Inflammation is a complex biological and pathophysiological response induced by infection and/or tissue damage and involves a network of pro- and anti-inflammatory mediating molecules and effects. The inflammatory response to a wide range of stimuli is a “double edged sword.” In its absence homeostasis cannot be resumed. On the other hand, inflammation may cause tissue damage, reversible or permanent, and induces disease processes. Inflammation involves a harmonized, consecutive, and often self-limiting sequence of events controlled by positive and negative regulatory networks. Thus, the molecular networks that regulate the initiation, spread, and resolution of inflammation must be appropriately tuned for optimization of the innate immune response. Besides protein regulatory factors, miRNAs have emerged as key regulators of inflammation, and it is likely that they modulate signaling of onset and termination of inflammation. Depending upon the target mRNAs, miRNAs may either promote or suppress inflammation. There-fore, the immune system utilizes multiple miRNAs to properly regulate its functional capacity thus establishing a fine balance between activation and inhibition. The interaction between miRNA function and inflammatory response is highlighted because this interaction can contribute to a better understanding on how depletion or downregulated immune homeostasis can be associated with autoimmunity conditions.
The regulation of inflammation by miRNAs is primarily through altered expression of specific miRNAs in stimulated immune- or bystander cells. There is also evidence that the biogenesis of miRNAs is regulated as part of the inflammatory response, by altering the transcription, processing or stabilization of mature or precursor miRNA transcripts. The initiation, spread, and resolution steps of inflammation are subject to both positive and negative regulatory events via miRNAs. The positive feedback initiates a cascade of molecular events that serve to combat against invasion of microbial pathogens and successful repair of tissue damage. The negative feedback, which is activated only during severe inflammation, is vital for preventing potentially damaging end-stage processes and maintaining tissue homeostasis.
Inflammation is a complex biological and pathophysiological response induced by infection and/or tissue damage and involves a network of pro- and anti-inflammatory mediating molecules and effects. The inflammatory response to a wide range of stimuli is a “double edged sword.” In its absence homeostasis cannot be resumed. On the other hand, inflammation may cause tissue damage, reversible or permanent, and induces disease processes. Inflammation involves a harmonized, consecutive, and often self-limiting sequence of events controlled by positive and negative regulatory networks. Thus, the molecular networks that regulate the initiation, spread, and resolution of inflammation must be appropriately tuned for optimization of the innate immune response. Besides protein regulatory factors, miRNAs have emerged as key regulators of inflammation, and it is likely that they modulate signaling of onset and termination of inflammation. Depending upon the target mRNAs, miRNAs may either promote or suppress inflammation. There-fore, the immune system utilizes multiple miRNAs to properly regulate its functional capacity thus establishing a fine balance between activation and inhibition. The interaction between miRNA function and inflammatory response is highlighted because this interaction can contribute to a better understanding on how depletion or downregulated immune homeostasis can be associated with autoimmunity conditions.
The regulation of inflammation by miRNAs is primarily through altered expression of specific miRNAs in stimulated immune- or bystander cells. There is also evidence that the biogenesis of miRNAs is regulated as part of the inflammatory response, by altering the transcription, processing or stabilization of mature or precursor miRNA transcripts. The initiation, spread, and resolution steps of inflammation are subject to both positive and negative regulatory events via miRNAs. The positive feedback initiates a cascade of molecular events that serve to combat against invasion of microbial pathogens and successful repair of tissue damage. The negative feedback, which is activated only during severe inflammation, is vital for preventing potentially damaging end-stage processes and maintaining tissue homeostasis.
