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The Toll Road Towards NGAL Expression: Exploring the Relationship Between Activation of Toll-Like Receptors and Expression of Neutrophil Gelatinase-Associated Lipocalin (NGAL) in Inflammatory Diseases

Zijlstra, I. (2016) The Toll Road Towards NGAL Expression: Exploring the Relationship Between Activation of Toll-Like Receptors and Expression of Neutrophil Gelatinase-Associated Lipocalin (NGAL) in Inflammatory Diseases. Bachelor's Thesis, Biology.

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Abstract

Members of the lipocalin protein family are involved in the regulation of innate immune responses. One family member of particular interest is neutrophil gelatinase-associated lipocalin (NGAL): NGAL is known for its classical function to limit bacterial growth during infection by binding to bacterial siderophores. Furthermore, NGAL might have an anti-inflammatory effect, since it can be detected in a large number of inflammatory conditions in different organ systems. Regulatory mechanisms for expression of NGAL during inflammation and tissue damage are poorly understood. One potential regulatory mechanism might be mediated by Toll-like receptors (TLRs). In this review, the relationship between TLR activation and induction of NGAL expression will be investigated. The potential molecular signalling pathway of TLR activation to NGAL expression will be highlighted as well. TLRs are activated by exogenous pathogen-associated molecular patterns (PAMPs) or endogenous damage-associated molecular patterns (DAMPs), which can be present during inflammatory conditions. An important transcription factor that is activated in the TLR activation signalling pathway is nuclear factor κB (NF-κB). Since the LCN2 gene, coding for NGAL, includes an NF-κB binding site in its promoter region, NF-κB might be one of the crucial factors in regulation of NGAL expression by TLR activation. In different inflammatory conditions in a large number of organ systems, including the central nervous system, respiratory, gastrointestinal, hepatic and renal system, it was found that NGAL expression was significantly increased due to activation of TLRs by specific PAMPs or DAMPs. It was confirmed that activation of TLR2, TLR3 and TLR4 has a crucial role in induction of NGAL expression in inflammatory diseases. Important functions of NGAL include the contribution to an anti-inflammatory response during bacterial infections by binding to siderophores, thus preventing bacterial growth and dissemination through the body. Furthermore, apoptosis seems to be regulated partly by NGAL, whereas NGAL inhibits necrosis. Stimulation of apoptosis and inhibition of necrosis also contributes to an anti-inflammatory state. In conclusion, this review describes that activation of TLRs induces expression of NGAL during inflammatory conditions. NF-κB activation is the crucial factor in TLR-mediated NGAL expression.

Item Type: Thesis (Bachelor's Thesis)
Degree programme: Biology
Thesis type: Bachelor's Thesis
Language: English
Date Deposited: 15 Feb 2018 08:12
Last Modified: 15 Feb 2018 08:12
URI: http://fse.studenttheses.ub.rug.nl/id/eprint/13987

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