Eosinophils and fibroblasts are believed to play important roles in the pathogenesis of bronchial asthma. This article focuses on the interaction between eosinophils and fibroblasts. Human eosinophil degranulation in the presence of lung fibroblasts is enhanced when both eosinophils and fibroblasts are activated by C5 a and TNF, respectively. This enhancement of eosinophil degranulation is partly dependent on GM-CSF from fibroblasts and on the adhesion of eosinophils to fibroblasts mediated by the ICAM-1/CD 18 dependent and CD 29-dependent mechanism. CD 11 b expression on human eosinophils increases after coculture with IL-1 β-stimulated fibroblasts, and this increase in CD 11 b expression is mediated by GM-CSF from fibroblasts and direct cell contact, similarly to above degranulation findings. On the other hand, IL-4 enhances SCF production by human lung fibroblasts, and IL-5-activated human eosinophils further augments SCF production stimulated by IL-4. Furthermore, eosinophil major basic protein interacts in a synergistic fashion with IL-1 a or TGF-β to further augment lung fibroblast IL-6-type cytokine production. It is possible that activated fibroblasts lead to the enhancement of eosinophil granule protein release and cytokine production, which results in the further activation of fibroblasts, leading to chronic asthmatic inflammation.
