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Questions and Answers
What is the role of phospholipase A2 in the synthesis of eicosanoids?
What is the role of phospholipase A2 in the synthesis of eicosanoids?
Phospholipase A2 catalyzes the release of arachidonic acid from membrane phospholipids, initiating the synthesis of eicosanoids.
Name two types of eicosanoids derived from arachidonic acid.
Name two types of eicosanoids derived from arachidonic acid.
Prostaglandins and leukotrienes are two types of eicosanoids derived from arachidonic acid.
How do NSAIDs work in relation to the cyclooxygenase pathway?
How do NSAIDs work in relation to the cyclooxygenase pathway?
NSAIDs inhibit the cyclooxygenase (COX) enzymes, specifically blocking the formation of prostaglandins and thromboxane.
What critical role do eicosanoids play during inflammation?
What critical role do eicosanoids play during inflammation?
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What distinguishes COX-1 from COX-2 in the context of inflammation?
What distinguishes COX-1 from COX-2 in the context of inflammation?
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What are lipoxins and their significance in inflammation?
What are lipoxins and their significance in inflammation?
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Describe the significance of the metabolism of arachidonic acid.
Describe the significance of the metabolism of arachidonic acid.
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What is the function of prostacyclins in the body?
What is the function of prostacyclins in the body?
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What is the role of 5-LOX in the synthesis of inflammatory mediators?
What is the role of 5-LOX in the synthesis of inflammatory mediators?
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How do NSAIDs affect the synthesis of inflammatory mediators?
How do NSAIDs affect the synthesis of inflammatory mediators?
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What inflammatory mediators are derived from arachidonic acid through the LOX pathway?
What inflammatory mediators are derived from arachidonic acid through the LOX pathway?
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In what way do prostaglandins contribute to the inflammatory response?
In what way do prostaglandins contribute to the inflammatory response?
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What impact does blocking arachidonic acid pathways have on inflammation?
What impact does blocking arachidonic acid pathways have on inflammation?
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What is the difference between COX-1 and COX-2 in terms of their role in inflammation?
What is the difference between COX-1 and COX-2 in terms of their role in inflammation?
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Describe the synthesis and role of lipoxins in inflammation.
Describe the synthesis and role of lipoxins in inflammation.
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What is the significance of the irreversible action of aspirin compared to other NSAIDs?
What is the significance of the irreversible action of aspirin compared to other NSAIDs?
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What are the primary differences between COX-1 and COX-2 in terms of expression and tissue location?
What are the primary differences between COX-1 and COX-2 in terms of expression and tissue location?
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How do COX-1 and COX-2 differ in terms of their roles in inflammatory processes?
How do COX-1 and COX-2 differ in terms of their roles in inflammatory processes?
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What types of mediators are produced as a result of COX enzymatic activity on arachidonic acid?
What types of mediators are produced as a result of COX enzymatic activity on arachidonic acid?
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Describe the substrate that COX enzymes act upon and name one specific outcome of this enzymatic action.
Describe the substrate that COX enzymes act upon and name one specific outcome of this enzymatic action.
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What is the role of PGE2 in the inflammatory response?
What is the role of PGE2 in the inflammatory response?
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What pathway is involved in the synthesis of leukotrienes and lipoxins, and how does it relate to COX activity?
What pathway is involved in the synthesis of leukotrienes and lipoxins, and how does it relate to COX activity?
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Identify and explain the function of one inflammatory mediator produced by the COX pathways.
Identify and explain the function of one inflammatory mediator produced by the COX pathways.
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How does the location of COX-2's expression impact its function during inflammation?
How does the location of COX-2's expression impact its function during inflammation?
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Study Notes
Inflammatory Mediators
- Inflammation is the body's immune system response to stimuli, crucial for fighting harmful substances like pathogens, but uncontrolled inflammation can cause chronic disease.
- Inflammation is characterized by redness, swelling, warmth, and sometimes pain and immobility.
- Inflammation can be acute (temporary) or chronic (persistent). Acute inflammation often results from injuries, infections, or toxins, while chronic inflammation can lead to conditions like asthma and rheumatoid arthritis.
- The inflammatory process involves communication between injured tissue and the immune system, and a coordinated response that includes recruitment of immune cells to the site of damage, to help remove harmful stimuli and promote repair.
Types of Inflammatory Mediators
- Eicosanoids: Synthesized rapidly in response to stimuli, acting locally (e.g., prostaglandins and leukotrienes). A major target for pharmacological intervention.
- Complement (e.g., C3/C5): Essential early response to injury. Recognises pathogens, recruits phagocytes (cells that engulf and destroy pathogens).
- Histamine: Released by mast cells, primary mediator in allergic reactions; effects mainly occur in the blood vessels.
- Cytokines (e.g., interleukins, TNFα, TGFβ) and chemokines: Essential for the orchestration of the immune and inflammatory responses, playing a critical role in the acute inflammatory response and chronic inflammatory diseases. Secreted by various cell types like epithelial cells and immune cells.
- Other Agents: Include nitric oxide (NO) and bacterial products (e.g., LPS).
Causes of Acute Inflammation
- Injury: Physical injuries like cuts, trauma, surgical procedures, and hypoxia (lack of oxygen).
- Pathogenic: Microbial infections and parasites.
- Toxins: Toxins released by bacteria, plants, etc.
- All the above trigger an acute inflammatory response.
Acute Inflammation Process
- Dilation of blood vessels: Vasculature around injury site reacts to recruit immune cells.
- Recruitment of immune cells: Circulating immune cells migrate from vessels to the injured tissue.
- Chemotaxis: Immune cells move towards the location of the inflammation.
- Phagocytosis: Immune cells engulf and destroy harmful substances/ pathogens.
- Resolution: The inflammatory response ends, the damaged tissue heals.
Pharmacological Targets and Therapies
- Pharmacological targets in inflammation can differ based on the acute or chronic nature of the condition. Strategies focus on modulation of eicosanoids and histamine signaling.
- COX-1 and COX-2 inhibitors (NSAIDs) are commonly used. They inhibit prostaglandin synthesis.
- Leukotriene inhibitors target leukotrienes, important for inflammation and allergic responses.
- Antihistamines block histamine receptors, to help manage allergic reactions.
- Steroid-based anti-inflammatories (e.g., corticosteroids) regulate gene expression and suppress inflammation by acting on cytokines. They are commonly used.
Innate Immunity Cell Types and Their Function
- Macrophages: Phagocytose cellular and foreign debris and present antigens; link to the acquired immune response.
- Neutrophils: Phagocytose bacteria.
- Eosinophils: Defend against parasites.
- Basophils/Mast cells: Release histamine, leukotrienes, and other mediators after antigen exposure to activate an allergic response.
Summary
- Inflammation is an essential defense mechanism but can lead to chronic disease if not resolved properly.
- Acute inflammation has four key steps (dilation of vessels, recruitment, chemotaxis, phagocytosis- resolution). Inhibiting the arachidonic acid pathways can help manage the inflammation process.
- Various drugs target specific inflammatory mediators, such as cytokines, eicosanoids, and histamine, to control the inflammatory process.
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Description
This quiz delves into the role and types of inflammatory mediators in the body's immune response. Learn about the characteristics of inflammation, its acute and chronic forms, and the key mediators involved such as eicosanoids and complement proteins. Understand how these factors contribute to both healing and chronic diseases.