| First Author | Doyle NA | Year | 1997 |
| Journal | J Clin Invest | Volume | 99 |
| Issue | 3 | Pages | 526-33 |
| PubMed ID | 9022088 | Mgi Jnum | J:39042 |
| Mgi Id | MGI:86424 | Doi | 10.1172/JCI119189 |
| Citation | Doyle NA, et al. (1997) Neutrophil margination, sequestration, and emigration in the lungs of L-selectin-deficient mice. J Clin Invest 99(3):526-33 |
| abstractText | These studies tested the hypothesis that L-selectin plays a role in neutrophil traffic in the lungs, particularly in neutrophil margination, sequestration, and emigration, using L-selectin-deficient mice. No defect in neutrophil margination within either capillaries or arterioles and venules was observed in uninflamed lungs of L-selectin- deficient mice. The initial rapid sequestration of neutrophils within the pulmonary capillaries I min after intravascular injection of complement fragments was not prevented. In contrast, L-selectin did contribute to the prolonged neutrophil sequestration (greater than or equal to 5 min). Interestingly, neutrophil accumulation within noncapillary microvessels required L-selectin at both I and 5 min after complement injection. During bacterial pneumonias, L-selectin played a role in neutrophil accumulation within noncapillary microvessels in response to either Escherichia coli or Streptococcus pneumoniae and within capillaries in response to E. Coli but not S. Pneumoniae. However, L-selectin was not required for emigration of neutrophils or edema in response to either organism. These studies demonstrate a role for L-selectin in the prolonged sequestration of neutrophils in response to intravascular complement fragments, in the intracapillary accumulation of neutrophils during E. Coli- induced pneumonia, and in the accumulation of neutrophils within noncapillary microvessels when induced by either intravascular complement fragments or bacteria within the airways. |
