Infectious susceptibility and severe deficiency of leukocyte rolling and recruitment in E-selectin and P-selectin double mutant mice

@article{Bullard1996InfectiousSA,
  title={Infectious susceptibility and severe deficiency of leukocyte rolling and recruitment in E-selectin and P-selectin double mutant mice},
  author={D. Bullard and E. Kunkel and H. Kubo and M. Hicks and I. Lorenzo and N. A. Doyle and C. Doerschuk and K. Ley and A. Beaudet},
  journal={The Journal of Experimental Medicine},
  year={1996},
  volume={183},
  pages={2329 - 2336}
}
During the initial phase of the inflammatory response, leukocytes marginate and roll along the endothelial surface, a process mediated largely by the selectins and their ligands. Mice with mutations in individual selectins show no spontaneous disease and have mild or negligible deficiencies of inflammatory responses. In contrast, we find that mice with null mutations in both endothelial selectins (P and E) develop a phenotype of leukocyte adhesion deficiency characterized by mucocutaneous… Expand
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TLDR
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TLDR
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TLDR
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TLDR
The occurrence of skin and pulmonary disease in E/P double-Mutant mice but not E/L/P triple-mutant mice suggests that deficiency of L-selectin alters the inflammatory response in E-P mutants. Expand
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TLDR
A child with recurrent infections and clinical evidence of impaired pus formation reminiscent of a leukocyte adhesion deficiency syndrome, but whose neutrophils were functionally normal and expressed normal levels of CD18, L-selectin, and sialyl-Lewis(x) is described. Expand
Lack of Functional P-Selectin Ligand Exacerbates Salmonella Serovar Typhimurium Infection1
TLDR
A definitive phenotypic abnormality in mice lacking core 2, PS GL-1, or P-selectin is demonstrated, suggesting that the interaction of functional PSGL-1 with P- selectin is an important process in host defense against Salmonella infection. Expand
Importance of E-selectin for firm leukocyte adhesion in vivo.
TLDR
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TLDR
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References

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Leukocyte rolling and extravasation are severely compromised in P selectin-deficient mice
TLDR
It is reported that P selectin-deficient mice, generated by gene targeting in embryonic stem cells, exhibit a number of defects in leukocytes behavior, including elevated numbers of circulating neutrophils, virtually total absence of leukocyte rolling in mesenteric venules, and delayed recruitment of neutrophil to the peritoneal cavity upon experimentally induced inflammation. Expand
Characterization of E-selectin-deficient mice: demonstration of overlapping function of the endothelial selectins.
TLDR
It is demonstrated that the majority of neutrophil migration in both models requires an endothelial selectin but that E-selectin and P- selectin are functionally redundant, which has important implications in the use of selectin antagonists in the treatment of inflammatory disease. Expand
Lymphocyte homing and leukocyte rolling and migration are impaired in L-selectin-deficient mice.
TLDR
Homing experiments demonstrated that L-selectin plays an essential role in leukocyte homing to lymphoid tissues and sites of inflammation and significant defects inLeukocyte rolling and neutrophil migration into the peritoneum in response to an inflammatory stimulus were observed. Expand
L-selectin-deficient mice have impaired leukocyte recruitment into inflammatory sites
TLDR
It is demonstrated that L-selectin plays a prominent role in leukocyte homing to nonlymphoid tissues during inflammation and that blocking this process can be beneficial during pathological inflammatory responses. Expand
Sequential contribution of L- and P-selectin to leukocyte rolling in vivo
TLDR
Data show that P- selectin is important during the initial induction of leukocyte rolling after tissue trauma, and at later time points and in TNF-alpha-treated preparations, rolling is largely L-selectin dependent. Expand
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TLDR
Recognition of the molecular pathogenesis of this disorder has allowed rich insights into the role of cellular adherence reactions in inflammation and host defense. Expand
P-selectin/ICAM-1 double mutant mice: acute emigration of neutrophils into the peritoneum is completely absent but is normal into pulmonary alveoli.
TLDR
These data demonstrate organ-specific differences, since emigration into the peritoneum requires both adhesion molecules while emigrating into the lung requires neither, and P-selectin-independent mechanisms cannot lead to ICAM-1-independent firm adhesion and emigration. Expand
In vivo behavior of neutrophils from two patients with distinct inherited leukocyte adhesion deficiency syndromes.
TLDR
Testing the behavior of neutrophils from two patients with distinct inherited leukocyte adhesion deficiency syndromes demonstrates that both selectin-carbohydrate-mediated initiation of adhesion and subsequent activation-induced beta 2-integrin engagement are essential for the normal function of human neutrophil in vivo. Expand
Absence of trauma-induced leukocyte rolling in mice deficient in both P- selectin and intercellular adhesion molecule 1
TLDR
It is concluded that the residual trauma-induced leukocyte rolling seen in P-selectin-deficient mice is completely abolished by concomitant ICAM-1 deficiency. Expand
In vivo neutrophil and lymphocyte function studies in a patient with leukocyte adhesion deficiency type II.
TLDR
In vivo neutrophil and lymphocyte function in a patient who lacks Sialyl-Lewis-X, a ligand for the selectin family of leukocyte adhesion molecules, provides direct evidence that theSelectin family and its ligands play an important role in neutrophils function. Expand
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