Response of body to injury




Vascular Phase

- redness, heat & swelling

- transient vasoconstriction after injury

- then vasodilatation of arterioles

- increased permeability followed by plasma exuded into extravascular space


Cellular Phase

- leukocytes adhere to endothelium

- margination - migrate into extravascular space


Inflammatory Cells



- attracted by chemotactic agents

- phagocytose bacteria, immune complexes & particulate matter

- particulate matter may be opsonised (coated with complement or IgG)

- opsonisation helps phagocytosis by aiding recognition

- during phagocytosis particle encased by vacuole

- lysosomes fuse with vacuole and enzymes destroy particle



- Involved in host defence from parasitic infections


Mast Cells & Basophils

- involved in allergic or immediate hypersensitivity reactions



- important in chronic inflammation

- produced as monocytes in bone marrow

- function to phagocytose matter and present antigens to T Cells



- identify antigens

- help eliminate these antigens

- B Cells become plasma cells - humoral immunity (antibodies)

- T Cells mediate cellular immunity




Complement functions

1.  Activation of inflammatory cells

2.  Cytolysis of infected cells / insert pores

3.  Opsonisation of antigen to facilitate phagocytosis



- proteins that circulate in plasma in inactive form

- increase permeability blood vessels / Vasodilatation

- hypotension / pain / leukocyte margination


Vasoactive Amines



- stored in mast cell granules

- released on activation by IgE

- produces increased BV permeability / vasodilation / bronchospasm



- stored in platelets

- causes vasoconstriction / increased BV permeability / fibrogenesis




Arachidonic Acid 

- AA is a fatty acid found in most tissues

- released by phospholipases




Cyclo-oxygenase (COX) catalyses AA to PGG

- many types

- PGI2 (Prostacyclin) / Thromboxane A / PGE2


Effects of PGE2 & PGI2

- vasodilation

- increase BV permeability

- stimulate osteoclastic bone resorption

- anti-inflammatory effects

- inhibit T Cell activation

- inhibit B Cell proliferation

- inhibit IL-2 production



- stimulates platelet aggregation




Lipoxygenase catalyse conversion of AA to Leukotrienes

- important mediators


1. Chemotactic for leukocytes

2. Activate neutrophil enzyme secretion

3. Increase BV permeability

4. Cause bronchospasm




1.  NSAID 

- inhibit COX activity / inhibits PG synthesis

- suppress inflammation

- explains many of its side effects

- decrease cytoprotective effect of PGE2 on gastric mucosa (ulcers)

- increase leukotrienes (bronchoconstriction)


2.  COX 2 selective

- don't inhibit COX 1

- maintain production of PGE2 in gastric mucosa


2.  Glucocorticoids 

- inhibit release of AA from phospholipids

- inhibit production of leukotrienes AND prostaglandins


Growth Factors / Cytokines


Polypeptides that regulate inflammatory cells

- Interleukins

- IL-1, IL-6 & TNF

- similar actions

- produced by monocytes



1.  Pyrogenic

2.  Stimulate synthesis of Acute Phase Reactants

3.  Facilitates B & T Cell proliferation

4.  Stimulate stem cell growth for neutrophils & monocytes


IL-2 & IL-4

- stimulate proliferation of T Cells & IG production

- stimulate fusion of macrophages to form MNGC (multinucleated giant cells)


Il-3, Il-5 & Il-7

- promote growth & differentiation of haemopoietic stem cells




Interferon Gamma

- produced by activated T cells

- induces expression of Type II MHC antigens

- activates macrophages for antigen presentation


Neutral Proteinases


Acid Proteinases

- most stored in lysosomes of leukocytes

- degrade microbes & cell debris at low pH within phagolysosomes

- degrade extracellular proteins in connective tissue at neutral pH


1. Metalloenzymes

- require metal ions (eg Zn) as cofactor


2. Serine Proteinases 

- collagenase - degrades extracellular collagen

- gelatinase - degrades denatured collagen

- proteoglycanase - degrades PG