Biomedical Engineering Reference
In-Depth Information
Table 3 Inducers of increased endothelial expression of ICAM-1 and/or VCAM-1 in
leukocyte adhesion and activation (Ersson et al. 1998, 2002, Duan et al . 2008, Zang et al .
2009)
Interleukin-1 (IL-1); IL-1β
Interleukin-6 (IL-6)
Interleukin-18 (IL-18)
Tumor necrosis factor-α (TNF-α)
Reactive oxygen species (ROS including oxygen-free radical)
Interferon-γ (IFN-γ)
Cytokines and ROS in leukocyte activation and adhesion to endothelia.
Definitions
Inl ammatory Molecules
a. Cytokines called interleukins (ILs)
• IL-1 causes endothelial activation in inl ammation/coagulation,
fever, acute phase protein synthesis by liver; it is produced mainly by
macrophages, endothelial cells, and some epithelial cells.
• IL-6 causes the liver to produce acute phase proteins associated with
inl ammation and proliferation of antibody-producing B cells; it is
produced mainly by macrophages, endothelial cells, and T cells.
• IL-17 causes macrophages and endothelial cells to produce increased
amounts of chemokine (IL-8); it causes epithelial cells to produce
granulocyte-monocyte-colony stimulating factor (GM-CSF) and
granulocyte-colony-stimulating factor (G-CSF). IL-17 is produced by
T cells (δ:γ T cells) and a subset of CD4 T cells.
• IL-8 is a chemoattractant molecule (chemokine) now designated as
CXCL8, an ef ector of neutrophil recruitment; it is produced by blood
monocytes.
• IL-18 is a macrophage product that synergizes with IL-12 to stimulate
production of IFN-γ by NK and T cells.
• IL-12 activates NK cells and CD4 T cells to produce IFN-γ and
promotes development of T H 1 cells (CD4 T cells that produce IFN-γ
and TNF); produced by macrophages and dendritic cells.
• TNF (tumor necrosis factor) causes activation of endothelial cells in
inl ammation/coagulation, fever, and acute phase protein synthesis
by liver, and it af ects many cell types, causing apoptosis; it is mainly
produced by macrophages and T cells. It is also stimulated by
complement components (membrane attack complex) binding to
endothelial cells (Table 5) .
 
 
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