Regulatory mechanisms of eosinophil adhesion to and transmigration across endothelial cells by alpha4 and beta2 integrins.
To participate in allergic airway inflammation, it is necessary for blood eosinophils (Eos) to adhere to and migrate across pulmonary vascular endothelial cells (EC). Accumulating evidence has established that Eos adhesion molecules, such as alpha4 and beta2 integrins, play central roles in these processes. We have reported that Eos spontaneously adhere to recombinant human (rh)-VCAM-1, while adhesion to rh-ICAM-1 requires a second stimulus such as GM-CSF. Furthermore, our study employing human pulmonary microvascular endothelial cells (HPMEC) revealed that although the alpha4 integrin/VCAM-1 pathway is crucial for the firm adhesion of Eos, subsequent transendothelial migration occurred dependent on the beta2 integrin/ICAM-1 pathway. We also discuss secretagogues that would affect Eos recruitment to the airways via regulation of alpha4 and beta2 integrins.
Yamamoto
H
H
Pulmonary Division, Second Department of Internal Medicine, Saitama Medical School, Irumagun, Saitama, Japan.
Nagata
M
M
D000818:Animals; D015703:Antigens, CD / Q000502:physiology*; D018821:CD18 Antigens / Q000502:physiology*; D002465:Cell Movement / Q000502:physiology*; D004730:Endothelium, Vascular / Q000473:pathology* / Q000502:physiology*; D004804:Eosinophils / Q000473:pathology*; D006801:Humans; D039441:Integrin alpha4
D015703:Antigens, CD; D018821:CD18 Antigens; D039441:Integrin alpha4