BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Memento EPFL//
BEGIN:VEVENT
SUMMARY:The Effect of Immune Modulation of Tuberculosis on Pathogenesis an
 d Response to TB Drugs
DTSTART:20100416T121500
DTSTAMP:20260428T020517Z
UID:06675951aca08b6b742f662df9d4cbb1d987ddce5a21b08ff9baa3fc
CATEGORIES:Conferences - Seminars
DESCRIPTION:Dr Gilla Kaplan\, Laboratory Mycobacterial Immunity and Pathog
 enesis\, Public Health Research Institute / UMDNJ\nTuberculosis (TB) cause
 d by Mycobacterium tuberculosis (Mtb) is one of the leading infectious dis
 ease causes of morbidity and mortality worldwide. Though current antibioti
 c regimens can control TB\, treatment requires at least six months to be c
 ompleted. Moreover\, the currently available TB drugs were selected for th
 eir ability to inhibit or kill growing organisms and are less effective ag
 ainst non-replicating bacilli. We hypothesized that a strong host immune r
 esponse can drive some bacilli into a non-replicating state\, thereby inad
 vertently rendering the organisms more able to withstand the activities of
  TB drugs. We predicted that selective modulation of the host immune respo
 nse to alter the environmental pressure on the bacilli would result in bet
 ter bacterial clearance during anti-TB treatment. We have demonstrate that
  adjunctive treatment of Mtb-infected mice or rabbits with an immunomodula
 tory thalidomide analog\, CC-3052\, plus the anti-TB drug isoniazid (INH) 
 improves bacillary clearance over treatment with INH alone. We show that C
 C-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.
LOCATION:SV 1717A
STATUS:CONFIRMED
END:VEVENT
END:VCALENDAR