Biomedical Engineering Reference
In-Depth Information
Table 4
Putative roles of bone marrow-derived and kidney cells in ischemia-reperfusion
(acute kidney) injury (Rahman and Fazal 2008)
1. Bone marrow-derived cells cause increases in ini ltration, activation, cytokine production.
a. neutrophils produce reactive oxygen and nitrogen species
b. monocytes/macrophages produce reactive oxygen and nitrogen species and inl ammatory
cytokines (IL-1, IL-6, TNF-α) and chemokines (IL-8)
c. Resident dendritic cells are prominent secretors of TNF-α
d. NK cells cause cytokine secretion
e. Invariant NKT (iNKT) cells result in cytokine (IL-4, IL-10, IFN-γ) production
f. Gamma delta (γδ) T cells
g. CD4 T cells: T
H
1 subsets damaging; T
H
2 subsets protective
h. B-1 B cells
2. Endothelial cells show increases in vascular permeability and adhesion molecule expression.
3. Epithelial cells display increases in complement deposition, toll-like receptor TLR2/4 expression.
TLR signaling is involved in mediating renal damage.
4. Renal dendritic cells are involved in producing increases in cytokine production and in antigen
presentation by draining lymph node.
Table 5
Role of innate immune complement pathways in hypoxic injury (Rahman and
Fazal 2008)
1. A monoclonal antibody against Factor B (alternative complement pathway) protects mice from
renal tubular injury and apoptosis at er I/R.
2. Activation of lectin pathway triggered by pattern recognition receptors (mannose-binding lectin
and i colin), which bind endogenous ligands expressed on necrotic and apoptotic host cells, also
bind cytokeratin exposed on hypoxic endothelia.
3. h e membrane attack complex of all complement pathways (C5-C9) deposits on epithelial cells
to stimulate production of TNF-α.
h e complement pathways contribute to production of TNF-α following deposition of membrane
attack complex on endothelial and epithelial cell membranes.
transplantation (2 hr following ischemia) and increases in ICAM-1 protein were
apparent by immunohistochemistry at er 6 hr of reperfusion (Wang
et al.
1998).
A kappa-opiod receptor (kOR) agonist protected cardiomyocytes and neuron
cells against I/R injury through activation of protein kinase C (Yu
et al.
2009).
Treatment of male Spraque Dawley rats with the KOR agonist signii cantly reduced
(p < 0.001) the number of leukocytes adhering and transmigration in protecting
the microcirculation of skeletal muscle from I/R injury. Expression of ICAM-1 in
the cremaster muscle of the protected rats was reduced (Yu
et al.
2009).
Key Point
Blood leukocytes expressing certain CAMs interact with endothelial
co-ligands, e.g. ICAM-1/β-2 integrin interaction, which permits transmigration of
blood leukocytes into the injured tissue site.
