02809nas a2200529 4500000000100000008004100001260005600042653001500098653001000113653002500123653003200148653002300180653003000203653001100233653002000244653002000264653001100284653002500295653001200320653000900332653002300341653001600364653001700380653002500397653002500422653001600447100001500463700001600478700001700494700001300511700001600524700001600540700001300556700001600569700001300585700001900598700001200617700001300629700001200642700001400654700001600668245017100684300001000855490000800865520139200873022001402265 2012 d c2012 Jul bBlackwell Scientific Publications aOxford 10 aAdolescent 10 aAdult 10 aAnalysis of Variance 10 aAntibiotics, Antitubercular 10 aDNA, Complementary 10 aDrug Therapy, Combination 10 aFemale 10 aGene Expression 10 aGlucocorticoids 10 aHumans 10 aImmunohistochemistry 10 aleprosy 10 aMale 10 aMethylprednisolone 10 aMiddle Aged 10 aPrednisolone 10 aToll-Like Receptor 2 10 aToll-Like Receptor 4 10 aYoung Adult 1 aWalker S L 1 aRoberts C H 1 aAtkinson S E 1 aKhadge S 1 aMacdonald M 1 aNeupane K D 1 aRanjit C 1 aSapkota B R 1 aDhakal S 1 aHawksworth R A 1 aMahat K 1 aRuchal S 1 aHamal S 1 aHagge D A 1 aLockwood DN 00 aThe effect of systemic corticosteroid therapy on the expression of toll-like receptor 2 and toll-like receptor 4 in the cutaneous lesions of leprosy Type 1 reactions. a29-35 0 v167 3 aBACKGROUND: Leprosy is complicated by immunological reactions which can occur before, during and after successful completion of multidrug therapy. Genetic studies have suggested that polymorphisms in toll-like receptors (TLRs) may affect the susceptibility of an individual with leprosy to developing Type 1 reactions.
OBJECTIVES: To examine the gene and protein expression of TLRs in the cutaneous lesions of leprosy Type 1 reactions at the onset of reaction and during systemic corticosteroid therapy.
METHODS: Patients who were being treated for leprosy type 1 reactions with corticosteroids as part of a randomized controlled trial of corticosteroid treatment had skin biopsies performed before, during and at the end of treatment. The gene and protein expression of TLR2 and TLR4 were measured.
RESULTS: We have demonstrated that the gene hARP-P0 is a suitable control gene for TLR gene expression studies in this population. The gene and protein expression of TLR2 and TLR4 were both reduced significantly during corticosteroid treatment.
CONCLUSIONS: This is the first study to examine the expression of TLR2 and TLR4 in vivo in individuals experiencing leprosy Type 1 reactions. The data support the possibility of an important role for TLR2 and TLR4 in the pathogenesis of this important complication of leprosy.
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