Acute Inflammatory Response: The Chemistry, Molecular Signals and Regulatory Networks | ||||
| Egyptian Journal of Chemistry | ||||
| Articles in Press, Accepted Manuscript, Available Online from 05 September 2025 | ||||
| Document Type: Review Articles | ||||
| DOI: 10.21608/ejchem.2025.390958.11850 | ||||
 View on SCiNiTO | ||||
| Author | ||||
Maged Essa ALhawsawi 
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| National Guard Prince Mohammad Bin Abdulaziz Hospital, Health Information System, Ministry of health, Saudi Arabia | ||||
| Abstract | ||||
| Background: Acute inflammation is a fundamental component of the innate immune system, serving as the body's immediate response to harmful stimuli, whether infectious or noninfectious. It is characterized by five cardinal signs—redness, heat, swelling, pain, and loss of function—resulting from vascular, cellular, and molecular changes. While acute inflammation is protective, dysregulation can lead to chronic inflammation or systemic complications such as septic shock. Aim: This article explores the biochemical, molecular, and genetic mechanisms underlying acute inflammation, its clinical manifestations, and its role in various organ-specific pathologies. It also highlights key inflammatory markers used in diagnosis and management. Methods: A comprehensive review of inflammatory pathways, including toll-like receptor (TLR) signaling, arachidonic acid metabolism, mast cell activation, and complement system involvement, was conducted. Clinical correlations in cardiovascular, pancreatic, hepatic, renal, and gastrointestinal diseases were examined, along with diagnostic biomarkers such as C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and procalcitonin (PCT). Results: Acute inflammation involves a complex interplay of mediators (cytokines, chemokines, prostaglandins) and immune cells (neutrophils, macrophages). Dysregulation contributes to chronic conditions like atherosclerosis, pancreatitis, and inflammatory bowel disease. CRP, ESR, and PCT serve as valuable diagnostic tools, with CRP being the most sensitive acute-phase reactant. Conclusion: Understanding the mechanisms of acute inflammation is crucial for developing targeted therapies that enhance its protective effects while minimizing tissue damage. Future research should focus on modulating inflammatory pathways to prevent progression to chronic disease. | ||||
| Keywords | ||||
| Acute inflammation; innate immunity; cytokines; CRP; TLR signaling; inflammatory biomarkers; organ-specific inflammation | ||||
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