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Massachusetts Chapter of the American College of Surgeons Massachusetts Chapter of the American College of Surgeons Massachusetts Chapter of the American College of Surgeons Massachusetts Chapter of the American College of Surgeons Massachusetts Chapter of the American College of Surgeons
57th Annual Meeting Abstracts


Poster 16

Abstract Title

Anti-inflammatory Effects of Intestinal Alkaline Phosphatase on Intestinal Luminal Fluids

 

Author Block

Angela K. Moss, MD, Madhu S. Malo, MD, PhD, Halim Yammine, MD, Sayeda Nasrin Alam, MD, Sundaram Ramasamy, PharmD, PhD, H. Shaw Warren, MD, Elizabeth Hohmann, MD, Richard Hodin, MD

Massachusetts GeneralHospital, Boston, MA

 

Abstract Body

Background: The gastrointestinal tract has a dual responsibility of supporting bacterial growth while limiting the hostís inflammatory response to bacteria.† Oral supplementation of intestinal alkaline phosphatase (IAP), a brush border enzyme, reduces inflammation in chronic colitis models, but its precise mechanism of action remains unclear.† Here we examined the effects of IAP on bacterial products and luminal fluids in vitro.

Methods: Overnight bacterial cultures were sonicated, centrifuged, and the supernatant was filtered.† Supernatant was incubated with IAP then applied to THP-1 monocytes.† Mouse proximal small intestine contents and scrapings and cecal contents were obtained.† These fluids were incubated +/- IAP and applied to THP-1 monocytes.† Monocyte supernatant was assayed for IL-8 content by ELISA.

Results: IAP inhibited the ability of sonicated E. coli to induce IL-8 production by monocytes in a dose-dependent fashion with an 18% decrease with IAP treatment.†† In contrast, sonicated Enterococcus did not increase IL-8 production.† Treatment of monocytes with luminal fluids caused vigorous IL-8 production, which was decreased by preincubation of fluids with IAP, most dramatically in cecal contents, followed by proximal small intestine contents and proximal small intestine scrapings.

Conclusions: IAP prevents stimulation of inflammatory cells by sonicated E. coli and, more dramatically, by intestinal luminal fluids.† This anti-inflammatory effect likely underlies the protection IAP confers to the host and may explain its efficacy as an IBD treatment.

 

 

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