L05: Cellular mediators of innate immunity 2

Question 1

Neutrophil extracellular trap (NETs):

Answer 1

Released by neutrophils to ensnare and destroy microbes, contain chromatin and anti-microbial products that kill microbe and immobilise microbe

Question 2

Phagocyte deficiency: Leukocyte adhesion deficiency (LAD)

Answer 2

1. Failure of neutrophils and monocytes to migrate to site of infection
2. Type 1 = defect in firm adhesion (component of LFA-1 on neutrophil)
3. Type 2 = defect in rolling adhesion (synthesis of ligand for Selectins)

Question 3

Phagocyte deficiency: CGD, G6PD, myeloperoxidase deficiency and Chediak-Higashi syndrome

Answer 3

1. Deficiencies in anti-microbial responses

2. E.g. ROS prod. (CGD), phagosome/lysosome fusion (Chediak-Higashi Syndrome)

Question 4

Acute inflammation

Answer 4

Body’s immediate response to infection or injury. Movement of white blood cells and leakage of plasma (and soluble mediators) to inflammatory site. Characterised by swelling, redness, pain and warmth. Inflammation resolution is where the injury has repaired itself or infection is cleared. Acute inflammatory diseases include sepsis, trauma where inflammatory mediators are hyperactivated.

Question 5

Chronic inflammation

Answer 5

Long term inflammation with tissue destruction and attempt at repair. Mononuclear cells are recruited, however there is abnormal repair as there is constant stimuli present. This results in more tissue damage or failure and host destructive processes. Chronic inflammation can occur when T and B cells activate macrophages in the absence of a trigger called sterile inflammation. Diseases include: Rheumatoid arthritis and atherosclerosis.