2 Inflammation, Inflammatory Disorders, & Healing

Question 1

Inflammation

Answer 1

Inflammatory cells, plasma proteins, & fluid leave blood vessels for the interstitial space

Acute - Neutrophils
Chronic - Lymphocytes

Question 2

Acute Inflammation

Answer 2

Edema & neutrophils

To eliminate pathogen causing infection, OR
To clear necrotic debris after infarction

(Innate immunity, limited specificity)

Question 3

Mediators of Acute Inflammation

Answer 3

1. TLRs on macrophages & dendritic cells recognize PAMPs
   (Ex. CD14 recognizes LPS on G- bacteria)
2. NF-kB upregulated to activate other immune response genes & mediators
3. Arachidonic acid released from bilayer by phospholipase A2

a. COX pathway
- PGI2, PGD2, PGE2 for vasodilation, inc vascular permeability (+PGE2 for fever & pain)

b. 5-Lipooxygenase pathway
- LTB4 (+C5a, IL8, bacteria) for neutrophils
- LTC4, LTD4, LTE4 for vasoconstriction, bronchospasm, inc vascular permeability

4. Mast cells activated by…
   -Tissue trauma
   -Complement C3a 7 C5a
   -Cross-linking of mast cell surface IgE’s by antigen

Immediate: Release of pre-formed histamine granules to vasodilate & inc vascular permeability

Delayed: Produce arachidonic acid metabolites, especially LT’s

5. Complement = Pro-inflammatory serum proteins, circulate as inactive precursors

a. Classical ~ C1 binds to antigen bound IgG or IgM
b. Alternative ~ Microbial products directly bind
c. Mannose-Binding Lectin ~ MBL binds mannose on microbes

~ All pathways generate C3 convertase (to create C3a & C3b), ***