Characterization of the rat leukocyte integrin, CD11/CD18, by the use of LFA‐1 subunit‐specific monoclonal antibodies

Tamatani, Takuya; Kotani, Masaharu; Miyasaka, Masayuki

doi:10.1002/eji.1830210314

Cited by 209 publications

(95 citation statements)

References 25 publications

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“…Circulating granulocytes expressed high levels of L-selectin and b 2 , and to a lesser extent a 4 (Figure 1a-c), in line with other studies (Tamatani et al, 1991;Issekutz TB et al, 1996;van den Berg et al, 2001). In inflamed paws, CD45 þ cells expressed high levels of b 2 and low levels of L-selectin (Figure 1e and f).…”

Section: Coexpression Of Selectins Integrins and Pecam-1 With Opioidssupporting

confidence: 89%

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Selectins and integrins but not platelet–endothelial cell adhesion molecule‐1 regulate opioid inhibition of inflammatory pain

Machelska

Brack

Mousa

et al. 2004

British J Pharmacology

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1 Control of inflammatory pain can result from activation of opioid receptors on peripheral sensory nerves by opioid peptides secreted from leukocytes in response to stress (e.g. experimental swim stress or surgery). The extravasation of immunocytes to injured tissues involves rolling, adhesion and transmigration through the vessel wall, orchestrated by various adhesion molecules. 2 Here we evaluate the relative contribution of selectins, integrins a 4 and b 2 , and platelet-endothelial cell adhesion molecule-1 (PECAM-1) to the opioid-mediated inhibition of inflammatory pain. 3 We use flow cytometry, double immunofluorescence and nociceptive (paw pressure) testing in rats with unilateral hind paw inflammation induced by complete Freund's adjuvant. 4 In inflamed tissue, 43-58% of hematopoietic cells (CD45 þ ) expressed opioid peptides. L-selectin and b 2 were coexpressed by 7 and 98% of opioid-containing leukocytes, respectively. Alpha 4 integrin was expressed in low levels by the majority of leukocytes. Opioid-containing cells, vascular P-and E-selectin and PECAM-1 were simultaneously upregulated. 5 Swim stress produced potent opioid-mediated antinociception in inflamed tissue, unaffected by blockade of PECAM-1. However, blockade of L-and P-selectins by fucoidin, or of a 4 and b 2 by monoclonal antibodies completely abolished peripheral stress-induced antinociception. This coincided with a 40% decrease in the migration of opioid-containing leukocytes to inflamed tissue. 6 These findings establish selectins and integrins a 4 and b 2 , but not PECAM-1, as important molecules involved in stress-induced opioid-mediated antinociception in inflammation. They point to a cautious use of anti-inflammatory treatments applying anti-selectin, anti-a 4 and anti-b 2 strategies because they may impair intrinsic pain inhibition.

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Section: Coexpression Of Selectins Integrins and Pecam-1 With Opioidssupporting

confidence: 89%

“…Issekutz AC et al, 1996;Issekutz TB et al, 1996). The WT.3 mAb recognizes the b 2 subunit (Tamatani et al, 1991), which is shared by the three integrins CD11a (lymphocyte functionassociated antigen-1; LFA-1), CD11b (Mac-1) and CD11c (p150,95) (Sanchez-Madrid et al, 1983).…”

Section: Antibodiesmentioning

confidence: 99%

Selectins and integrins but not platelet–endothelial cell adhesion molecule‐1 regulate opioid inhibition of inflammatory pain

Machelska

Brack

Mousa

et al. 2004

British J Pharmacology

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“…mAbs. Hybridoma cell lines producing mouse IgGl anti-rat ICAM-1 (anti-CD54) mAb (IA29) (11) and mouse IgG2 antirat LFA-1 (anti-CD11a) mAb (WT.1) (12) …”

Section: Methodsmentioning

confidence: 99%

Antibody to intercellular adhesion molecule 1 protects the kidney against ischemic injury.

