Signaling mechanism inflammatory response

Harmon EB, Porter JM, Porter JE (2005) Beta-adrenergic receptor activation in immortalized human urothelial cells stimulates inflammatory responses by PKA-independent mechanisms. Cell Commun. Signal. 3 10. 

The failure of antioxidant mechanisms to correct redox disequilibrium could lead to the escalation of oxidative to tier 2. Tier 2 cellular responses are characterized by the activation of cellular signaling pathway such as stress-activated kinases (p38 MAP kinase and JNK) along with activation and nuclear translocation of transcription factors NF-kB and STAT-1. NF-KB-induced transcriptional activation leads to the production of a number of pro-inflammatory cytokines, including the neutrophil chemoattractant IL-8. STAT-1 activation stimulates the increased production of CXC-motif chemokines that function in lymphocyte recruitment and activation. Therefore, tier 2 oxidative responses result in an inflammatory response in the lung. 

Excessive inflammatory responses may result from inappropriate cellular signaling. On the other hand, inflammation is normally a protective response, and its lack can lead to increased susceptibility to infections. Dysregulation of cellular division can lead to neoplasia or aplasia. Neoplastic changes reflect a dysregulation of cell growth, whether from failure of apoptosis or other mechanisms. 

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