Cloning, expression, and functional characterization of rat MIP-2: a neutrophil chemoattractant and epithelial cell mitogen

Driscoll, Kevin E.; Hassenbein, Diana G.; Howard, Brian W.; Isfort, Robert J.; Cody, David B.; Tindal, M H; Suchanek, Maureen K.; Carter, Janet M.

doi:10.1002/jlb.58.3.359

Cited by 138 publications

(88 citation statements)

References 16 publications

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“…It is therefore reasonable to speculate that soluble factors produced by activated macrophages trigger additional cells types, such as epithelial cells and leukocytes, thus provoking an inflammatory cascade. A related observation is the induction of MIP-2 by chitosan, since Driscoll and colleagues have reported that MIP-2 stimulates epithelial cell proliferation [8]. Hence, MIP-2 production by activated macrophages may play a critical role in epithelial regeneration.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Macrophage Activation by Chitin Derivatives

Mori

Murakami

Okumura

et al. 2005

The Journal of Veterinary Medical Science

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ABSTRACT. In order to analyze the detailed mechanisms responsible for macrophage activation by chitin derivatives, resident peritoneal macrophages were prepared and stimulated with chitin, chitosan and low-molecular weight chitosan. Our findings were as follows: (i) chitosan induced apoptosis of peritoneal macrophages, but this did not occur when chitin or water soluble low-molecular weight chitosan were used; (ii) chitosan treatment induced activation markers, such as the major histocompatibility complex (MHC) class I, class II, Fc receptors, transferrin receptor, mannose receptor, Fas, and macrophage inflammatory protein (MIP)-2, whereas chitin and low molecular weight soluble chitosan induced only the expression of MHC class I and II molecules; (iii) apoptosis induced by chitosan was mediated by the Fas signaling pathway, in response to phagocytosis via the mannose receptor. We conclude that since chitosan activates macrophages, this may be the mechanism by which it accelerates wound healing.

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Section: Discussionmentioning

confidence: 99%

Mechanism of Macrophage Activation by Chitin Derivatives

Mori

Murakami

Okumura

et al. 2005

The Journal of Veterinary Medical Science

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“…Reverse transcription. A 1-g portion of total RNA was subjected to first-strand cDNA synthesis in a 25-l reaction mixture containing avian myeloblastosis virus reverse transcriptase (10 U), dNTP mixture (2 mM concentrations of each dNTP), oligo(dT) [12][13][14][15][16][17][18] primers (10 M), and reaction buffer as supplied with the enzyme (50 mM Tris-HCl (pH 8.3), 50 mM KCl, 10 mM MgCl 2 , 0.5 mM spermidine, and 10 mM DDT). The samples were incubated in a PerkinElmer 480 thermal cycler (PerkinElmer, Wellesley, MA) at 42°C for 60 min followed by enzyme denaturation step at 94°C for 2 min.…”

Section: Lung Cytokine Gene Expression (Rt-pcr)mentioning

confidence: 99%

“…Within the CXC chemokine subfamily, the presence of a glutamate-leucine-arginine (ELR) motif before the first conserved cysteine residue confers selectivity in recruiting neutrophils (30), and the ELR-containing CXC chemokines, CINC, and MIP-2 are potent inducers of neutrophil activation and their directional migration (17,18,(31)(32)(33). We have therefore investigated whether the effect of ebselen on neutrophil recruitment might be achieved through inhibition of the macrophage CXC chemokines CINC-1 and MIP-2.…”

Section: Effect Of Ebselen On Airway CXC Chemokine Expressionmentioning

confidence: 99%

“…The mechanism of pulmonary PMN migration in rats given intratracheal LPS has been partially characterized and involves production by airway cells of inflammatory cytokines such as TNF-␣ and IL-1␤ as well as neutrophil-specific chemoattractants known as CXC chemokines, which in rats include the family of cytokineinduced neutrophil chemoattractants (CINCs) and macrophage-inflammatory protein-2 (MIP-2) also known as CINC-3 (12)(13)(14)(15)(16)(17)(18)(19). CD18 integrins have also been shown to play a role for full polymorphonuclear cell (PMN) migration.…”

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confidence: 99%

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Differential Effects of Ebselen on Neutrophil Recruitment, Chemokine, and Inflammatory Mediator Expression in a Rat Model of Lipopolysaccharide-Induced Pulmonary Inflammation

