IL-10 AND GM-CSF EXPRESSION AND THE PRESENCE OF ANTIGEN-PRESENTING CELLS IN CHRONIC VENOUS ULCERS

Citation
Yq. Li et al., IL-10 AND GM-CSF EXPRESSION AND THE PRESENCE OF ANTIGEN-PRESENTING CELLS IN CHRONIC VENOUS ULCERS, The Journal of surgical research (Print), 79(2), 1998, pp. 128-135
Citations number
37
Categorie Soggetti
Surgery
ISSN journal
00224804
Volume
79
Issue
2
Year of publication
1998
Pages
128 - 135
Database
ISI
SICI code
0022-4804(1998)79:2<128:IAGEAT>2.0.ZU;2-I
Abstract
Background. White cell trapping and activation occurs in the legs of p atients having chronic venous insufficiency (CVI), and it is thought t hat this process may be important in the development of CVI ulcers. Th is study has compared the tissue distribution of proinflammatory (GM-C SF) and anti-inflammatory cytokines (IL-10) and inflammatory cell mark ers (CD68, HLA-DR) between CVI ulcers, other chronic and acute wounds, and autologous nonwounded skin to determine whether cell-mediated imm unity (CMI) is impaired in CVI ulcers. Methods. Wound and donor site t issue was obtained from 10 patients with CVI ulcers and 10 patients wi th other chronic and acute wounds. Serial Formalin-fixed sections were processed by standard hematoxylin and eosin staining or by indirect i mmunoperoxidase histochemical staining. Results. BLA-DR-positive antig en-presenting cells (APC), including CD68-positive macrophages and der mal dendritic cells, were found with greater frequency in CVI ulcers t han in other chronic or acute wounds (P = 0.0015) or in the autologous CVI donor site tissue (P = 0.006). CVI ulcers also demonstrated incre ased IL-IO staining of the entire epidermis compared to non-CVI wounds (P = 0.0019) or autologous donor site tissue (P = 0.004), whereas the re was no significant change in the presence of the counteracting cyto kine, GM-CSF. Conclusions. These findings suggest that although the ce llular components of CMI are present in CVI ulcers, their function may be impaired by the increased level of IL-10. Future studies will exam ine whether IL-10-mediated suppression of CMI and/or inhibition of GM- CSF-stimulated keratinocyte proliferation may contribute to the chroni c nature of CVI ulcers. (C) 1998 Academic Press.