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Am J Physiol Gastrointest Liver Physiol (March 6, 2002). doi:10.1152/ajpgi.00491.2001
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Articles in PresS, published online ahead of print March 6, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00491.2001
Submitted on November 16, 2001
Accepted on February 11, 2002

IL4 Inhibits Vasoactive Intestinal Peptide (VIP) Production by Macrophages

Ahmed Metwali1*, Arthur M Blum1, David E Elliott1, and Joel V Weinstock1

1 Department of Internal Medicine, University of Iowa, Iowa City, Iowa, USA

* To whom correspondence should be addressed. E-mail: joel-weinstock{at}uiowa.edu.

In schistosomiasis, eggs induce granulomas that have a VIP immunoregulatory circuit. This study explored the regulation of VIP production at sites of inflammation. Splenocytes from uninfected C57BL/6 mice expressed VIP mRNA and protein, which stopped following egg deposition. Eggs induce a Th2 response suggesting that Th2 cytokines like IL4 can regulate VIP. To address this issue, splenocytes from uninfected mice were incubated 4h with or without rIL4. IL4 inhibited VIP mRNA expression. F4/80+ macrophages were the source of constitutively expressed VIP, subject to IL4 regulation. In IL4 KO mice, splenic VIP production did not down-modulate during schistosome infection suggesting that IL4 is a critical cytokine regulating VIP production in WT mice spleen. IL4 producing granulomas in schistosomiasis made VIP. Experiments showed that granuloma VIP derived from F4/80 negative (non-macrophage) cell populations, explaining this paradox. Granuloma F4/80+ cells from IL4 KO mice expressed VIP. Thus, macrophages can make VIP, which is subject to IL4 regulation. However, in the Th2 granulomas other cell types produce VIP, which compensates for loss of macrophages as a source of this molecule.






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