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
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.