The Effect of Immune Modulation of Tuberculosis on Pathogenesis and Response to TB Drugs
Event details
| Date | 16.04.2010 |
| Hour | 12:15 |
| Speaker | Dr Gilla Kaplan, Laboratory Mycobacterial Immunity and Pathogenesis, Public Health Research Institute / UMDNJ |
| Location |
SV 1717A
|
| Category | Conferences - Seminars |
Tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb) is one of the leading infectious disease causes of morbidity and mortality worldwide. Though current antibiotic regimens can control TB, treatment requires at least six months to be completed. Moreover, the currently available TB drugs were selected for their ability to inhibit or kill growing organisms and are less effective against non-replicating bacilli. We hypothesized that a strong host immune response can drive some bacilli into a non-replicating state, thereby inadvertently rendering the organisms more able to withstand the activities of TB drugs. We predicted that selective modulation of the host immune response to alter the environmental pressure on the bacilli would result in better bacterial clearance during anti-TB treatment. We have demonstrate that adjunctive treatment of Mtb-infected mice or rabbits with an immunomodulatory thalidomide analog, CC-3052, plus the anti-TB drug isoniazid (INH) improves bacillary clearance over treatment with INH alone. We show that CC-3052 treatment results in smaller granulomas and reduced lung pathology, compared to treatment with INH alone. We suggest that the combination of an anti-TB drug with an immune modulating molecule is a novel strategy to shorten the duration of TB treatment and improve treatment outcome.
Links
Practical information
- General public
- Free
Organizer
- Stewart Cole
Contact
- Caroline Guinchard