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Types of Chronic Inflammation

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CHRONIC  INFLAMMATION

DEFINITION

Inflammation of prolonged duration

(weeks and months) in which:

  • Active inflammation
  • Tissue injury
  • Attempts at repair

coexist, in a varying combination

CAUSES

  • •Persistent infection by certain microorganism (of low toxicity)
  • •Prolonged exposure to toxic agents
    •            exogenous (silicosis)
    •            endogenous (atherosclerosis)
    • Autoimmunity

GENERAL FEATURES

Mononuclear cell infiltration

Tissue destruction and necrosis

Proliferative changes

DIFFERENCES BETWEEN ACUTE AND CHRONIC INFLAMMATION

ACUTE INFLAMMATION

  • •Duration= short
  • •Onset= acute
  • •Inflammatory cells= neutrophils, macrophages
  • •Vascular changes= Active vasodilation, increased permeability
  • •Fluid exudation and edema= +
  • •Tissue necrosis= -, seen in suppurative and necrotizing inflammation

CHRONIC INFLAMMATION

Long (weeks to months)

Insidious

Lymphocytes, plasma cells, macrophages and fibroblasts

Angiogenesis, granulation tissue

SYSTEMIC EFFECTS

Fever

Anemia

Leucocytosis

Raised ESR

Secondary systemic amyloidosis

CELLS INVOLVED IN CHRONIC INFLAMMATION

Mononuclear- phagocyte system

Lymphocytes

Plasma cells

Eosinophils

Mast cells

Neutrophils (in some cases)

MONONUCLEAR-PHAGOCYTE SYSTEM

  • •Closely related cells of bone marrow origin-

Blood monocytes (t=1/2 1 day)

Tissue macrophages (t=1/2 several months)

Kupffer cells (liver)

Histiocytes

Alveolar macrophages

Microglia (CNS)

Osteoclast (bone)

Dendritic cells and Langerhans cells (skin)

Macrophages of bone marrow

Tingible body cells of germinal centres (lymph node)

Littoral cells of splenic sinusoids

Mesengial cells of glomerulous

Key macrophage events

Recruitment from circulation

Local proliferation

Immobilization

Differentiation (kupffer cells, microglia, osteoclast)

ROLE OF MACROPHAGES IN INFLAMMATION

Phagocytosis and pinocytosis

Antigen processing and antigen presentation

Constituents of granulomas

Regulate lymphocytes response

Secretion of biologically active substances

PRODUCTS RELEASED BY MACROPHAGES

ENZYMES~

  • •Neutral proteases (elastases, collagenases)
  • •Acid hydrolases (phosphatases, lipases)
  • •Plasma proteins~ Complement components (e.g. C1 to C5, properdin)
  • •Coagulation factors (e.g. Factor V, VIII, tissue factor)
  • •Reactive metabolites of oxygen
  • •Nitric oxide
  • •Eicasonoids
  • •Cytokines (IL-1, TNF, IL-8)
  • •Growth factors (PDGF, EGF, TGF-b, TGF)

LYMPHOCYTES

  • •Ab production and humoral immunity (B-cells)
  • •Cell mediated immunity (T-cells)
  • CD4+ helper T cells
  • CD8+ suppressor T cells
  • •Regulate macrophage response

PLASMA CELLS

Develop from activated B- lymphocytes

Antibody synthesis and secretion

against persistant antigen or altered tissue components

EOSINOPHILS

Inflammation associated with

Allergic responses

Parasitic infestations

Weakly phagocytic

Effector function by degranulation

Eosinophilic granule protein

Biologically active proteins

Includes

Major basic protein (MBP)

Eosinophilic cationic protein

Eosinophilic derived neurotoxins

Eosinophil peroxidase

MAST CELL

Bear receptor for Fc portion of IgE antibody

Degranulate when crosslinked with antigen

Basophilic granules

  • Histamine
  • Proteoglycans
  • Glycosidases

ROLE OF NEUTROPHILS

Persist in some forms of chronic inflammation

Induced by

  • persistent microbes or
  • mediators produced by macrophages and T-lymphocytes

Examples: Chronic osteomyletis, Chronic damage in lungs (Smokers)

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 bowel diseases (Crohns disease, ulcerative colitis)

Silicosis and other pneumoconioses

Peptic ulcer of the duodenum and stomach

Liver cirrhosis

CLASSIFICATION

  • •Chronic inflammation
    • Chronic non specific inflammation
    • Chronic granulomatous inflammation

Chronic granulomatous inflammation:

Characterized by focal accumulation of activated macrophages, which often develop an epithelial like (epitheliod) appearance (granuloma).

