalian target of rapamycin (mTOR-KD) have been performed in mice. They have found elevated antibody production, higher level of IFN-γ secretion, and augmented Ag85B-specific cytotoxic Tlymphocyte response in the murine splenocytes [27]. In agreement with the results of the present study, it has been previously shown that Beclin1 activates autophagy in human MCF7 breast carcinoma cells by gene-transfer techniques.…”

Section: Discussionsupporting

confidence: 93%

Design and construction of Beclin1-expressing plasmid as an autophagy inducing system: a novel strategy for enhancing the potency of DNA vaccines

Naziri

Abdoli

Tahmtan

et al. 2016

vacres

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Introduction: Autophagy is a complicated process which is involved in many biological events such as antigen presentation by immune cells. Beclin1, as a key component of autophagic machinery, plays the main role in the induction and initiation of this process. In the present study, we hypothesized that overexpression of Beclin1 could be useful in autophagy induction as an immunostimulatory strategy for improving the efficiency of DNA vaccines. Methods: Beclin1 gene was cloned into pVITRO2 eukaryotic expression vector and was confirmed by agarose gel electrophoresis. Beclin1 expression was evaluated by Real-Time RT-PCR and Western blotting. The autophagy induction by pVITRO2 encoding Beclin1 in HEK293 cells was evaluated through detection of the expression levels of LC3II as a marker for autophagy induction by Western blotting. Results: Beclin1 expression by the constructed plasmid was detected in HEK293 cells. The pVITRO2 encoding Beclin1 showed autophagy enhancement as compared to the control condition. Our data showed significant increase in the expression of LC3II protein following Beclin1 transfection (P ˂0.05 or 0.01). Conclusion: Our results support a novel strategy for autophagy induction via up-regulation of Beclin1 expression. This could be useful for improvement of DNA vaccines through enhancing their antigen presentation.

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Section: Discussionsupporting

confidence: 93%

Design and construction of Beclin1-expressing plasmid as an autophagy inducing system: a novel strategy for enhancing the potency of DNA vaccines

Naziri

Abdoli

Tahmtan

et al. 2016

vacres

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“…In addition to the Beclin1, other autophagy inducers such as mammalian target of rapamycin-kinase defective (mTOR-KD) and LC3II have also been evaluated as an autophagy inducing system in vaccine development (30,31). Until now, It had not been tested that overexpression of Beclin1 induced autophagy in DNA vaccine; nevertheless, our study revealed that autophagy is induced through overexpression of this protein.…”

Section: Discussionmentioning

confidence: 87%

“…In parallel to the results of the present study, Meerak et al revealed that autophagy induction through mTOR-KD could improve the efficacy of a candidate DNA vaccine against mycobacterium tuberculosis (MTB). They found elevated levels of secreted IFN-γ, interleukin-2 (IL-2), and IgG2a in immunized mice with the autophagy-inducing based plasmid (30).…”

Section: Discussionmentioning

confidence: 99%

Enhancement of Hepatitis E Virus DNA Vaccine Immunity by Beclin-1- Mediated Autophagy

Naziri

Abdoli

Ghaemi

et al. 2017

Jundishapur J Microbiol

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Background: The Hepatitis E virus (HEV) infection is a serious public health problem, with a mortality rate of approximately 20-25% among pregnant women. DNA vaccination was reported to induce humoral and cellular immune responses in murine models; however, a major problem of the strategy is its limited potency. Methods: In this study, we have investigated whether Beclin1, as an autophagy-inducing based plasmid, can serve as an immunostimulatory agent and promote the HEV specific protective immunity of naked DNA vaccine encoding truncated ORF-2 (HEV239). Plasmids encoding HEV239 with or without Beclin1 were used for the BALB/c mice immunization. Results:The results demonstrated a significant increase microtubule-associated protein light chain-3 II (LC3 II) as a marker of autophagy in the HEK293 cell, which were transfected by pVITRO-Beclin1 plasmid. The immunological effects of adding Beclin1 to HEV239 ORF-2 DNA vaccines were associated with the induction of the antigen-specific lymphocyte proliferation and the Th1-type cytokine (gamma-interferon (IFN-γ)), while there were no differences in IL-4 levels between the groups. Examination of humoral immune responses in vaccinated mice represented that immunization with pVITRO-HEV239-Beclin1 notably increased serum level of IgG2a and total IgG against HEV in comparison to the HEV239 plasmid alone. Conclusions:The strong Th1 immune response induced by the Beclin1 suggest that induction of autophagy can be an efficient approach to enhance the immunogenicity of DNA vaccine. This promising procedure could be further exploited as a potential therapeutic vaccine candidate in future studies.

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“…DNA vaccines used directly or as prime-boost are alternative promising approaches to either improve the efficacy of the current BCG vaccine or to create a new more effective one (Rivas-Santiago and Cervantes-Villagrana, 2014). Plasmids containing M. tuberculosis DNA (from Ag85, Hsp65, and the 23 members of Esx gene family) used in experimental DNA vaccines have been found to lead to higher INF-g production and consequent induction of autophagy (Meerak et al, 2013;Zarate-Blades et al, 2013;Villarreal et al, 2014).…”

Section: Arg677trp (C2029t)mentioning

confidence: 99%

Autophagy in the Fight Against Tuberculosis

Bento

Empadinhas

Mendes

2015

DNA and Cell Biology

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Tuberculosis (TB), a chronic infectious disease mainly caused by the tubercle bacillus Mycobacterium tuberculosis, is one of the world's deadliest diseases that has afflicted humanity since ancient times. Although the number of people falling ill with TB each year is declining, its incidence in many developing countries is still a major cause of concern. Upon invading host cells by phagocytosis, M. tuberculosis can replicate within infected cells by arresting the maturation of the phagosome whose function is to target the pathogen for elimination. Host cells have mechanisms of controlling this evasion by inducing autophagy, an elaborate cellular process that targets bacteria for progressive elimination, decreasing bacterial loads within infected cells. In addition, autophagy activation also aids in the control of inflammation, contributing to a more efficient innate immune response against M. tuberculosis. Several innovative TB therapies have been envisaged based on autophagy manipulation, with some of them revealing high potential for future clinical trials and eventual implementation in healthcare systems. Thus, this review highlights the recent advances on the innate immune response regulation by autophagy upon M. tuberculosis infection and the promising new autophagy-based therapies for TB. Mycobacterium tuberculosis: Biology and Infection

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Enhancement of immune response to a DNA vaccine against Mycobacterium tuberculosis Ag85B by incorporation of an autophagy inducing system

Cited by 42 publications

References 31 publications

Design and construction of Beclin1-expressing plasmid as an autophagy inducing system: a novel strategy for enhancing the potency of DNA vaccines

Design and construction of Beclin1-expressing plasmid as an autophagy inducing system: a novel strategy for enhancing the potency of DNA vaccines

Enhancement of Hepatitis E Virus DNA Vaccine Immunity by Beclin-1- Mediated Autophagy

Autophagy in the Fight Against Tuberculosis

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