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Monoclonal antibody to murine PECAM-1 (CD31) blocks acute inflammation in vivo
1Department of Pathology, Boston University School of Medicine, Massachusetts 02118-2394.
Abstract:
A murine model of peritonitis was used to test the role of platelet/endothelial cell adhesion molecule 1 (PECAM-1/CD31) in acute inflammation. A monoclonal antibody (mAb) specific for murine PECAM-1 injected intravenously 4 h before the intraperitoneal injection of thioglycollate broth blocked leukocyte emigration into the peritoneal cavity for up to 48 h. This block was particularly evident for neutrophils. Control mAb, including one that bound to murine CD18 without blocking its function, failed to block emigration when used at the same or higher concentrations. The decreased emigration seen with the anti-PECAM-1 antibody was not due to neutropenia or neutrophil sequestration in the lung, spleen, or other organs; peripheral blood leukocyte counts were not diminished in these mice. In the mesenteric venules of the mice treated with anti-PECAM-1 mAb, leukocytes were frequently seen in association with the luminal surface of the vessel, but did not appear to emigrate. Thus, the requirement for PECAM-1 in the transendothelial migration of leukocytes previously seen in an in vitro model holds true in this in vivo model of acute inflammation.
Insights
Platelet/endothelial cell adhesion molecule 1 (PECAM-1) is crucial for acute inflammation, as blocking it prevents leukocytes, especially neutrophils, from emigrating into the peritoneal cavity in a mouse model. This confirms PECAM-1
Area of Science:
- Immunology
- Cell Biology
- Inflammation Research
Background:
- Acute inflammation involves leukocyte recruitment to sites of injury.
- Platelet/endothelial cell adhesion molecule 1 (PECAM-1/CD31) is implicated in leukocyte trafficking.
- Previous in vitro studies suggested PECAM-1's role in transendothelial migration.
Purpose of the Study:
- To investigate the in vivo role of PECAM-1 in acute inflammation using a murine peritonitis model.
- To determine if blocking PECAM-1 function affects leukocyte emigration.
- To confirm findings from in vitro models in a relevant in vivo setting.
Main Methods:
- A murine model of thioglycollate-induced peritonitis was established.
- Mice were intravenously injected with a monoclonal antibody (mAb) against murine PECAM-1.
- Leukocyte emigration into the peritoneal cavity was assessed up to 48 hours post-injection.
- Control mAbs, including anti-CD18, were used for comparison.
- Peripheral blood leukocyte counts and organ sequestration were evaluated.
Main Results:
- Intravenous injection of anti-PECAM-1 mAb significantly blocked leukocyte emigration into the peritoneal cavity.
- Neutrophil emigration was particularly inhibited by anti-PECAM-1 treatment.
- Control mAbs did not inhibit leukocyte emigration.
- The observed effect was not due to neutropenia or neutrophil sequestration in other organs.
- Leukocytes were observed adhered to mesenteric venule surfaces but failed to transmigrate.
Conclusions:
- PECAM-1 is essential for leukocyte transendothelial migration in vivo during acute inflammation.
- Blocking PECAM-1 function effectively inhibits neutrophil recruitment.
- The in vitro role of PECAM-1 in leukocyte migration is validated in a relevant in vivo model.
- PECAM-1 represents a potential therapeutic target for modulating inflammatory responses.