TY - JOUR
T1 - Mycobacterium indicus pranii (MIP) mediated host protective intracellular mechanisms against tuberculosis infection
T2 - Involvement of TLR-4 mediated signaling
AU - Das, Shibali
AU - Chowdhury, Bidisha Paul
AU - Goswami, Avranil
AU - Parveen, Shabina
AU - Jawed, Junaid
AU - Pal, Nishith
AU - Majumdar, Subrata
N1 - Funding Information:
This work was supported by Council of Scientific and Industrial Research (CSIR) , New Delhi and Bose Institute , DST funded institute , Govt. of India .
Funding Information:
We are thankful to The Director, Bose institute for providing the research facilities. We are grateful to the Council of Scientific and Industrial Research, New Delhi, India for providing Senior Research Fellowship to Shibali Das.
Publisher Copyright:
© 2016
PY - 2016/12/1
Y1 - 2016/12/1
N2 - 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.
AB - 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.
KW - Cytokine
KW - MAP kinase
KW - Mycobacterium indicus pranii
KW - TLR-4
KW - Tuberculosis
UR - http://www.scopus.com/inward/record.url?scp=84994344458&partnerID=8YFLogxK
U2 - 10.1016/j.tube.2016.09.027
DO - 10.1016/j.tube.2016.09.027
M3 - Article
C2 - 27865392
AN - SCOPUS:84994344458
SN - 1472-9792
VL - 101
SP - 201
EP - 209
JO - Tuberculosis
JF - Tuberculosis
ER -