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Published on: November 7, 2013
Decreased systemic polymorphonuclear neutrophil (PMN) rolling without increased PMN adhesion in peritonitis at remote
D E Swartz1, A J Seely, L Ferri
1Division of General Surgery, McGill University Health Center, Royal Victoria Hospital, 687 Pine Ave W, Montreal, Quebec, Canada H3A 1A1.
Background:
Previous in vitro studies have demonstrated that the host response to intra-abdominal infection produces increased generalized polymorphonuclear neutrophil (PMN) adherence to vascular endothelial cells (ECs), which may lead to subsequent endothelial damage, leaky capillaries, and organ dysfunction. There are scant data to demonstrate this enhanced systemic PMN adherence in vivo or the influence of PMN rolling on PMN endothelial adherence.
Hypothesis:
Systemic PMN adherence in the animal with sepsis is increased.
Design:
In vivo murine model of a 2-front infection using intravital microscopy of the cremasteric muscle to quantify PMN-EC adherence in a septic response.
Setting:
Basic science laboratory and animal surgical facility.
Patients Or Other Participants:
One hundred CD1 male mice.
Interventions:
Animals underwent cecal ligation and puncture peritonitis, cremasteric muscle Escherichia coli infection, both infections, or neither (controls). Eighteen hours later, the mice underwent exteriorization of the cremasteric muscle under an intravital microscope for measurement of PMN-EC interactions. Blood was then drawn for calculation of circulating PMN counts.
Main Outcome Measures:
Adherence of PMNs, PMN rolling flux, PMN rolling velocity, and circulating PMN counts.
Results:
Circulatory mechanics did not differ between the groups. Unlike static in vitro systems, we could not detect an increase in PMN adherence after peritonitis with this dynamic in vivo model. A local (cremasteric) infection was associated with marked PMN adherence. Peritonitis was associated with reduced PMN adherence at a local infection site as well as reduced rolling adhesion and PMN rolling velocity.
Conclusions:
The data suggest that intra-abdominal infection does not increase remote PMN adherence, and may actually result in reduction of systemic adherence via modulation of PMN rolling.
Insights
Intra-abdominal infection does not increase systemic polymorphonuclear neutrophil (PMN) adherence in vivo. Instead, sepsis may reduce PMN adherence and rolling velocity, contrary to in vitro findings.
Area of Science:
- Immunology
- Sepsis Pathophysiology
- Microcirculation
Background:
- In vitro studies suggest intra-abdominal infection increases polymorphonuclear neutrophil (PMN) adherence to endothelial cells (ECs), potentially causing organ dysfunction.
- However, in vivo data demonstrating this enhanced systemic PMN adherence and the role of PMN rolling are limited.
Purpose of the Study:
- To investigate systemic PMN adherence in vivo during a septic response in a murine model.
- To evaluate the influence of PMN rolling on PMN-EC adherence in sepsis.
Main Methods:
- An in vivo murine model utilizing intravital microscopy of the cremasteric muscle was employed.
- Mice underwent cecal ligation and puncture peritonitis, localized Escherichia coli infection, or both.
- PMN-EC interactions, PMN rolling flux, PMN rolling velocity, and circulating PMN counts were quantified.
Main Results:
- Systemic PMN adherence did not increase following peritonitis in this dynamic in vivo model.
- A local infection significantly increased PMN adherence.
- Peritonitis was associated with reduced PMN adherence, rolling adhesion, and rolling velocity at the local infection site.
Conclusions:
- Intra-abdominal infection does not appear to increase remote PMN adherence in vivo.
- Sepsis may modulate PMN rolling, potentially reducing systemic PMN adherence.
