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Intravital microscopy of the murine urinary bladder microcirculation
Paulina M Kowalewska1, Lori L Burrows, Alison E Fox-Robichaud
1Medical Sciences Graduate Program, McMaster University, Hamilton, ON, Canada.
Microcirculation (New York, N.Y. : 1994)
|July 28, 2011
Summary
This study establishes a mouse model of bladder microcirculation to investigate endotoxin-induced leukocyte recruitment. It reveals key molecular mechanisms, including α(4)-integrins and ICAM-1, involved in leukocyte adhesion during urinary tract infections.
Area of Science:
- Urology
- Immunology
- Microcirculation Research
Background:
- Urinary tract infections (UTIs) involve complex inflammatory responses in the bladder.
- Understanding leukocyte recruitment is crucial for developing effective UTI treatments.
- Existing models may not fully capture the dynamics of bladder microcirculation.
Purpose of the Study:
- To develop and validate an in vivo mouse model of the urinary bladder microcirculation.
- To characterize the molecular mechanisms driving leukocyte recruitment in response to endotoxins.
- To provide a platform for studying inflammatory processes in UTIs.
Main Methods:
- Adapted a rat model technique for murine bladder microcirculation observation using intravital microscopy.
- Administered intravesical lipopolysaccharide (LPS) from E. coli and P. aeruginosa.
- Examined leukocyte-endothelial interactions and identified molecular mediators using antibodies.
Main Results:
- LPS induced significant leukocyte adhesion and rolling in the bladder microcirculation within four hours.
- Leukocyte adhesion was dependent on α(4)-integrins and ICAM-1; rolling was P-selectin dependent.
- Endothelial expression of VCAM-1 increased significantly post-LPS, while MIP-2 and KC blockade had no effect.
Conclusions:
- The established mouse model is suitable for studying inflammatory responses in vivo.
- This model facilitates research into the pathogenesis of urinary tract infections.
- Identified specific molecular players in endotoxin-induced leukocyte recruitment in the bladder.
