Abstract
Acute inflammation, an integral part of host defence and immunity, is a highly conserved cellular response to pathogens and other harmful stimuli. An inflammatory stimulation triggers transcriptional activation of selective pro-inflammatory genes that carry out specific functions such as anti-microbial activity or tissue healing. Based on the nature of inflammatory stimuli, an extensive exploitation of selective transcriptional activations of pro-inflammatory genes is performed by the host to ensure a defined inflammatory response. Inflammatory signal transductions are initiated by the recognition of inflammatory stimuli by transmembrane receptors, followed by the transmission of the signals to the nucleus for differential gene activations. The differential transcriptional activation of pro-inflammatory genes is precisely controlled by the selective binding of transcription factors to the promoters of these genes. Among a number of transcription factors identified to date, NF-κB still remains the most prominent and studied factor for its diverse range of selective transcriptional activities. Differential transcriptional activities of NF-κB are dictated by post-translational modifications, specificities in dimer formation, and variability in activation kinetics. Apart from the differential functions of transcription factors, the transcriptional activation of selective pro-inflammatory genes is also governed by chromatin structures, epigenetic markers, and other regulators as the field is continuously expanding.
Highlights
The survival of all living organisms relies on their ability to respond to a wide range of harmful stimuli such as microbial infection, environmental stresses, and tissue injures
Inflammatory stimuli activate transcriptional repressive pathways. An example of this is the post-translational modification of promyelocytic leukaemia zinc finger protein (PLZF) in response to Toll-like receptors (TLRs) or tumour necrosis factor alpha (TNF-)α signaling, which results in calcium/calmodulin-dependent protein kinase (CaMK2) activation of the type-B histone acetylase-1 (HAT1) and acetylation of PLZF
We have recently reported that integrin-linked kinase (ILK) mediates pro-inflammatory cytokine TNF- production by modulating phosphorylation of NF-B p65 at Ser536 in response to pathogenic microorganisms [42]
Summary
The survival of all living organisms relies on their ability to respond to a wide range of harmful stimuli such as microbial infection, environmental stresses, and tissue injures. The inflammatory response triggers transcriptional activation of numerous genes, which carry out diverse physiological functions ranging from initiation of antimicrobial activities to the development of acquired immunity. Some of these gene products, such as antimicrobial peptides, directly target pathogenic microorganisms, while others, such as inflammatory cytokines and chemokines, activate the host defence by recruiting immune cells to the site of infection, as well as initiating healing of the injured tissues. Due to the enormous variety of pathogenic microorganisms and harmful stimuli routinely experienced by an organism, the inflammatory response involves an extensive exploitation of the transcriptional activation of selective genes intended for specific antimicrobial defence and tissue repairs. Since the latter has been reviewed in detail elsewhere [2], it will not be discussed further in this article
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