Involvement of IL‐6 in a Glucan Model of Vascular Injury

Abstract

The role of interleukin-6 (IL-6) in granulomatous vasculitis is not yet fully understood. To investigate its involvement in granulomatosis injury an interleukin-6 deficient (IL6−/−) mouse model of glucan-induced pulmonary vasculitis was employed. Briefly, IL-6−/− mice and C57B/J6 (IL-6+/+) mice were injected intravenously with a suspension of glucan isolated from the cell wall of bakers yeast. Histologic examination of paraffin embedded sections demonstrated no significant difference in the number of infiltrating leukocytes between the IL-6+/+ and IL-6−/− glucan injured mice. Similar numbers of granulomatous formations were noted in both the IL-6+/+ and IL-6−/− injured animals, while no granulomas are seen in saline injected control mice. Cells recovered from the bronchioalveolar lavage (BAL) fluid were differentially stained and counted. While there was a significant increase in infiltrating leukocytes recovered from the BAL following glucan-induced injury, there was no significant difference between the IL-6−/− and IL-6+/+ mice. In addition, no difference was demonstrated in total protein content in the BAL fluid between IL-6−/− and IL-6+/+ mice. An additional marker of neutrophil activity, myeloperoxidase (MPO) activity in IL6−/− mice demonstrated significantly less (p<0.005) MPO activity than their IL-6+/+ counterparts. These studies suggest that IL-6, while possibly influencing the role that neutrophils play in glucan-induced vasculitis, does not exacerbate or attenuate the overall T cell mediated pulmonary injury. Work supported by NIH RO1 HL07097