Kelly

Williams

Colvin

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

456

237

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The pathophysiology of ischemic acute renal failure is complex, and the role of leukocyte adhesion in this process is not well defined. A monoclonal antibody (mAb) against intracellular adhesion molecule 1 (anti-ICAM-1), administered at the time of bilateral renal ischemia in the rat, prevented both functional impairment and histologic changes of acute renal failure. Plasma creatinine measured (mg/dl) 24 hr after 30 min of ischemia was 0.61 ± 0.05 in the anti-ICAM-1-treated animals compared with 2.4 ± 0.14 (P < 0.0001) in the vehicle-treated ischemic group. Forty-eight hours after ischemia, creatinine values were 0.46 ± 0.05 and 2.03 ± 0.22 (P < 0.0001) in anti-ICAM-1 and vehicle-treated groups, respectively. A low dose of anti-ICAM-1 that was itself nonprotective, when given with partially protective doses of a mAb against lymphocyte function-associated antigen-i (anti-LFA-1), acted synergistically to prevent renal failure. Anti-ICAM-1 mAb also protected the kidney when administered 0.5 or 2 hr but not 8 hr after restoration of blood flow and when the ischemic period was extended to 40 min. Ischemia-induced increases in tissue myeloperoxidase, a marker of neutrophil infitration, were mitigated with anti-ICAM-1 treatment. Thus, anti-ICAM-1 mAb protected the kidney against ischemic renal failure, even when the antibody was administered after the ischemic period. These results suggest a critical role for leukocytes and adhesion molecules in the pathophysiology of ischemic inijury and may have important therapeutic implications.The pathophysiology of acute ischemic renal failure is poorly understood. Therapeutic interventions designed to inhibit cellular injury have frequently been either ineffective or equivocal in their effectiveness in both experimental animals and man, and rarely has an agent been effective when administered after the ischemic insult (1).We hypothesized that leukocyte adhesion plays a critical role in renal ischemia-reperfusion injury. Outer medullary vascular congestion that occurs in ischemic acute renal failure (2) may result from leukocyte-endothelial cell interactions with obstruction of the vasa recta or leukocyte-mediated increases in endothelial permeability leading to erythrocyte aggregation (3). This would sustain ischemia to the outer medulla, even if total renal blood flow were restored.Leukocyte adhesion to various cell types is mediated in large part by the three P2 integrins: CD11a/CD18 [lymphocyte function-associated antigen 1 (LFA-1)], CD11b/CD18 (Mac-i), and CD11c/CD18. The intercellular adhesion molecule 1 (ICAM-1, CD54) is a ligand for CD11a/CD18 and CD11b/CD18. The CD54-CD11/CD18 interactions are important determinants of leukocyte-endothelial cell adhesion (4). The purpose of our studies was to evaluate the effects of a monoclonal antibody (mAb) directed against ICAM-1 on ischemic acute renal failure in the rat.Ischemia results in increased tissue levels of proinflammatory mediators, including cytokines (5, 6) and products of arachidonic acid metabolism (7), which ...

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“…17 Anti-CD18 mAb, or isotypematched control mAb (10 g/mL) was infused for 30 minutes, commencing 10 minutes prior to a 10-minute infusion of MIP-2 or vehicle. The basal release of neutrophils from the bone marrow was not altered by the infusion of anti-CD18 mAb ( Figure 3B-C).…”

Section: Blockade Of Cd18 Integrins Increases Neutrophil Mobilizationmentioning

confidence: 99%

The CXC chemokine MIP-2 stimulates neutrophil mobilization from the rat bone marrow in a CD49d-dependent manner

Burdon

Martin

Rankin

2005

Blood

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The acute release of neutrophils from the bone marrow is a critical step in their trafficking to sites of inflammation. This process is stimulated by systemically acting inflammatory mediators, such as the CXC chemokines. In this study we have used a novel in situ perfusion system of the rat femoral bone marrow to directly investigate the role of specific adhesion molecules in chemokine-stimulated neutrophil mobilization. We show here that neutrophils mobilized in response to rat macrophage inflammatory protein-2 (MIP-2) shed L-selectin and expressed significantly higher levels of CD11b and CD49d. However, inhibition of L-selectin sheddase activity with KD-IX-73-4 had no effect on the number of neutrophils mobilized in response to rat MIP-2. Blockade of CD18, using a neutralizing monoclonal antibody (mAb), did not inhibit neutrophil mobilization but unexpectedly increased the rate and number of neutrophils released from the bone marrow in response to chemokine, suggesting that CD18 could play a role in neutrophil retention within the bone marrow. Blockade of CD49d using either a selective mAb or a specific antagonist resulted in a dramatic inhibition (> 75%) of the chemokine-stimulated neutrophil mobilization from the bone marrow. These data reveal contrasting roles for CD18 and CD49d in the retention and release of neutrophils from the bone marrow. (Blood. 2005;105:2543-2548)

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Characterization of the rat leukocyte integrin, CD11/CD18, by the use of LFA‐1 subunit‐specific monoclonal antibodies

Cited by 209 publications

References 25 publications

Selectins and integrins but not platelet–endothelial cell adhesion molecule‐1 regulate opioid inhibition of inflammatory pain

Selectins and integrins but not platelet–endothelial cell adhesion molecule‐1 regulate opioid inhibition of inflammatory pain

Antibody to intercellular adhesion molecule 1 protects the kidney against ischemic injury.

The CXC chemokine MIP-2 stimulates neutrophil mobilization from the rat bone marrow in a CD49d-dependent manner

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