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Chronic inflammation
- 1. INFLAMMATIO N AND HEALING Mohammad MuztabaKhan Assistant professor(Jr.) Department of Pharmacology Bhavdiya institute sibar Sohawal Ayodhya
- 2. Chronic inflammation • Itis the inflammation of prolong duration (weeks or months). • It is occurred as: • Following acute inflammation. • Occurs, incidentally as active inflammation. • With tissue destruction. With repair process.
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- 6. Causes of Chronicinflammation I - Persistent infection. II - Prolonged exposure to potentially toxic agents. III - Autoimmunity.
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- 10. Causes of Chronicinflammation I - Persistent infection: • Bacteria. • Viruses. • Fungi. • Parasites
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- 14. Causes of Chronicinflammation II - Prolonged exposure to potentially toxic agents: • Endogenous, (atherosclerosis). • Exogenous, ( particulate silica-Silicosis).
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- 16. Lesions of Atherosclerosisin Aorta
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- 19. Causes of Chronicinflammation III - Autoimmunity: Occurs in: • Rheumatoid arthritis. • Lupus erythmatosus.
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- 22. 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)
- 23. Morphological Features of ChronicInflammation These are characterized by: I - Infiltration by mononuclear cells. II - Tissue destruction. III - Removal of damaged tissue, (healing).
- 24. Morphological Features of ChronicInflammation I - Infiltration by mononuclear cells: The mononuclear cells are become predominant after 48 hours. These include: • Macrophages. • Lymphocytes. • Plasma cells. • Eosinophils. • Mast cells.
- 25. Morphological Features of ChronicInflammation • 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
- 26. Morphological Features of ChronicInflammation • 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 (of lymphocytes). – Produce antibodies.
- 27. Morphological Features of ChronicInflammation Eosinophils – Found especially at sites of parasitic infection, or at allergic (IgE-mediated) sites. – Eosinophils have highly cationic proteins, which are toxic to parasites.
- 28. Morphological Features of ChronicInflammation II - Tissue destruction Occur due to: • Inflammatory cells. • Persistent infecting material.
- 29. Morphological Features of ChronicInflammation III - Removal of damaged tissue, (healing): • Occur by proliferation of small blood vessels, (angiogenesis). • Proliferation of fibroblast, (fibrosis-repair).
- 30. Granulomatous Inflammation • Clustersof T cell-activated macrophages, which engulf and surround indigestible foreign bodies (mycobacteria, H. capsulatum, silica, suture material) • Resemble squamous cells, therefore called “epithelioid” granulomas with peripheral lymphocytes, fibrosis & multinucleated giant cells.
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- 34. Lymph Nodes andLymphatics • 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
- 35. 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
- 36. Systemic effects (cont’d) –Bacterial infection (neutrophilia) – Parasitic infection (eosinophilia) – Viral infection (lymphocytosis)
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