Cytokine production in a model of wound healing: The appearance of MIP-1, MIP-2, cachectin/TNF and IL-I

Macrophage inflammatory protein-2 gene therapy attenuates adenovirus- and acetaminophen-mediated hepatic injury

“…A regenerative role for MIP-2 in the liver would be consistent with its critical role in wound healing responses. 26 Recombinant adenoviruses have been tested extensively in gene delivery protocols because of their ability to infect many cell types with high efficiencies in vivo. 24 After intravenous infusion, the majority of the adenoviral vector can ultimately be found in the liver but delivery of recombinant adenovirus in this manner elicits a powerful systemic immune response that limits gene expression and the ability to re-administer the viral vector.…”

MIP-1alpha as a critical macrophage chemoattractant in murine wound repair.

“…Among the many candidates for a wound monocyte chemoattractant is macrophage inflammatory protein 1 ␣ (MIP-1 ␣ ) 1 (13). MIP-1 ␣ is an LPS-inducible chemokine of the C-C family that is a strong chemoattractant for monocytes (14).…”

TNF-α promotes LPA1- and LPA3-mediated recruitment of leukocytes in vivo through CXCR2 ligand chemokines

“…Some chemokines, particularly CXC chemokines containing the ELR motif (including CXCL1, 2, 3, 5, 6, 7, and 8) are crucial for neutrophil recruitment via binding to and activation of their receptors CXCR1 or CXCR2 ( 13,14 ). In the mouse, IL-8/CXCL8 and a functional homolog of CXCR1 are absent, and keratinocytederived chemokine (KC, Gro ␣ , CXCL1) and macrophage infl ammatory protein-2 (MIP-2) appear to be the major ELR CXC chemokines expressed at sites of tissue infl ammation following injury and/or infection (15)(16)(17)(18)(19). It is assumed that neutrophil migration in this species is mediated mainly by KC and MIP-2 via binding to their sole receptor CXCR2 ( 20,21 ).…”