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Unexpected Macrophage Activity Might Alter the Inflammatory Process in Necrotizing Enterocolitis
Jessica Raque^*, Jessica Shepherd, Paul J. Matheson, Jason Smith, Cynthia Downard

Surgery, University of Louisville, Louisville, KY

Purpose: The pathophysiology of necrotizing enterocolitis (NEC) is not well understood. Macrophages might play a role in clearing bacteria from the gut in the initial stages of NEC. Macrophage Inhibitory Peptide 1α (MIP-1α) is a cytokine produced by T-cells that works to inhibit macrophage chemotaxis and activation. Interleukin12 (IL-12) is a pro-inflammatory chemotactant produced primarily by macrophages. We hypothesized that the pro-inflammatory state associated with NEC pathophysiology would inhibit MIP-1α expression and induce IL-12 expression in serum.
Methods: Timed pregnant Sprague-Dawley rats were randomized by litter. Controls were delivered vaginally and dam-fed. NEC groups were prematurely delivered, formula fed, given a single oral dose of lipopolysaccharide, and subjected to intermittent cold and hypoxia. Animals were sacrificed at 12, 24, 48, 72, and 96 hours of life and serum samples were taken for cytokine analysis by Luminex MagPix multianalyte cytokine array.
Results: As shown below, MIP-1α was upregulated , and IL-12 was downregulated in NEC groups compared to controls. (See figure 1).
Conclusion: In the first 48 hours of life, MIP-1α levels are increased in NEC animals compared to Controls, and this correlates with decreased IL-12 levels in NEC animals. These findings suggest that macrophage function plays a central role in the first 48 hours of NEC, and that either a paucity of macrophages or macrophage inhibition is present in NEC, which is an unexpected finding.

Figure 1

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