Primary granulomatous conditions

Bacterial

Tuberculosis

Leprosy

Syphilis

Granuloma inguinale

Brucellosis

Cat scratch disease

Tularemia

Fungal

Histoplasmosis

Coccidiomycosis

Blastomycosis

Cryptococcosis

Actinomycosis

Parasitic

Schistosomiasis

Trichiniasis

Primary granulomatous condition (CONTD)

Foreign body type

Foreign body granulomatosis

Silicosis

Talc granuloma

Metal induced

Berylliosis

Zerconium

granulomatosis

Miscellaneous

Sarcoidosis

Crohn’s disease

Wegener’s granulomatosis

Giant cell arteritis

Major features

  • •Mononuclear cell infiltrate
  • Lymphocytes
  • Macrophages
  • Plasma cells
  • •Epitheliod cells
  • •Giant cell
  • •Necrosis(+/-)
  • •Fibrosis

Epitheliod cells

These are activated macrophages with epithelial (squamous) cell like appearance

Cells with indistinct cell boundaries

  • Abundant pale staining granular

cytoplasm

  • Elongated/oval slipper shaped nuclei

Weakly phagocytic

Giant cells

When macrophages (epitheliod) cells fail to deal with microbes to be removed, they fuse together to form multinucleated giant cells

40-50 µm

Weakly phagocytic

Giant cells

Giant cells in inflammation

Langhan’s giant cells

Foreign body type

Touton giant cell

Aschoff cells

Tumour giant cells

Reed-Sternberg cells

Anaplastic tumour giant cells

Giant cells in giant cell tumour of the bone

Giant cells (Contd)

Miscellaneous-

Warthin finkeldy cells (measles)

Osteoclasts, megakaryocyte, syncytiotrophoblast

Langhans giant cell

GIANT FOREIGN BODY CELL

Granuloma

A microscopic aggregation of activated macrophages transformed into epitheliod cells surrounded by a collar of mononuclear leukocytes

With time, develops an enclosing rim of fibroblasts and connective tissue

Types of granuloma

Foreign body granuloma

Immune granuloma

GRANULOMA

Formation of granuloma

Injury

Failure to digest the agent

Weak inflammatory response

Persistence of injurious agent

T-cell mediated immune response

Activation of T cells, monocyte chemotactic factor(C5a, MCP-1, growth factor PDGF, TGF-β)

Recruitment of circulating monocytes and proliferation of tissue macrophages

accumulation and activation of macrophages

Transformation into epitheliod and giant cells

GRANULOMA

GRANULOMA FORMATION

Tuberculosis

Protype of immune granuloma

Caseating garnulomatous lesion

Mycobacterium tuberculosis (Acid fast bacilli)

Pathogenicity is related to ability to escape killing by macrophages and induce delayed type IV hypersensitivity reaction

Formation of tubercle

Initial neutrophilic response to TB bacilli

Neutrophils destroyed by organism

Proliferation of macrophages (after~12 hrs)

Phagocytosis of  TB bacilli by macrophages

Activate CD4 + T lymphocytes

Morphological transformation of activated macrophages

Epitheliod cells

Fuse to form giant cells

Hard tubercle formation

(role of cytokines released in response to sensitized CD4 + T cells and constituents of bacterial cell wall

Interaction of mycobacteria with activated T-cells

- direct action of CD8+ suppressor T cells

-action of CD4+helper T cells (via INF-γ)

Direct toxicity of mycobacteria to macrophages

Development of central caseation necrosis

Soft tubercle

(caseating granuloma of tuberculosis)

Tubercular granuloma

ZN staining

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