Important cells in chronic inflammation a. Macrophages i. Macrophages are derived from blood monocytes ii. Tissue-based macrophages

• Connective tissue (histiocyte)

• Lung (pulmonary alveolar macrophages)

iii. During inflammation macrophages are mainly recruited from the blood (circulating monocytes)

iv. Chemotactic factors: C5a, MCP-1, MlP-la, PDGF, TGF-P

v. Secretes a wide variety of active products (monokines)

vi. May be modified into an epithelioid cell in granulomatous processes b. Lymphocytes i. B cells and plasma cells ii. T cells iii. Lymphocyte chemokine: lymphotaxin c. Eosinophils i. Play an important role in parasitic infections and IgE-mediated allergic reactions ii. Eosinophilic chemokine: eotaxin iii. Granules contain major basic protein, which is toxic to parasites d. Basophils i. Tissue-based basophils are called mast cells ij. Mast cells are present in high numbers in the lung and skin iii. Play an important role in IgE mediated reactions (allergies and anaphylaxis)

iv. Release histamine

Chronic granulomatous inflammation a. Definition: specialized form of chronic inflammation characterized by small aggregates of modified macrophages (epithelioid cells and multinucleated giant cells) usually surrounded by a rim of lymphocytes b. Composition of a granuloma i. Epithelioid cell

• IPN-y transforms macrophages —» epithelioid cells

■ Enlarged cell with abundant pink cytoplasm ii. Multinucleated giant cells

■ Formed by the fusion of epithelioid ceUs

• Langerhans-type giant cell (peripheral arrangement of nuclei)

• Foreign body type giant cell (haphazard arrangement of nuclei)

iii. Lymphocytes and plasma cells iv. Central caseous necrosis

• Present in granulomas due to tuberculosis

■ Is rare in other granulomatous diseases c. Granulomatousdiseases

■ Tuberculosis (caseating granulomas)

• Cat-scratch fever

■ Fungal infections (e.g., coccidioidomycosis)

• Parasitic infections (e.g., schistosomiasis)

• Foreign bodies

• Sarcoidosis

Tissue Responses to Infectious Agents

1. General a. Infectious diseases are very prevalent worldwide and are a major cause of morbidity and mortality b. Infectious agents tend to have tropisno for specific tissues and organs

2. Five major histologic patterns a. Exudative inflammation i. Acute inflammatory response with neutrophils

■ Bacterial meningitis

■ Bronchopneumonia

• Abscess b. Necrotizing inflammation i. Virulent organism producing severe tissue damage and extensive cell death

■ Necrotizing fasciitis

■ Necrotizing pharyngitis c. Granulomatous inflammation i. Granulomatous response predominates ii. Slow-growing organisms

• Mycobacteria

• Parasites d. Interstitial inflammation i. Diffuse mononuclear interstitial infiltrate ii. Common response to viral infectious agents

• Myocarditis (Coxsackie virus)

• Viral hepatitis

USMLEStepl: Pathology e. Cytopathic/cytoproliferative inflammation i. Definition: infected/injured cell is altered ii. Intranuclear/cytoplasmicinclusions

• Cytomegalic inclusion disease

• Rabies—Negri body iii. Syncytia formation

■ Respiratory syncytial virus

• Herpes virus iv. Apoptosis: Councilman body in viral hepatitis

Chapter Summary

Acute inflammation is an immediate response to injury that can cause redress, heat swelling, pain, and loss of function.

Hemodynamic changes in acute inflammation are mediated by vasoactive chemicals and, after a transient initial vasoconstriction, produce massive dilation with increased vascular permeability.

Neutrophils are important white blood cells in acute inflammation that contain granules with many degradative enzymes.

Neutrophils leave the bloodstream in a highly regulated process involving margination (moving toward the vessel wall), adhesion (binding to the endothelium), and emigration (moving between endothelial cells to leave the vessel. Defects in adhesion can contribute to the immunosuppression seen in diabetes mellitus and corticosteroid use.

Chemotaxis is the attraction of cells toward a chemical mediator, which is released in the area of inflammation.

The phagocytosis of bacteria by neutrophils is improved if opsonins, such as the Fc portion of immunoglobulin (Ig) G or the complement product GB, are bound to the surface of the bacteria. Chediak-Higashi syndrome is an example of a genetic disease with defective neutrophil phagocytosis.

Once a bacterium has been phagocytized, both oxygen-requiring and oxygen-independent enzymes can contribute to the killing of the bacteria. Chronic granulomatous disease of childhood and myeloperoxidase deficiency are genetic immunodeficiencies related to a deficiency of oxygen-dependent killing.

Chemical mediators of inflammation include vasoactive amines, the kinin system, arachidonic acid products, the complement cascade, and cytokines.

Acute inflammation may lead to tissue regeneration, scarring, abscess formation, or chronic inflammation.

Cells important in chronic inflammation include macrophages, lymphocytes, eosinophils, and basophils.

Chronic granulomatous inflammation is a specialized form of chronic inflammation with modified macrophages (epithelioid cells and multinucleated giant cells) usually surrounded by a rim of lymphocytes. A wide variety of diseases can cause chronic granulomatous inflammation, most notably tuberculosis, syphilis, leprosy, and fungal infections.

Patterns of tissue response to infectious agents can include exudative inflammation, necrotizing inflammation, granulomatous inflammation, interstitial inflammation, and cytopathic/cytoproliferative inflammation.

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