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Protective response of the body to cell injury to remove the noxious stimulus that caused the injury in the first place.

Acute or Chronic if the noxious stimulus persists.

Acute inflammation lasts for minutes to days while chronic inflammation may persist from days to years
Inflammation and repair are the important steps in healing process but the inflammation can cause harm to our native tissues, eg

Autoimmune diseases
Constrictive pericarditis

Cardinal signs of inflammation:

Calor: hot
Rubor: red
Dolor: pain
Tumor: swelling
Function laesa

CellularComponents of inflammation:


Polymorphonuclear cells( neutrophils)


B cells and humoral immunity
T cells and cell mediated immunity
Monocytes and macrophages
Smooth muscle cells
Mast cells
Natural killer cells

Events in Acute Inflammation:

1.Vascular Events

Vascular dilatation: histamine, bradykinin

Increased vascular permeability and exudation:

Endothelial cell contraction( early) and retraction( late)
Direct endothelial injury: toxins, burn, etc
Leucocyte dependent endothelial injury
Increased transcytosis
Neoangiogenesis: increased gap junctions

2.Cellular events:

Neutrohils initially
Monocytes after 6-24 hours
Rolling and margination
Adhesion: interaction between selectins, integrins and cell adhesion molecules like VCAM
Transmigration by diapedesis


Chemokines: bacterial peptides, C5a, LTB4( Leukotreine), IL 8( interleukin)
Actin myosin interactions in the leucocyte are responsible for diapedesis

Phagocytosis and degranulation

Opsonisation: c3b, IgG, collectins
Oxidative burst

How do neutrophils kill?

Oxidative burst resulting in free radicals

2O2+NADPH ....NADPH.....2O2- ions+NADP+H+

2O2- ions+ 2H+ .....oxidase........ H2O2

H2O2+ Cl-...myeloperoxidase....... HOCl-

Dead organisms digested by lysosomal hydrolases

Bacterial killing also aided by lysozymes and defensins, the latter increase the permeability of bacterial cell.

Body’s defense against free radical injuries

Catalase which neutralises H2O2 into water and O2
Superoxide Dismutase
Glutathione Peroxidase
Antioxidant Vitamins like vitamin A, C and E

Disorders of cellular events of inflammation

Adhesion deficiency
Myeloperoxidase deficiency: Chediak Higasi disease
NADPH Oxidase deficiency: chronic granulomatous diseases

Chemical mediators of inflammation


Preformed mediator so released early on
Secreted by mast cells and basophils
Secreted in response to
cross linking of IgE during reexposure to allergen in type I hypersensitivity
Anaphylotoxins: C3a, C5a

Substance P: responsible for pain

Chemical mediators of inflammation

Kinin Cascade:

Coagulation factor XIIa activates Prekallikrein into Kallikrein
Kallikrein activates HMWK( High Molecular Weight Kininogen) into Bradykinin

Coagulation cascade:

Fibrinolytic cascade: tPA activates plasmin

Complement cascade:

Proteases that are nine in number: c1 to c9

Activated by
classic pathway due to Ag-Ab complexes
alternative pathway by microbial LPS or endotoxins

One activated complement activates another
C3a and C5a are anaphylotoxins
C5a is a chemokine
C3b along with IgG work as opsonins
C5b to C9 make the MAC: membrance attack complex

Lysosomal proteases, endonucleases and antiproteases to protect the cells against own enzyme, eg α antitrypsin.

NO( previously called EDRF) by NO synthase

Reactive oxygen species

Arachidonic acid metabolites


Interleukins: more than 20 types


Colony stimulating factors eg GM-CSF

IL 1 and TNFα are responsible for all the acute phase response including fever, cachexia, neutrophil aggregation, septic shock and synthesis of acute phase reactants from liver( eg CRP, ceruloplasmin)

Chronic Inflammation

Outcomes of acute inflammation can either be resolution, chronic inflammation or scarring

Persistence of noxious stimulus causes chronic inflam.

Eg. Chronic viral hepatitis, syphilis, TB and fungi( delayed hypersensitivity), silicosis and other pneumoconioses, autoimmune diseases, etc

Interference in the healing process

3 main components

Mononuclear cell( macrophages) infiltration
Tissue destruction
Repair: by either tissue regeneration or fibrosis

Tissue injury in chronic inflammation is caused by Radical oxygen species, proteases and tissue plasmin activator( tPA)

Fibrosis is a common component in chronic inflammation caused by cytokines like PDGF, FGF, TGFβ, VEGF, etc

Granulomatous inflammation

Type IV hypersensitivity

Attempt at walling off the noxious material

CD4 T helper lymphocyes crucial in recruiting monocytes which turn into macrophages( epitheloid cells) and giant cells

Granuloma with caseous necrosis seen in TB

Other examples are

tuberculoid leprosy
syphilitic gumma
fungal infections like histoplasmosis, blastomyces, cryptococcosis, coccidioides
foreign body like suture materials
pneumoconiosis like silicosis
idiopathic like sarcoidosis

Morphology of a granuloma

lymphocytes( esp CD4 type T helper cells)

macrophages( epitheloid cells, so called because of their resemblance to squamous cells)

epitheloid giant cells formed by the fusion of many epitheloid cells with multiple nucleus in different patterns of arrangement like horseshoe pattern in Langhan’s giant cell seen in TB granuloma.

Necrotic material in centre in case of caseous granuloma as seen in TB

Morphologic types of inflammation


Exudative Inflammation: excess fluid. TB lung.
Suppuration/Purulent – Bacterial - neutrophils
Fibrinous – pneumonia – fibrin
Serous – excess clear fluid – Heart, lung
Haemorrhagic – b.v.damage - anthrax.

Chronic inflammation:

with healing.
Granulomatous – clusters of epitheloid* cells eg. TB, Fungus, Foreign body.

Lewis Triple Response:

Flush: capillary dilatation.
Flare: arteriolar dilatation.
Wheal:exudation, edema.

Gastric Ulcer:


Mouth Aphthous ulcer:

Acute Enteritis:


Neutrophil Margination:

Vascular changes:

Pneumonia - Exudation:

Chronic Inflammation:

Serous Inflammation - Effusion :

Fibrinous Inflammation:

Purulent - Inflammation:

Chronic Inflammation:

Lung Abscess



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