Mycobacterium indicus pranii (MIP) mediated host protective intracellular mechanisms against tuberculosis infection: Involvement of TLR-4 mediated signaling

Das, Shibali; Chowdhury, Bidisha Paul; Goswami, Anupam; Parveen, Shabina; Jawed, Junaid Jibran; Pal, Nishith Kumar; Majumdar, Subrata

doi:10.1016/j.tube.2016.09.027

Cited by 21 publications

(21 citation statements)

References 36 publications

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“…Bacteria, viruses, fungi, and parasites can be recognized by TLR2. TLR4, with an adaptor molecule MyD88, is essential in the recognition of and response to antigenic components of multiple Gram-negative bacteria [56]. At present, in pro-inflammatory cytokines analysis and signal pathway investigation, we found TLR4 and not TLR2, was involved in positive control of cytokine production by PotD in H. parasuis, which was different from a previous finding for GALT in A. pleuropneumoniae, in which TLR2 played a contrary role against TLR4.…”

Section: Discussioncontrasting

confidence: 99%

Polyamine Transport Protein PotD Protects Mice against Haemophilus parasuis and Elevates the Secretion of Pro-Inflammatory Cytokines of Macrophage via JNK–MAPK and NF–κB Signal Pathways through TLR4

Dai

Yang

et al. 2019

Vaccines

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The potD gene, belonging to the well-conserved ABC (ATP-binding cassette) transport system potABCD, encodes the bacterial substrate-binding subunit of the polyamine transport system. In this study, we found PotD in Haemophilus (Glaesserella) parasuis could actively stimulate both humoral immune and cellular immune responses and elevate lymphocyte proliferation, thus eliciting a Th1-type immune response in a murine immunity and infection model. Stimulation of Raw 264.7 macrophages with PotD validated that Toll-like receptor 4, rather than 2, participated in the positive transcription and expression of pro-inflammatory cytokines IL–1β, IL–6, and TNF–α using qPCR and ELISA. Blocking signal-regulated JNK–MAPK and RelA(p65) pathways significantly decreased PotD-induced pro-inflammatory cytokine production. Overall, we conclude that vaccination of PotD could induce both humoral and cellular immune responses and provide immunoprotection against H. parasuis challenge. The data also suggest that Glaesserella PotD is a novel pro-inflammatory mediator and induces TLR4-dependent pro-inflammatory activity in Raw 264.7 macrophages through JNK–MAPK and RelA(p65) pathways.

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Section: Discussioncontrasting

confidence: 99%

Polyamine Transport Protein PotD Protects Mice against Haemophilus parasuis and Elevates the Secretion of Pro-Inflammatory Cytokines of Macrophage via JNK–MAPK and NF–κB Signal Pathways through TLR4

Dai

Yang

et al. 2019

Vaccines

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“…TLR4 belongs to the TLR family and locates in the cell membrane and cytoplasm. Mycobacterium indicus pranii treatment can activate NF‐kB via regulating TLR4 signaling, which results in the enhanced pro‐inflammatory cytokine production in the infected macrophages …”

Section: Introductionmentioning

confidence: 99%

MiR‐1178 regulates mycobacterial survival and inflammatory responses in Mycobacterium tuberculosis‐infected macrophages partly via TLR4

Shi

Mao

Xie

et al. 2018

J of Cellular Biochemistry

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Tuberculosis is chronic respiratory infectious disease and is caused by the infection of Mycobacterium tuberculosis (M.tb). Macrophages play an important role in host immune response against M.tb infection, which is regulated by various factors, including microRNAs (miRNAs). The present study aimed to examine the in vitro functional role of miR-1178 in mycobacterial survival and inflammatory responses induced by M.tb infection in human macrophages. Our results showed that M.tb infection increased the expression of miR-1178 in human macrophages (HTP-1 and U937 cells) in a concentration- and time-dependent manner. Overexpression of miR-1178 enhanced the intracellular growth of mycobacteria during M.tb infection, while knockdown of miR-1178 suppressed the mycobacteria survival. Overexpression of miR-1178 also significantly attenuated the accumulation of proinflammatory cytokines including interferon-γ (IFN-γ), interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in the M.tb-infected macrophages, while knockdown of miR-1178 caused enhancement in these proinflammatory cytokines in the M.tb-infected macrophage. Bioinformatics analysis and luciferase reporter assay showed that toll-like receptor 4 (TLR4) was a direct target of miR-1178, and miR-1178 negatively regulated the expression of TLR4. In addition, enforced expression of TLR4 attenuated the effects of miR-1178 overexpression on promoting the production of proinflammatory cytokines including IFN-γ, IL-6, IL-1β, and TNF-α in the M.tb-infected macrophages. Collectively, our findings showed that overexpression of miR-1178 promoted mycobacteria survival and miR-1178 also modulated the immune response of M.tb-infected macrophages partly via targeting TLR4.

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“…In guinea pig models of tuberculosis [176], MIP enhanced bacterial killing by increasing the number of antigen-presenting cells (APCs) and lymphocytes in lung tissue infected with a low dose aerosol of M. tuberculosis H37Rv. In infected peritoneal macrophages [177], it was also demonstrated that MIP significantly upregulates TLR-4 signaling, including its downstream components, indicating that MIP enhances the host immune response against tuberculosis. Furthermore, MIP activates NF-κB, resulting in increased levels of pro-inflammatory cytokines and NO production, enhancing the immune response.…”

Section: Modulators Of Autophagy For Immune Controlmentioning

confidence: 99%

Modulation of Autophagy for Controlling Immunity

Jang

Kim

Byun

2019

Cells

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Autophagy is an essential process that maintains physiological homeostasis by promoting the transfer of cytoplasmic constituents to autophagolysosomes for degradation. In immune cells, the autophagy pathway plays an additional role in facilitating proper immunological functions. Specifically, the autophagy pathway can participate in controlling key steps in innate and adaptive immunity. Accordingly, alterations in autophagy have been linked to inflammatory diseases and defective immune responses against pathogens. In this review, we discuss the various roles of autophagy signaling in coordinating immune responses and how these activities are connected to pathological conditions. We highlight the therapeutic potential of autophagy modulators that can impact immune responses and the mechanisms of action responsible.

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Mycobacterium indicus pranii (MIP) mediated host protective intracellular mechanisms against tuberculosis infection: Involvement of TLR-4 mediated signaling

Cited by 21 publications

References 36 publications

Polyamine Transport Protein PotD Protects Mice against Haemophilus parasuis and Elevates the Secretion of Pro-Inflammatory Cytokines of Macrophage via JNK–MAPK and NF–κB Signal Pathways through TLR4

Polyamine Transport Protein PotD Protects Mice against Haemophilus parasuis and Elevates the Secretion of Pro-Inflammatory Cytokines of Macrophage via JNK–MAPK and NF–κB Signal Pathways through TLR4

MiR‐1178 regulates mycobacterial survival and inflammatory responses in Mycobacterium tuberculosis‐infected macrophages partly via TLR4

Modulation of Autophagy for Controlling Immunity

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