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TLRs can be viewed as crucial surveillance receptors for innate

TLRs are highly conserved receptors that have been implicated in the immune response to a variety of pathogens. TLRs detect exogenous microbial components, which can lead to the induction of innate immune responses (1) and the development of antigen-specific adaptive immunity (2). Interestingly, over the past few years, it has become clear that TLRs also recognize endogenous host material that is released during cellular injury, such as degradation products of macromolecules, products of proteolytic cascades, intracellular components of ruptured cells, and products of genes that are activated by inflammation (3). In this way, TLRs can be viewed as crucial surveillance receptors for innate and adaptive immunity to detect tissue damage, infection, and remodeling (4). Whereas TLRs are preferentially expressed on antigen-presenting cells, recent observations suggest that these receptors are also expressed on cells that are traditionally not regarded as being involved in host defense. Indeed, the majority of TLR2 mRNA in the kidney is constitutively expressed on renal tubular epithelial cells (TECs) and epithelial cells from the Bowman capsule in the murine kidney and is markedly enhanced on these cells upon renal ischemic injury (5). The functional significance of this upregulation, however, remains unknown. Interestingly, the endogenous cellular injury signals that can activate TLR2, such as heat shock proteins (6), and the contents of necrotic cells (7) are known to accumulate upon renal ischemic tissue injury (8, 9).

Following injury of TECs in renal ischemia, a cascade of proinflammatory mediators that can lead to amplification of injury either directly or indirectly is activated. The primary mechanism through which the kidney initiates this inflammatory cascade has, however, not yet been elucidated. As TECs belong to the nonimmune cells that express and upregulate TLR2 after ischemic injury, it might be hypothesized that this TEC-associated receptor plays a key role in the initiation of inflammation after renal ischemia. In support of this, the role of TLR2 in chemokine production by mouse renal TECs after stimulation with bacterial products in vitro has already been reported (10). Since renal ischemia is a major cause of acute (11) and end-stage renal failure (12), producing serious morbidity and mortality, and in addition is an important inducer of acute renal transplant rejection and delayed allograft function (13, 14), improved knowledge of the primary mechanisms involved in monitoring and mediating renal ischemia/reperfusion (I/R) injury is essential for the development of therapeutic strategies. The activation of TLR by ligands released during I/R injury may be an important link between an inflammatory immune response in the kidney and damage in this organ and in addition might trigger renal allograft rejection by activating innate and adaptive immune responses.

Together, these data prompted us to investigate the role of TLR2 in ischemic injury and repair in the kidney. For this, we induced renal I/R injury in TLR2-/- or TLR2+/+ mice, chimeric mice deficient in leukocyte or renal TLR2, and analyzed the subsequent pathophysiology. In addition, we evaluated the therapeutic potential of TLR2 antisense therapy for the treatment of renal ischemia as these nucleotides are known to be taken up mainly by the kidney, i. e., TECs.

Tuesday, 23-Aug-2011 06:58

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Thursday, 18-Aug-2011 08:50

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Wednesday, 17-Aug-2011 03:25

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Wednesday, 17-Aug-2011 03:21

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Tuesday, 16-Aug-2011 09:48

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Monday, 15-Aug-2011 09:29

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