Differential Roles of Toll-like Receptor (TLR) 2 and 4 between PPD- and 38-kDa-induced Proinflammatory Cytokine Productions in Human Monocytes.
- Author:
Saet Byel JUNG
1
;
Ji Sook LEE
;
Chul Su YANG
;
Chang Hwa SONG
;
Kil Soo LEE
;
Hwa Jung KIM
;
Jeong Kyu PARK
;
Tae Hyun PAIK
;
Eun Kyeong JO
Author Information
- Publication Type:Original Article
- Keywords: PPD antigen; 38-kDa antigen; Monocyte; TNF-alpha; IL-6; MAPK; Mycobacterium tuberculosis
- MeSH: Antibodies; Humans*; Interleukin-6; Interleukins; Monocytes*; Mycobacterium tuberculosis; Phosphotransferases; Protein Kinases; Toll-Like Receptors*; Tuberculosis; Tumor Necrosis Factor-alpha
- From:Journal of Bacteriology and Virology 2007;37(1):11-21
- CountryRepublic of Korea
- Language:Korean
- Abstract: In this study, we investigated the role of toll-like receptor (TLR) and mitogen-activated protein kinase (MAPK) pathways involved in the tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 expression after stimulation with purified protein derivatives (PPD) or native 38-kDa protein antigen (Ag) of Mycobacterium tuberculosis H37Rv in human primary monocytes. Both PPD and 38-kDa Ag significantly induced TNF-alpha and IL-6 in human primary monocytes. MAPK [extracellular signal-regulated kinase (ERK) 1/2 and p38] are rapidly phosphorylated in human monocytes stimulated with the PPD or 38-kDa Ag. Both p38 and ERK 1/2 activation are essential for PPD- or 38-kDa-induced TNF-alpha and IL-6 production. The inhibition of TLR2 and TLR4 by specific antibodies significantly abrogated the 38-kDa-induced secretion of TNF-alpha and IL-6, whereas blockade of TLR2, but not TLR4, was responsible for the PPD-induced TNF-alpha and IL-6 production in human monocytes. Collectively, these data suggest that the PPD and 38-kDa Ag differentially interact with TLR2 and TLR4, which in turn mediate an essential role for the early inflammatory immune responses during human tuberculosis.
