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Since many inflammatory responses are beneficial, directing and instructing the inflammatory machinery may be a better therapeutic objective than suppressing it.
The ELR+ CXC chemokines are critical for protective neutrophil responses to most bacterial infections, but nevertheless can contribute importantly to the pathogenic effects of many inflammatory responses.
Marked oxidative stress has been consistently reported in patients with sepsis and acts as a trigger for up-regulation of many inflammatory responses.
Complement and FcγRs act in concert in many inflammatory responses, with complement both attracting and activating FcγR-bearing cells at sites of inflammation.
We focused on examining the activity of NF-κB and AP-1, two families of transcription factors that regulate the activation of iNOS and COX-2 genes and are critical in many inflammatory responses [ 28, 29].
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Furthermore, many inflammatory response-related genes have potential xenobiotic-responsive elements (XREs) embedded in upstream sequences.
Most of the immune cells respond to such modulation, and many inflammatory response-related genes contain multiple xenobiotic-responsive elements (XREs) boxes upstream.
Ligand binding to TLR9 results in the recruitment of adaptor proteins, MyD88, to ultimately lead to the activation of NF-κB, a key regulator of many inflammatory response pathways [8].
Many inflammatory response gene transcripts are inherently unstable as a mechanism to control cellular response to certain stimuli [ 18].
The promoters of many inflammatory response genes, especially those encoding cytokines and chemokines, have functional AP-1 binding sites [ 6].
The degradation of IκBs facilitates the migration of NF-κB into the nucleus, where they typically form homodimers or heterodimers that bind to the promoters of many inflammatory response genes and activate transcription [ 14, 15].
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