Biomedical Engineering Reference
In-Depth Information
necrotic cells via Toll-like receptors, intracellular pattern-recognition receptors, and
interleukin-1 receptor, as well as adaptor MyD88 (myeloid differentiation primary-
response gene product).
Breathing and eating are associated with penetration of foreign substances and
pathogens to the gut and lungs. The immune system must then be poised for attack
against pathogens and damage to the body's tissues.
Alveolar macrophages in the lower respiratory tract abundantly express receptor
CD200R for membrane glycoprotein CD200 of airway epithelial cells to restrain
cytokine secretion and inflammation [
306
].
In the intestinal mucosa, the immune system must tolerate antigens of the
intestinal commensal flora and food, whereas it must fight against pathogens.
An intestinal subset of dendritic cells that expresses
α
E
β
7
-integrin
175
activates
T lymphocytes that transform into T
Reg
cells and produce less interferon-
.
In macrophages, supplementation of arachidonic acid, eicosapentaenoic acid,
and docosahexaenoic acid
176
and activation of Toll-like (TLR4) and purinergic
(P2X
7
) receptors involved in short- and long-term inflammation, respectively, lead
to the release of 22-carbon fatty acids. These molecules can indeed be incor-
porated in membrane phospholipids under arachidonic and eicosapentaenoic acid
supplementation via rapid elongation. These fatty acids inhibit the cyclooxygenase
pathways (more strongly COx1 than COx2) and shunt arachidonic acid metabolism
to the lipoxygenase (Lox1) axis, thereby augmenting leukotriene synthesis [
308
].
γ
175
Integrin-
7
is expressed almost exclusively by mucosal T lymphocytes. E-cadherin on
epithelial cells is a ligand of
α
β
E
α
β
7
-integrin. Production of
α
β
7
-integrin often rises during inflam-
E
E
mation. Integrin-
7
also mediates the specific connection to human intestinal microvascular
endothelial cells, thus intestinal T-cell homing, independently of E-cadherin [
307
].
176
Dietary fish oil that contains
α
β
E
3-fatty acids, eicosapentaenoic acid, and docosahexaenoic acid
has cardioprotective and anti-inflammatory effects. Eicosapentaenoic and docosahexaenoic acids
are important
ω
3-polyunsaturated fatty acids with beneficial effects. A lower mortality rate results
from intake of polyunsaturated fatty acids rather than saturated fatty acids, and more precisely
ω
ω
3-polyunsaturated fatty acids (with a carbon-carbon double bond (C
=
C) in the
−
3 position
[position 3 from the methyl (-CH
3
) end, or
ω
end]) rather than
ω
6-polyunsaturated fatty acids
(with a carbon-carbon double bond in the
−
6 position [position 6 from the
ω
end]). Arachidonic
acid (CH
3
(CH
2
)
18
COOH), a 20:4 fatty acid (the lipid number
referring to the numbers of
carbon atoms [20 C] and of double bonds in the fatty acid) is the most common highly unsaturated
fatty acid.
•
:
•
3] fatty acid); linoleic
acid ([18:2],[
−
6]) is the shortest
ω
6-fatty acid.
ω
3-Polyunsaturated fatty acid supplementation
can lower the ratio of arachidonic acid to
ω
3-polyunsaturated fatty acids in cell membrane
phospholipids. Membrane arachidonic acid can be released by phospholipase-A2 upon various
stimuli. Free arachidonic acid can then be oxygenated by cyclooxygenases, lipoxygenases, and
cytochrome-P450 enzymes to generate numerous lipid mediators, the eicosanoids, or icosanoids.
Eicosanoids can initiate the innate immune response and operate in inflammation. Like arachidonic
acid-derived eicosanoids, eicosapentaenoic and docosahexaenoic acid-derived eicosanoids can be
produced.
α
-Linolenic acid is an essential
ω
3-fatty acid ([18:3],[
−
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