Interplay between Cellular and Molecular Mechanisms Underlying Inflammatory Bowel Diseases Development-A Focus on...

Area of Science:

• Gastroenterology
• Immunology
• Molecular Biology

Background:

• Inflammatory bowel diseases (IBD) are characterized by chronic gastrointestinal inflammation.
• Increased intestinal pathogens trigger inflammasome assembly, a key immune response.
• While protective, excessive inflammasome activation, particularly NLRP3, drives pro-inflammatory cytokine production.

Purpose of the Study:

• To review the cellular and molecular mechanisms driving inflammation in ulcerative colitis (UC).
• To elucidate the role of inflammasome activation and non-coding RNAs in IBD pathogenesis.

Main Methods:

• Literature review of cellular and molecular mechanisms in UC.
• Analysis of inflammasome pathways, autophagy, unfolded protein response, and non-coding RNAs (miRNAs, lncRNAs).

Main Results:

• Excessive nucleotide-binding oligomerization domain-like receptor and pyrin domain-containing protein 3 (NLRP3) inflammasome assembly leads to high pro-inflammatory cytokine synthesis.
• Autophagy and unfolded protein response pathways are activated to restore homeostasis.
• Aberrant expression of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) significantly impacts IBD mechanisms.

Conclusions:

• Understanding these pathways is crucial for IBD management.
• Targeting inflammasomes and non-coding RNAs may offer therapeutic strategies for UC.