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First published online June 5, 2008
Experimental Biology and Medicine 233:1099-1108 (2008)
doi: 10.3181/0802-RM-53
© 2008 by the Society for Experimental Biology and Medicine
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ORIGINAL RESEARCH ARTICLE

Dietary Lactoferrin Does Not Prevent Dextran Sulfate Sodium Induced Murine Intestinal Lymphocyte Death

Paul A. Spagnuolo and Laurie Hoffman-Goetz1

Department of Health Studies and Gerontology, Faculty of Applied Health Sciences, University of Waterloo, Waterloo, Ontario N2L 3G1 Canada

To whom requests for reprints should be addressed at 1 Department of Health Studies and Gerontology, Faculty of Applied Health Sciences, University of Waterloo, 200 University Avenue West, Waterloo, Ontario N2L 3G1 Canada. E-mail: lhgoetz{at}healthy.uwaterloo.ca

Dextran sulfate sodium (DSS) induced intestinal inflammation is characterized by pronounced mucosal and epithelial cell damage. Bovine lactoferrin (bLf), a common dietary protein, influences inflammatory cytokines and intestinal lymphocyte (IL) apoptosis. The objectives of this study were to determine if 1) DSS induces IL necrotic or apoptotic death, 2) dietary bLf affects DSS induced IL death and 3) bLf alters cytokine profiles during DSS induced inflammation. Female C57BL/6 mice were randomized to 2% or 0% bLf diets for 12 d and within diets to 5% or 0% DSS in the drinking water for 4 d after which intestinal histology, IL number, IL apoptosis/necrosis, IL phenotypes, protein levels of pro-inflammatory cytokine (TNF-{alpha}) and transcription factor (NF{kappa}B), apoptotic (caspase 3, Bax) proteins, anti-inflammatory cytokine (IL-10) and anti-apoptotic (Bcl-2) protein in IL were evaluated. DSS treatment resulted in shortened intestinal length, decreased body weight and widespread mucosal damage as well as increased IL death as determined by a decreased percentage of viable (PI–/ANN–, P < 0.005) and increased percentage of necrotic/late apoptotic (PI+/ ANN+, P < 0.05) and necrotic (PI+/ANN–, P < 0.05) IL. DSS exposure increased caspase 3 (P < 0.05) and decreased Bcl-2 (P < 0.01) protein levels in mouse IL. Dietary bLf did not influence these cell death outcome measures. However, bLf reduced protein levels of the pro-inflammatory transcription factor, NF{kappa}B, in IL (P < 0.05) and was associated with a 34%, albeit non-significant, reduction in TNF-{alpha} relative to non-bLf fed mice. DSS treatment increased apoptosis and necrosis of mouse IL and elevated pro-apoptotic and reduced anti-apoptotic protein levels in these cells. Dietary bLf did not influence necrosis or apoptosis of IL but may provide limited protection in the intestine by affecting the pro-inflammatory transcription factor NF{kappa}B, and potentially, cytokine expression.

Key Words: intestinal lymphocytes • DSS • lactoferrin • apoptosis/necrosis • NF{kappa}B






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