Abstract

Curcumin, the bioactive component of turmeric also known as “Indian Yellow Gold,” exhibits therapeutic efficacy against several chronic inflammatory and infectious diseases. Even though considered as a wonder drug pertaining to a myriad of reported benefits, the translational potential of curcumin is limited by its low systemic bioavailability due to its poor intestinal absorption, rapid metabolism, and rapid systemic elimination. Therefore, the translational potential of this compound is specifically challenged by bioavailability issues, and several laboratories are making efforts to improve its bioavailability. We developed a simple one-step process to generate curcumin nanoparticles of ~200 nm in size, which yielded a fivefold enhanced bioavailability in mice over regular curcumin. Curcumin nanoparticles drastically reduced hepatotoxicity induced by antitubercular antibiotics during treatment in mice. Most interestingly, co-treatment of nanoparticle-formulated curcumin along with antitubercular antibiotics dramatically reduced the risk for disease reactivation and reinfection, which is the major shortfall of current antibiotic treatment adopted by Directly Observed Treatment Short-course. Furthermore, nanoparticle-formulated curcumin significantly reduced the time needed for antibiotic therapy to obtain sterile immunity, thereby reducing the possibility of generating drug-resistant variants of the organisms. Therefore, adjunct therapy of nano-formulated curcumin with enhanced bioavailability may be beneficial to treatment of tuberculosis and possibly other diseases.

Highlights

  • Tuberculosis (TB) remains a major global health problem that claims ~2 million lives and causes 9.6 million infections every year [1]

  • which have a uniform size of ~200 nm

  • More than 90% of people exposed to Mycobacterium tubercu­ losis

Read more

Summary

Introduction

Tuberculosis (TB) remains a major global health problem that claims ~2 million lives and causes 9.6 million infections every year [1]. The vast majority of infected individuals successfully eliminates the harbored M.tb organisms and remains resistant to TB throughout life [5, 6]. Taken together, these observations suggest that the immune system can effectively control M.tb infection. IL-4-producing Th2 cells and regulatory T (Treg) cells promote disease progression by inhibiting Th1 responses [9,10,11,12,13]. We recently showed that Stat-6−/−TGF-βRIIDN animals, which are devoid of Th2 cells and contain reduced numbers of functional Treg cells, mount exuberant inflammatory Th1 responses and display suppressed bacterial burden, yet this response was not sufficient to induce sterile immunity [9]. Immunotherapy directed toward promoting Th1-mediated inflammatory responses may not be sufficient for achieving sterile immunity

Methods
Results
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.