Acute and chronic inflammation - Semantic Scholar...Inflammation • Components of the inflammatory...
Transcript of Acute and chronic inflammation - Semantic Scholar...Inflammation • Components of the inflammatory...
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Outline • Introduction to inflammation • Acute inflammation – Clinical examples of acute inflammation
• Chronic inflammation – Clinical examples of chronic inflammation
• Leukocyte activation and mechanisms of microbial killing
• Chemical mediators of inflammation
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Inflammation • A protective response involving host cells,
blood vessels and proteins – Goals are: • eliminate the initial cause of cell injury • Remove necrotic cells and tissue • Initiate the process of repair
• Also a potentially harmful process – Components of inflammation that are capable of
destroying microbes can also injury bystander normal tissue
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Inflammation • Components of the inflammatory process
include white blood cells and plasma proteins – Normally present in the blood – The inflammatory reaction’s goal is to bring these
to the site of infection and/or tissue damage • Inflammation is induced by chemical
mediators produced by damaged host cells – Cytokines and other mediators
• Inflammation is normally controlled and self-limited
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Excess inflammatory reactions • Inappropriate
inflammatory response when there are no foreign substances to fight off leads to autoimmunity
• Inflammatory process must be tightly regulated by the immune system to avoid excessive tissue damage and spillover to normal tissue
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Cardinal signs of inflammation • Heat (calor) • Redness (rubor) • Swelling (tumor) • Pain (dolor) – Celsus, De Medicina – Roman encyclopedia of
medicine, >2000 years ago
• Loss of function – Rudolf Virchow (“father
of modern pathology”) – Late 19th century
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Robbins Basic Pathology, 9th Ed.
Components of acute and chronic inflammation
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Acute vs. Chronic inflammation
Robbins Basic Pathology, 9th Ed.
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Acute inflammation
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Stimuli for Acute Inflammation
• Infections (bacterial, viral, fungal, parasitic) & microbial toxins
• Tissue necrosis: ischemia, trauma, physical or chemical injury (e.g., thermal injury; irradiation; some environmental chemicals)
• Foreign bodies (splinters, dirt, sutures) • Immune reactions (aka hypersensitivity
reactions)
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• Main components: – Vascular changes • Vasodilation • Vascular permeability • Increased adhesion of
white blood cells – Cellular events • Cellular recruitment
and activation of neutrophils (polymorphonuclear leukocytes)
Robbins Basic Pathology, 9th Ed.
Acute inflammation
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Acute Inflammation 1. Vasodilation:
- The reactions of blood vessels - Alterations in vascular caliber (diameter)
- Causes decrease in blood pressure
2. Vascular leakage and edema: - The accumulation of fluid and proteins of plasma in the extravascular tissues (interstitium)
3. Leukocyte emigration to extravascular tissues A. Margination and rolling B. Activation and adhesion C. Transmigration
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1. Vasodilation • Change in vessel flow – NO, histamineèvascular smooth muscleè
vasodilationèincreased blood flow (heat & redness) – Stasis: slowed blood flow, hyperviscosity – Margination of circulating leukocytes & endothelial
activation
• Followed by increased permeability of the vasculature – Formation of an early transudate (protein-poor filtrate
of plasma) gives way to exudate (protein-rich filtrate) into extracellular tissues
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2. Vascular leakage and edema
• Change in vessel permeability – Histamines, bradykinins, leukotrienes cause
endothelial cell contraction that widens intercellular gaps of venules
– Outpouring of protein-rich fluid (exudate) into the extracellular tissues leads to: • Reduction of intravascular osmotic pressure • Increase in extravascular/interstitial osmotic pressure
– Increase of interstitial osmotic pressure leads to edema (water and ions)
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Robbins Basic Pathology, 9th Ed.
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AnCbody + complement Serum alone
Gap formaCon in monolayers of porcine endothelial cells induced by the combinaCon of anCbody and complement
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Acute inflammation: skin blister
Robbins Basic Pathology, 9th Ed.
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Acute inflammation: bacterial bronchopneumonia
Robbins Basic Pathology, 9th Ed.
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Acute inflammation: chronic gastric ulcer
Robbins Basic Pathology, 9th Ed.
Chronic ulcer with an acute inflammatory exudate at the
base
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Outcomes of acute inflammation
Robbins Basic Pathology, 9th Ed.
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Chronic inflammation
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Features of chronic inflammation • Chronic inflammation = long duration • Components: – Lymphocyte, plasma cell, macrophage (mononuclear
cell) infiltration – Tissue destruction by inflammatory cells – Repair with fibrosis and angiogenesis (new vessel
formation)
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Acute vs. Chronic inflammation
Robbins Basic Pathology, 9th Ed.
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Causes of chronic inflammation • Persistent injury or infection – Ulcer, tuberculosis
• Prolonged exposure to a toxic agent – Pulmonary silicosis (silica in the lung)
• Autoimmune disease—self-perpetuating immune reaction that results in tissue damage and inflammation – Rheumatoid arthritis – Systemic lupus erythematosus – Multiple sclerosis
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Clinical examples of chronic inflammation
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Chronic inflammation: tuberculous granuloma
Robbins Basic Pathology, 9th Ed.
Features: 1. Central
necrosis 2. Epithelioid
macrophages 3. Langhans-type
giant cells 4. Peripheral
lymphocytes
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Chronic inflammation: chronic pancreatitis with fibrosis
Klöppel, Modern Pathology (2007)
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Chronic inflammation: pulmonary silicosis
hSp://radiology.rsna.org/
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Leukocyte activation and mechanisms of microbial killing
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Leukocyte activation
Robbins Basic Pathology, 9th Ed.
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Phagocytosis
Robbins Basic Pathology, 9th Ed.
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Neutrophil extracellular traps (NETs)
Robbins Basic Pathology, 9th Ed.
• Extracellular fibrillar networks that are produced by neutrophils in response to infecCous pathogens and inflammatory mediators • contain a framework of nuclear chroma,n with embedded granule proteins,
such as an,microbial pep,des and enzymes
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Chemical mediators of inflammation
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Chemical mediators • Source of chemical mediators: – May be produced locally by cells at the site of inflammation – may be derived from circulating inactive precursors (typically
synthesized by the liver) that are activated at the site of inflammation
• Cell-derived mediators: – normally sequestered in intracellular granules – rapidly secreted upon cellular activation or are synthesized de
novo in response to a stimulus
• Plasma protein–derived mediators: – complement proteins, kinins – circulate in an inactive form – typically undergo proteolytic cleavage to acquire their biologic
activities.
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Chemical mediators
Robbins Basic Pathology, 9th Ed.
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Chemical mediators
hSp://wenliang.myweb.uga.edu/
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Cytokines and inflammation
Robbins Basic Pathology, 9th Ed.
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Important points • Know the 5 cardinal signs of inflammation • Know the main features of acute vs chronic
inflammation and the predominant cell types in each
• Know some clinical examples of acute and chronic inflammation
• Know the stages of immune cell emigration from the blood vessels
• Understand the basics of immune cell activation and chemical mediators
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Recommended books • Robbins Basic Pathology,
Ninth Edition – Vinay Kumar, Abul K.
Abbas, and Jon C. Aster
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Questions??