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Acute and Chronic Inflammation

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Outline of Lecture

Acute and Chronic Inflammation

Possible Outcomes of Acute Inflammation

Abscess formation occurs with some bacterial or fungal infections

Progression to chronic inflammation (next)

Chronic Inflammation

CHRONIC  INFLAMMATION

Definition of chronic inflammation

an inflammatory response of prolonged duration (weeks – months – years)

provoked by the persistence of the causative stimulus

simultaneous presence of acute inflammation, tissue destruction and repair

Causes of chronic inflammation

Infectious organisms that resist clearance and form a persistent infection in tissue or undrained abscess cavities

e.g mycobacterium tuberculosis, actinomycetes, treponema palidum and Staph aureus (in bone and pleural cavities)

Exposure to irritant non-living foreign material that can not be removed

implanted materials into wounds (wood splinters), inhaled materials (silica, asbestos), deliberately introduced material (surgical suture material or prosthesis)

Potentially normal tissue components as seen in auto-immune diseases

Beta islet cell in diabetes mellitus type I, Acetyl cholin receptor in Myastenia gravis

Characteristics of chronic inflammation

Infiltration of mononuclear cells

Tissue destruction

Healing with scar formation and fibrosis

Chronic inflammation

Lymphocyte, macrophage, plasma cell (mononuclear cell) infiltration

Tissue destruction by inflammatory cells

Attempts at repair with fibrosis and angiogenesis (new vessel formation)

When acute phase cannot be resolved

Persistent injury or infection (ulcer, TB)

Prolonged toxic agent exposure (silica)

Autoimmune disease states (RA, SLE)

The Players (mononuclear phagocyte system)

Macrophages

Scattered all  over (microglia, Kupffer cells, sinus histiocytes, alveolar macrophages, etc.

Circulate as monocytes and reach site of injury within 24 – 48 hrs and transform

Become activated by T cell-derived cytokines, endotoxins, and other products of inflammation

The Players

T and B lymphocytes

Antigen-activated (via macrophages and dendritic cells)

Release macrophage-activating cytokines (in turn, macrophages release lymphocyte-activating cytokines until inflammatory stimulus is removed)

Plasma cells

Terminally differentiated B cells

The Players

Produce antibodies

Eosinophils

Found especially at sites of parasitic infection, or at allergic (IgE-mediated) sites

The dominant cellular player in chronic inflammation is the tissue macrophage
In chronic inflammation
macrophage accumulation persists by different mechanisms

Continued recruitment of monocytes from the circulation

Local proliferation

Prolonged survival and immobilization

Outcome of chronic inflammation

Ulcers

Fistulas

Granulomatous diseases

Fibrotic diseases

and combinations of the above

Examples of chronic inflammatory diseases

Tuberculosis

Sarcoidosis

Rheumatoid arthritis and other connective tissue diseases

Inflammatory bowl diseases (Crohns disease, ulcerative colitis)

Silicosis and other pneumoconioses

Peptic ulcer of the duodenum and stomach

Liver cirrhosis

Chronic Inflammation

Lymphocyte, macrophage, plasma cell (mononuclear cell) infiltration

Tissue destruction by inflammatory cells

Attempts at repair with fibrosis and angiogenesis (new vessel formation)

Unresolved acute phase

persistent injury or infection (ulcer, TB)

prolonged toxic agent exposure (silica)

autoimmune disease states (RA, SLE)

Mononuclear/ Phagocyte System

Macrophages

scattered all  over (microglia, Kupffer cells, sinus histiocytes, alveolar macrophages)

circulate as monocytes and reach site of injury within 24 – 48 hrs and transform

become activated by T cell-derived cytokines, endotoxins, and other products of inflammation

T and B Lymphocytes

Antigen-activated (via macrophages and dendritic cells)

Release macrophage-activating cytokines (in turn, macrophages release lymphocyte-activating cytokines until inflammatory stimulus is removed)

Plasma Cells

Terminally differentiated B cells

Produce antibodies

Eosinophils

Found especially at sites of parasitic infection, or at allergic (IgE-mediated) sites

Lymph Nodes and Lymphatics

Lymphatics drain tissues

flow increased in inflammation

antigen to the lymph node

toxins, infectious agents also to the node

lymphadenitis, lymphangitis

usually contained there, otherwise bacteremia  ensues

tissue-resident macrophages must then prevent overwhelming infection

Patterns of Acute and Chronic Inflammation

Serous

watery, protein-poor effusion (e.g., blister)

Fibrinous

fibrin accumulation

either entirely removed or becomes fibrotic

Suppurative (abscess)

presence of pus (pyogenic staph spp.)

often walled-off if persistent

Patterns of Acute and Chronic Inflammation

Serous

watery, protein-poor effusion (e.g., blister)

Fibrinous

fibrin accumulation

either entirely removed or becomes fibrotic

Suppurative (abscess)

presence of pus (pyogenic staph spp.)

often walled-off if persistent

Patterns of Acute and Chronic Inflammation

Serous

watery, protein-poor effusion (e.g., blister)

Fibrinous

fibrin accumulation

either entirely removed or becomes fibrotic

Suppurative (abscess)

presence of pus (pyogenic staph spp.)

often walled-off if persistent

Granulomatous Inflammation

Distinct pattern of chronic inflammation

Macrophage is the major player

Granuloma is a focal area of inflammation made up of macrophages, lymphocytes and plasma cells

Granulomatous Inflammation

Clusters of T cell-activated macrophages, which engulf and surround indigestible foreign bodies (mycobacteria, H. capsulatum, silica, suture material)

Resemble squamous cells, therefore called “epithelioid” granulomas

Ulcerative

Necrotic and eroded epithelial surface

Underlying acute and chronic inflammation

Trauma, toxins, vascular insufficiency

Systemic Effects

Fever

one of the easily recognized cytokine-mediated (esp. IL-1, IL-6, TNF) acute-phase reactions including

anorexia

skeletal muscle protein degradation

hypotension

Leukocytosis

elevated white blood cell count

Systemic Effects

bacterial infection (neutrophilia)

parasitic infection (eosinophilia)

viral infection (lymphocytosis)

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