Haddad

McCluskie

Birrell

et al. 2002

The Journal of Immunology

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We postulated that the seleno-organic compound ebselen would attenuate neutrophil recruitment and activation after aerosolized challenge with endotoxin (LPS) through its effect as an antioxidant and inhibitor of gene activation. Rats were given ebselen (1–100 mg/kg i.p.) followed by aerosolized LPS exposure (0.3 mg/ml for 30 min). Airway inflammatory indices were measured 4 h postchallenge. Bronchoalveolar lavage (BAL) fluid cellularity and myeloperoxidase activity were used as a measure of neutrophil recruitment and activation. RT-PCR analysis was performed in lung tissue to assess gene expression of TNF-α, cytokine-induced neutrophil chemoattractant-1 (CINC-1), macrophage-inflammatory protein-2 (MIP-2), ICAM-1, IL-10, and inducible NO synthase. Protein levels in lung and BAL were also determined by ELISA. Ebselen pretreatment inhibited neutrophil influx and activation as assessed by BAL fluid cellularity and myeloperoxidase activity in cell-free BAL and BAL cell homogenates. This protective effect was accompanied by a significant reduction in lung and BAL fluid TNF-α and IL-1β protein and/or mRNA levels. Ebselen pretreatment also prevented lung ICAM-1 mRNA up-regulation in response to airway challenge with LPS. This was not a global effect of ebselen on LPS-induced gene expression, because the rise in lung and BAL CINC-1 and MIP-2 protein levels were unaffected as were lung mRNA expressions for CINC-1, MIP-2, IL-10, and inducible NO synthase. These data suggest that the anti-inflammatory properties of ebselen are achieved through an inhibition of lung ICAM-1 expression possibly through an inhibition of TNF-α and IL-1β, which are potent neutrophil recruiting mediators and effective inducers of ICAM-1 expression.

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“…[6][7][8][9][10] Similarly, ENA-78 and MIP-2 are also produced by many cell types in response to TNF. [11][12][13][14] Recently, both Herbert and associates and ClarkLewis and colleagues have shown an important amino acid sequence in the primary CXC chemokine structure that appears to account for the disparate abilities of these molecules to function as promoters or inhibitors of neutrophil chemotaxis. [15][16][17] The 3 amino acid residues that immediately precede the first cysteine amino acid are critically important in receptor binding and neutrophil activation.…”

Section: -445)mentioning

confidence: 99%

The ratio of ELR+ to ELR− CXC chemokines affects the lung and liver injury following hepatic ischemia/reperfusion in the rat

et al. 2000

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Hepatic ischemia/reperfusion (I/R) results in a neutrophildependent lung and liver injury. The process of neutrophil recruitment and activation in this injury is at least partially dependent on the presence of the ELR؉ CXC chemokines. Other investigations have shown that ELR؊ CXC chemokines can block ELR؉ CXC chemokine neutrophil recruitment and activation in vitro. To begin to investigate the role of the balance between these 2 types of molecules in vivo in neutrophil recruitment and activation following hepatic I/R, we used our rat model of lobar hepatic I/R and pretreated animals with pharmacologic doses of gamma-interferon (␥-IFN). ␥-IFN is known to upregulate some of the ELR؊ CXC chemokines, including ␥-IFN-inducible protein (IP-10) and monokine-induced by ␥-IFN (MIG), as well as down-regulate ELR؉ CXC chemokine production. Following hepatic I/R or sham laparotomy, hepatic and pulmonary levels of the ELR؊ chemokines, IP-10 and MIG, and the ELR؉ chemokines, rat cytokine-induced neutrophil chemoattractant (KC), macrophage inflammatory protein-2 (MIP-2), and epithelial neutrophil activating protein (ENA-78) were determined by ELISA, and lung and liver injury were assessed. In response to ␥-IFN, hepatic and pulmonary levels of the ELR؊ chemokines were increased and the levels of the ELR؉ chemokines were decreased. Immunohistochemical staining confirmed the hepatocyte as the source of these molecules, as well as the changes in chemokine levels in response to ␥-IFN. There was an associated significant decrease in liver and lung injury, although there was no significant decrease in neutrophil influx in either tissue. This suggests that the alteration in the balance of ELR؉ to ELR؊ CXC chemokines results in a decrease in tissue injury through a mechanism other than through an alteration in tissue neutrophil levels. (HEPATOLOGY 2000;31: 435-445.)

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Cloning, expression, and functional characterization of rat MIP-2: a neutrophil chemoattractant and epithelial cell mitogen

Cited by 138 publications

References 16 publications

Mechanism of Macrophage Activation by Chitin Derivatives

Mechanism of Macrophage Activation by Chitin Derivatives

Differential Effects of Ebselen on Neutrophil Recruitment, Chemokine, and Inflammatory Mediator Expression in a Rat Model of Lipopolysaccharide-Induced Pulmonary Inflammation

The ratio of ELR+ to ELR− CXC chemokines affects the lung and liver injury following hepatic ischemia/reperfusion in the rat

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