Previous studies have shown that a non-HS-binding mutant form of the inflammatorychemokineCCL7 can block inflammation produced by wild-type chemokines.
The current study was designed to assess the potential of the non-HS-binding form of the homeostatic chemokineCXCL12 to modulate normal chemokine-mediated inflammation.
Together, these data suggest that systemic administration of non-HS-binding CXCL12 is able to inhibit localized, CXCL12-mediated inflammation within the air pouch.
However, the mixture of either of these mutants with wild-type chemokines can abrogate the potential of the latter to induce transendothelial leukocyte migration in vitro and normal chemokine-mediated inflammation in vivo .
The second part is a systems physiology-based overview of the roles that chemokines play in tissue-specific homing of lymphocyte subsets and in trafficking of inflammatory cells.
Release of immuno-regulatory cytokines and chemokines during inflammatory response is mediated by a complex signaling network.
A main component of the inflammatory response is the production and release of immuno-regulatory cytokines and chemokines by macrophages.
Pro-inflammatory cytokines, such as tumor necrosis factor (TNF)α, interleukin (IL)-1, IL-6, IL-12, granulocyte macrophage colony stimulating factor (GM-CSF) and interferon (IFN)γ, induce both acute and chronic inflammatory responses; the chemokines MIP(macrophage inflammatory protein)-1α and RANTES (Regulated on Activation, Normal T Expressed and Secreted) are involved in the chemotaxis of leucocytes; and anti-inflammatory cytokines, such as IL-4, IL-10 and transforming growth factor (TGF)β, limit the magnitude and the extent of inflammation .
Thus, CXCL12 and CXCR4 have a constitutive and inflammatory role in the intestinal mucosa and their selective therapeutic manipulation may be considered in IBD management.
Inflammatory bowel disease (IBD) is characterized by increased lymphocytic infiltrate to the lamina propria (LP) and upregulation of inflammatorychemokines and receptors.
In the patients with GPC, three inflammation-related factors, IL-6, M-CSF, and monokine-induced gamma interferon (MIG), increased to four times those in the control group, and five inflammation-related factors, eotaxin-2, IL-6sR, IL-11, MIP-1delta, and TIMP-2, increased to eight times the control values.
In the patients with VKC, four inflammation-related factors, eotaxin, interleukin (IL)-11, monocyte chemoattractant protein (MCP)-1, and macrophage-colony stimulating factor (M-CSF) increased to four times the values in the control group, and seven inflammation-related factors, eotaxin-2, IL-4, IL-6, interleukin-6 soluble receptor (IL-6sR), IL-7, macrophage inflammatory protein (MIP)-1delta, and tissue inhibitor of metalloproteinases (TIMP)-2, increased to eight times the control values.
Thus, IL-6sR may play an important pathophysiological role in giant papillary proliferation in VKC and GPC, and eotaxin-2 may play an important role in eosinophilic inflammation in VKC.
Although the mediators involved in immunomodulation and synovial cell function, including cytokines, chemokines, and adhesion molecules, have primary roles in the inflammatory and catabolic processes in the joint, they may also promote cartilage damage, directly or indirectly.
In addition to the requirement of chemokines for the recruitment of T lymphocytes and other inflammatory cells to the subsynovial lining, adhesion receptors must be available on synovial blood vessels for binding the circulating leukocytes and other cell types with which they interact in the inflamed tissue, including macrophages, dendritic cells, and fibro-blasts.
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