Phagocytosis
Inflammation
Fever
Complement
Interferons

Neutrophils (PMNs)
Basophils
Eosinophils
Lymphocytes
Monocytes

Highly phagocytic 
Most abundant type of white blood cells
Found in bloodstream
Also called PMN - polymorphonuclear (because nucleas changes shape)

Not phagocytic
Least common white blood cell
Contain cytoplasmic granules:
• Serotonin
• Heparin (an anticoagulant)
• Histamine
  • Release during inflammation and alergic reaction
  • Causes contraction of bronchial muscles
  • Causes vasodilation
  • Increases vessel permeability therefore causing edema (release of fluid into tissue)
  • In high levels can by fatal because of sudden drop in BP and Pulse

Somewhat phagocytic
Numbers increase during:
• Allergic reactions
• Parasitci worm infections i.e. pin worm

Not phagocytic
Found in lymphoid tissues
Circulate in blood
Three types NK, T and B
Play a major role in specific immunity

Not actively phagocytic until maturity
During infection they mature in macrophages
Macrophages play a role in specific immunity

Neutrophils (PMNs)
Mature monocytes - Macrophages

Activation of PMNs
Chemotaxis
Adherence
Ingestion and Formation of Phagosome (vacuole)
Killing and Digestion (Formation of Phagolysosome)
• Lysozymes (enzymes that lysis) in phagosome destroys or lysis bacteria
Expulsion - expels destroyed components of bacteria

By inflammatory mediators
The most important mediators are:
• Histamine (released by cells, basophils, platelets)
• Kinins (released by damaged tissue cells)
• Complement Components
• Microbial Products (anythings an MO releases)

The chemical attraction of PMNs to area of infection or inflammation
The chemical that initiate chemotaxis are:
• Microbial products
• Kinins
• Complement components

Capsules - gel like structure on MO that prevents adherence and is antiphagocytic.
• Examples: Bacillus anthracis, Streptococcus pneumoniae
Opsonization - coating / covering of MO by host molecules
• Increases phagocytosis by increasing adherence
• is any molecule that acts as a binding enhancer for the process of phagocytosis, for example, by coating the negatively-charged molecule on the membrane.

Complement components
Antibody molecules

Destroys pathogens
Walls off or seperates MO from body
Repairs damage

Initiated by damage to tissue or MO infection
A local response
A benefical response (but can also damage host tissues)
Symptoms: pain, redness, heat, swelling

What are the four steps in the mechanism of inflammation?

Damage to host tissues
Inflammatory mediators
Pus formation
Repair

Damaged host cells and MOs

Vasodilation - dilation of capillaries
• Increased diameter creates greater blood flow which creates increased redness and heat
Increased blood vessel permeability - leaks more
• phagocytes leak out into infected area
• increases swelling with added fluid

Activation and chemotaxis of phagocytes
Diapedesis - phagocytes change shape to exit capillaries

Accumulation of dead phagocytes, dead MOs and damaged tissues

Increases dilation
Activates phagocytes

PMNs respond first but die off quickly. Capicity is reached quickly.
Monocytes (peripheral blood vessels) move outside of vessels into tissue space and become macrophages.
• Macrophages have greater capacity than PMNs and can engulf dead PMNs, MO and dead host cells.

Fever is a systematic response to inflammation
Its benefits include:
• Higher temperatures inhibit pathogens (not ideal temp)
• Fever activates and speeds other body defenses:
  • Inflammatory response
  • Phagocytis
  • Chemotaxis
  • Interferon production
  • Antibody production

When MO are phagocytized by Macrophages they release a substance that effects the temperature control center (hypothalmus) in the brain.
These substances increase blood pressure and pulse and therefore increase the flow of PMNs and Macrophages to the infection site.
Some degree of fever is good to fight from infection.
If fever doesn't affect the MOs the temperture / fever will be reset to a higher level.

• They are 30 different proteins that are located in the blood.

Antigen - Antibody binding or complex formation
Endotoxins (GM-)

Activated complement proteins split into two subunits which activate two more additional subunits.
This is called the complement cascade.
Each subunit has a unique function

Cytolysis of MO - lysis of cell wall of MO to death
Contributes to development of phagocytes and inflammation because components acts as:
• Chemotactic factors
• Inflammatory mediators
Opsonization - complements can act as opsonins.

natural proteins produced by the cells
assist the immune response by inhibiting viral replication 

Interferons are produced inside the viral infected host cell.
When the host cell lysis the interferons are released and taken up by another neighboring host cell.

Interferons are host specific but not viral specific.
Interferons peak at 3 days and decrease by 1 week. Before antibodies peak.