Mycobacterium indicus pranii (MIP) mediated host protective intracellular mechanisms against tuberculosis infection: Involvement of TLR-4 mediated signaling
| Autor: | Nishith Kumar Pal, Shabina Parveen, Shibali Das, Junaid Jibran Jawed, Avranil Goswami, Subrata Majumdar, Bidisha Paul Chowdhury |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Microbiology (medical) Tuberculosis medicine.medical_treatment Mycobacterium indicus pranii Immunology Dose-Response Relationship Immunologic Microbial Sensitivity Tests Nitric Oxide p38 Mitogen-Activated Protein Kinases Microbiology Mycobacterium tuberculosis 03 medical and health sciences 0302 clinical medicine Immune system medicine Animals 030212 general & internal medicine Pathogen Cells Cultured Innate immune system biology Nontuberculous Mycobacteria medicine.disease biology.organism_classification Up-Regulation Mice Inbred C57BL Toll-Like Receptor 4 030104 developmental biology Infectious Diseases Cytokine Macrophages Peritoneal TLR4 Cytokines Signal Transduction |
| Zdroj: | Tuberculosis. 101:201-209 |
| ISSN: | 1472-9792 |
| DOI: | 10.1016/j.tube.2016.09.027 |
| Popis: | Mycobacterium tuberculosis infection inflicts the disease Tuberculosis (TB), which is fatal if left untreated. During M. tuberculosis infection, the pathogen modulates TLR-4 receptor down-stream signaling, indicating the possible involvement of TLR-4 in the regulation of the host immune response. Mycobacterium indicus pranii (MIP) possesses immuno-modulatory properties which induces the pro-inflammatory responses via induction of TLR-4-mediated signaling. Here, we observed the immunomodulatory properties of MIP against tuberculosis infection. We have studied the detailed signaling mechanisms employed by MIP in order to restore the host immune response against the in vitro tuberculosis infection. We observed that in infected macrophages MIP treatment significantly increased the TLR-4 expression as well as activation of its downstream signaling, facilitating the activation of P38 MAP kinase. MIP treatment was able to activate NF-κB via involvement of TLR-4 signaling leading to the enhanced pro-inflammatory cytokine and NO generation in the infected macrophages and generation of protective immune response. Therefore, we may suggest that, TLR4 may represent a novel therapeutic target for the activation of the innate immune response during Tuberculosis infection. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect