3.1 Acute and Chronic Inflammation

Inflammation is the body's protective response to injury or infection. It involves a complex interplay of immune cells, chemical mediators, and vascular changes that work together to eliminate threats and promote healing.

Understanding the inflammatory process is crucial for grasping how the body defends itself. From acute responses like sunburns to chronic conditions like arthritis, inflammation plays a key role in health and disease, affecting multiple body systems.

Inflammatory Response Characteristics

Acute vs chronic inflammation

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• Acute inflammation
  • Short-term response manifests rapidly within minutes to hours
  • Lasts days to weeks resolving with healing or progressing to chronic state
  • Neutrophils dominate cellular response engulfing pathogens and debris
  • Characterized by rapid onset and resolution (sunburn, minor cuts)
• Chronic inflammation
  • Long-term response develops slowly over days to years
  • Persists for months to years causing ongoing tissue damage and repair
  • Lymphocytes and macrophages predominate mediating adaptive immunity
  • Results in prolonged inflammation (rheumatoid arthritis, atherosclerosis)

Cardinal signs of inflammation

• Five cardinal signs
  • Rubor redness due to increased blood flow
  • Calor heat from elevated metabolic activity and blood flow
  • Tumor swelling caused by fluid accumulation in tissues
  • Dolor pain from nerve ending stimulation by inflammatory mediators
  • Functio laesa loss of function due to pain, swelling, and tissue damage
• Physiological explanations
  • Redness and heat result from vasodilation increasing blood flow to affected area
  • Swelling occurs as vascular permeability increases allowing fluid accumulation
  • Pain arises when chemical mediators stimulate local nerve endings
  • Loss of function stems from combined effects of pain, swelling, and tissue injury

Inflammatory Process Mechanisms

Immune cells in inflammation

• Key immune cells
  • Neutrophils arrive first performing phagocytosis of pathogens and debris
  • Macrophages engulf pathogens and present antigens to adaptive immune cells
  • Lymphocytes coordinate adaptive immune responses (T cells, B cells)
  • Mast cells release histamine and other mediators triggering early inflammatory response
• Chemical mediators
  • Histamine causes vasodilation and increased vascular permeability
  • Prostaglandins promote vasodilation and sensitize pain receptors
  • Leukotrienes guide chemotaxis and increase vascular permeability
  • Cytokines facilitate cell signaling and regulate immune responses
  • Complement proteins enhance opsonization and induce cell lysis
• Vascular changes
  • Vasodilation increases blood flow to affected area
  • Increased permeability allows fluid and protein exudation into tissues
• Cellular events
  1. Margination leukocytes adhere to vessel walls
  2. Diapedesis leukocytes migrate through vessel walls into tissues
  3. Chemotaxis directs leukocyte movement towards inflammatory stimuli

Systemic effects of inflammation

• Fever
  • Pyrogens (IL-1, TNF-α) elevate body temperature
  • Increases metabolic rate and oxygen consumption
• Acute phase response
  • Liver produces acute phase proteins
  • C-reactive protein enhances opsonization and activates complement
  • Fibrinogen increases blood viscosity and clotting risk
• Leukocytosis
  • Elevated white blood cell count in circulation
• Fatigue and malaise
  • Energy redirected to support immune response
• Anorexia
  • Decreased appetite from cytokine effects on hypothalamus
• Muscle protein catabolism
  • Muscle breakdown provides energy and materials for acute phase proteins
• Neuroendocrine changes
  • Increased cortisol production modulates inflammation
  • Altered insulin sensitivity affects glucose metabolism
• Anemia of chronic disease
  • Decreased red blood cell production and iron sequestration
• Cachexia
  • Severe weight loss and muscle wasting in prolonged inflammation (cancer)