Molecular therapy for tuberculosis: MiRNA-494-3p increases the expression of MKP-1, inhibits TLR2 signalling, secretion of Chemokine CXCL5, and recruitment of polymorphonuclear leukocytes (PMNs), decreases destructive pulmonary inflammation, promotes M. tuberculosis clearance and inhibits pulmonary tuberculosis via up-regulation of its target gene, 30/January/2017, 5.30 am

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IntroductionWhat they say

A study from the Max Plank Institute for Infection Biology, Berlin, Germany shows that “CXCL5-secreting pulmonary epithelial cells drive destructive neutrophilic inflammation in tuberculosis.” This study was published in the 10 February 2014 issue of the“Journal of Clinical Investigation” [One of the best research journals in clinical medicine with an impact factor of 12.575] by Prof. Stefan H.E. Kaufman MJ, Geraldine Nouailles, and others.


What we say: 

price-100

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for tuberculosis: MiRNA-494-3p increases the expression of MKP-1, inhibits TLR2 signalling, secretion of Chemokine CXCL5, and recruitment of polymorphonuclear leukocytes (PMNs), decreases destructive pulmonary inflammation, promotes M. tuberculosis clearance and inhibits pulmonary tuberculosis via up-regulation of its target gene


What is known? 

Prof. Stefan Kaufman’s research team has shown earlier that knockdown of CXCL5 in mice inhibits recruitment of polymorphonuclear leukocytes, decreases pulmonary inflammation and inhibits the progression of pulmonary tuberculosis.


From Significance to Public health relevance:

Given that: (1) nearly 2.5 billion people out of 7.4 billion total world population are infected with M. tuberculosis; (2) majority of population in Asian and African countries test positive in tuberculin tests; (3) molecular pathways involved and the mechanism of development of drug-resistant tuberculosis is far from understood; (4) treating drug-resistant tuberculosis is still a daunting task; (5) tuberculosis is the second-leading cause of death–first being the HIV–due to an infectious disease; (6) in 2010, out of the 88 lakhs patients test positive for TB, 14.5 lakhs patients died; (7) billions of dollars are being spent each year globally for the treatment of tuberculosis; and (8) most of the TB cases are registered in developing countries—that cannot afford high-cost required for the treatment of drug-resistant TB—compared to developed countries, there is an urgent need to find: (i) a way to inhibit drug-resistant tuberculosis; (ii) a cheaper alternative to the existing expensive drugs; and (iii) a side-effect-free-Natural product-based drug that prevents relapse/recurrence of drug-resistant TB.


 From Research Findings to Therapeutic opportunity

This study suggests an MiRNA-based therapy for life-threatening tuberculosis. MiRNA-494-3p, by decreasing the expression of its target gene, it may: (1) inhibit TLR-2 expression; (2) increase the expression of phosphatase MKP-1; (3) suppress the expression of Chemokine CXCL5 (C-X-C Motif Chemokine Ligand 5); (4) inhibit the recruitment of polymorphonuclear leukocytes; (5) decrease lung inflammation/injury; (6) promote clearance of M.tuberculosis; and (7) inhibit the progression of pulmonary tuberculosis. Together, pharmacological formulations encompassing MiRNA-4943p activators may be used to treat pulmonary tuberculosis.


Details of the research findings

Idea Proposed/Formulated by: Dr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Undisclosed information: How MiRNA-494-3p: (1) increases the expression of MKP-1; (2) inhibits TLR-2 signaling; and (3) inhibits Chemokine CXCL5 expression

Amount: $100

# Research cooperation


References:

Web: http://genomediscovery.org or http://newbioideas.com

Citation: Boominathan, L.,  Molecular therapy for tuberculosis: MiRNA-494-3p increases the expression of MKP-1, inhibits TLR2 signalling, secretion of Chemokine CXCL5, and recruitment of polymorphonuclear leukocytes (PMNs), decreases destructive pulmonary inflammation, promotes M. tuberculosis clearance and inhibits pulmonary tuberculosis via up-regulation of its target gene, 30/January/2017, 5.30 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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