Cytotoxic and apoptotic effects of heat killed Mycobacterium indicus pranii (MIP) on various human cancer cell lines

Subramaniam, Menaga; In, Lionel Lian Aun; Kumar, Ashutosh; Ahmed, Niyaz; Nagoor, Noor Hasima

doi:10.1038/srep19833

Cited by 22 publications

(24 citation statements)

References 17 publications

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“…phlei, or HK MIP, inhibit BC proliferation similarly to live mycobacteria [63,[65][66][67], while other works found less growth inhibition of 253J and T24 cells significantly when HK BCG was used [68]. Unlike the observations made by the above mentioned authors, other authors found that HK BCG had no inhibitory effect in MGH BC cells [69].…”

Section: Purified Mycobacteria Antigens and Non-viable Mycobacteriacontrasting

confidence: 49%

Mycobacteria-Derived Agents for the Treatment of Urological and Renal Cancers

Noguera-Ortega¹,

Julián²

2018

Mycobacterium - Research and Development

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Mycobacteria are the unique group of bacteria that are currently used in antitumoral immunotherapy. Specifically, intravesical instillation of viable cells of Mycobacterium bovis Bacillus Calmette-Guérin (BCG), after transurethral resection of non-muscle invasive bladder cancer, is the most efficacious treatment for avoiding recurrence and progression of the disease. BCG has been used for the last 35 years for bladder cancer treatment, but other mycobacteria or mycobacteria components are currently under preclinical and clinical studies for the immunotherapeutic treatment of non-invasive bladder cancer and also of other types of tumors located at the urinary system. Those are, for instance, cell wall extracts or heat-killed forms from BCG or other mycobacteria such as Mycobacterium phlei or Mycobacterium indicus pranii (MIP) or even viable cells from non-pathogenic mycobacteria such us Mycobacterium brumae. A review of the literature in which mycobacteria components, non-viable mycobacteria, and viable mycobacteria have been used for these different cancers will be performed. In this chapter, the function of mycobacteria as antitumor agents will be then analyzed, awarding the audience a broad knowledge of one of the beneficial applications of mycobacteria, which are usually introduced as dangerous microorganisms.

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Section: Purified Mycobacteria Antigens and Non-viable Mycobacteriacontrasting

confidence: 49%

Mycobacteria-Derived Agents for the Treatment of Urological and Renal Cancers

Noguera-Ortega¹,

Julián²

2018

Mycobacterium - Research and Development

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“…[ 22 23 24 ] In addition, MIP-1α was mainly produced by hematopoietic cells (such as monocytes, macrophages, T lymphocytes, and B lymphocytes), and MIP-2 was secreted by both hematopoietic cells and nonhematopoietic cells. [ 25 ] Therefore, a possible reason why PDX could not regulate the release of MIP-2 may be associated with its binding on selective or specific cells.…”

Section: Discussionmentioning

confidence: 99%

Protectin DX Exhibits Protective Effects in Mouse Model of Lipopolysaccharide-Induced Acute Lung Injury

Tan

Chen

Wang

et al. 2018

Chinese Medical Journal

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Background:Acute lung injury (ALI) is a severe disease with high mortality and poor prognosis. Protectin DX (PDX), a pro-resolving lipid mediator, exhibits protective effects in ALI. Our experiment aimed to explore the effects and related mechanisms of PDX in mice with ALI induced by lipopolysaccharide (LPS).Methods:BALB/c mice were randomly divided into five groups: sham, LPS, LPS plus 1 ng of PDX (LPS + PDX-1 ng), LPS plus 10 ng of PDX (LPS + PDX-10 ng), and LPS plus 100 ng of PDX (LPS + PDX-100 ng). Bronchoalveolar lavage fluids (BALFs) were collected after 24 h, and total cells, polymorphonuclear leukocytes, monocyte-macrophages, and lymphocytes in BALF were enumerated. The concentration of interleukin (IL)-1β, IL-6, IL-10, tumor necrosis factor-alpha (TNF-α), macrophage inflammatory protein (MIP)-1α, and MIP-2 in BALF was determined, and histopathological changes of the lung were observed. The concentration of protein in BALF and lung wet/dry weight ratios were detected to evaluate pulmonary edema. After determining the optimal dose of PDX, neutrophil–platelet interactions in whole blood were evaluated by flow cytometry.Results:The highest dose of PDX (100 ng/mouse) failed to provide pulmonary protective effects, whereas lower doses of PDX (1 ng/mouse and 10 ng/mouse), especially 1 ng PDX, alleviated pulmonary histopathological changes, mitigated LPS-induced ALI and pulmonary edema, inhibited neutrophil infiltration, and reduced pro-inflammatory mediator (IL-1β, IL-6, TNF-α, and MIP-1α) levels. Meanwhile, 1 ng PDX exhibited pro-resolving functions in ALI including upregulation of monocyte-macrophage numbers and anti-inflammatory mediator IL-10 levels. The flow cytometry results showed that PDX could inhibit neutrophil–platelet interactions in ALI.Conclusion:PDX exerts protective effects in LPS-induced ALI by mitigating pulmonary inflammation and abrogating neutrophil–platelet interactions.

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“…On the other side, it has been described that overstimulation of PRRs can lead to induction of apoptosis. For example, TLR2 and TLR4 ligands present in the mycobacterial cell wall were identified as active ingredients of BCG treatment of superficial bladder tumors (Salaun et al, 2007; Subramaniam et al, 2016). This could be a reason for dose dependent decreased of cell viability caused by HV110 which was obtained in this study.…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus fermentum Postbiotic-induced Autophagy as Potential Approach for Treatment of Acetaminophen Hepatotoxicity

et al. 2017

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The aim of this study was to investigate the potential of postbiotics originated from Lactobacillus fermentum BGHV110 strain (HV110) to counteract acetaminophen (APAP)-induced hepatotoxicity in HepG2 cells. This strain was selected according to its autophagy inducing potential, based on previous studies reporting protective role of autophagy in APAP caused cellular damage. Cell viability was assessed using MTT and LDH assays, while autophagy was monitored by qPCR analysis of BECN1, Atg5, p62/SQSTM1, and PINK1 mRNA expression and by Western blot analysis of p62/SQSTM1 and lipidated LC3 accumulation. Our results showed that detrimental effect of APAP on cell viability was suppressed in the presence of HV110 which was linked with increased conversion of LC3 protein and p62/SQSTM1 protein degradation. Additionally, higher p62/SQSTM1 and PINK1 mRNA transcription were noticed in cells co-treated with APAP/HV110, simultaneously. In conclusion, this study suggests that HV110 enhances activation of PINK1-dependent autophagy in HepG2 cells and its eventual co-supplementation with APAP could be potentially used for alleviation of hepatotoxic side effects caused by APAP overdose.

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Cytotoxic and apoptotic effects of heat killed Mycobacterium indicus pranii (MIP) on various human cancer cell lines

Cited by 22 publications

References 17 publications

Mycobacteria-Derived Agents for the Treatment of Urological and Renal Cancers

Mycobacteria-Derived Agents for the Treatment of Urological and Renal Cancers

Protectin DX Exhibits Protective Effects in Mouse Model of Lipopolysaccharide-Induced Acute Lung Injury

Lactobacillus fermentum Postbiotic-induced Autophagy as Potential Approach for Treatment of Acetaminophen Hepatotoxicity

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