Volume 72, Issue 8, Pages (October 2007)

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Volume 72, Issue 8, Pages 918-925 (October 2007) Leptospirosis renal disease: Understanding the initiation by Toll-like receptors C.-W. Yang Kidney International Volume 72, Issue 8, Pages 918-925 (October 2007) DOI: 10.1038/sj.ki.5002393 Copyright © 2007 International Society of Nephrology Terms and Conditions

Figure 1 Differential induction of early inflammatory genes via TLR2 Pathway by leptospira OMP in renal proximal tubule cells. NF-κB and MAPK pathways can be activated and be inhibited by siRNA and inhibitors for each component and pathway. Kidney International 2007 72, 918-925DOI: (10.1038/sj.ki.5002393) Copyright © 2007 International Society of Nephrology Terms and Conditions

Figure 2 Leptospira induces fibrosis pathway in the tubule cells by activating TGF-β1/Smad pathway but not MAPK. The activation results in increased production of extracellular matrix in the renal tubule cells. These activations may lead to renal fibrosis in leptospirosis patients. Kidney International 2007 72, 918-925DOI: (10.1038/sj.ki.5002393) Copyright © 2007 International Society of Nephrology Terms and Conditions

Figure 3 The possible role of TLRs in initiation of kidney diseases. TLRs may be involved in the initiation of diverse renal diseases in response to exogenous and endogenous stimuli. On one hand, TLRs are the first line of defence for innate immune protection. Conversely, TLRs may act as a ‘danger signal’ by triggering inflammatory responses to stimuli when tailored immune reactions cannot adequately resolve the inflammation. The outcome may thus depend on a balanced or unbalanced immune reaction leading to either resolution or disease progression to renal fibrosis and end-stage renal disease. Kidney International 2007 72, 918-925DOI: (10.1038/sj.ki.5002393) Copyright © 2007 International Society of Nephrology Terms and Conditions