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2-1 inflammation

1. INFLAMMATION
A. Allows inflammatory cells, plasma proteins (e.g., complement), and fluid to exit
blood vessels and enter the interstitial space
B. Divided into acute and chronic inflammation
ACUTE INFLAMMATION
I. BASIC PRINCIPLES
A, Characterized by the presence of edema and neutrophils in tissue (Fig. 2.1 A)
B, Arises in response to infection (to eliminate pathogen) or tissue necrosis (to clear
necrotic debris)
C, Immediate response with limited specificity (innate immunity)
II. MEDIATORS OF ACUTE INFLAMMATION
A. Toll-like receptors (Tl.Rs)
1. Present on cells of the innate immune system (e.g., macrophages and dendritic
cells)
2. Activated by pathogen-associated molecular patterns (PAMPs) that are
commonly shared by microbes
i, CDI4 (a TLR) on macrophages recognizes I ipo polysaccharide (a PAMP) on
the outer membrane of gram-negative bacteria.
3. TLR activation results in upregulation of NF-kB, a nuclear transcription factor
that activates immune response genes leading to production of multiple immune
mediators.
4. TLRs are also present on cells of adaptive immunity (e.g., lymphocytes) and,
hence, play an important role in mediating chronic inflammation.
B. Arachidonic acid (AA) metabolites
1. AA is released from the phospholipid cell membrane by phospholipase A, and
then acted upon by cyclooxygenase or 5-lipoxygenase.
i. Cyclooxygenase produces prostaglandins (PG).
a. PGI,, PGD„ and PGE3 mediate vasodilation and increased vascular
permeability.
b. PGEj also mediates pain.
ii. 5-lipoxygenase produces leukotrienes (LT).
a. LTB, attracts and activates neutrophils.
b. LTC^ LTD4, and LTE4 (slow reacting substances of anaphylaxis) mediate
vasoconstriction, broncho spasm, and increased vascular permeability.

C. Mast cells
1, Widely distributed throughout connective tissue
2. Activated by (1) tissue trauma, (2) complement proteins C3a and C5a, or (3)
cross-linking of cell-surface IgE by antigen

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