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1 Medicine, Emory University, Atlanta, Georgia, United States
2 Pathology, Emory University, Atlanta, Georgia, United States
3 Atlanta, Georgia, United States; Medicine, Emory University, Atlanta, Georgia, United States
4 Nutrition and Health Science Program, EMORY UNIVERSITY, ATLANTA, Georgia, United States
5 Surgery, Emory University, Atlanta, Georgia, United States
6 Department of Medicine, Emory University, Atlanta, Georgia, United States
* To whom correspondence should be addressed. E-mail: tzieg01{at}emory.edu.
Background and Aims: Gut barrier dysfunction may occur in short bowel syndrome (SBS). We hypothesized that systemic exposure to flagellin and lipopolysaccharide (LPS) in SBS may regulate specific immune responses. We analyzed serial serum samples obtained from parenteral nutrition (PN)-dependent patients with SBS versus non-SBS control serum. Methods: Serum from 23 adult SBS patients was obtained at baseline and 4, 8, 12, 16, 20 and 24 weeks in a trial of modified diet with or without growth hormone. Control serum was obtained from 48 healthy adults and 37 adults requiring PN during critical illness. Serum flagellin was detected by ELISA, recognizing an array of Gram-negative flagellins and LPS by limulus assay. Serum flagellin- and LPS-specific immunoglobulin levels (IgM, IgA and IgG) were determined by ELISA. Results: Serum flagellin and LPS were undetectable in control subjects. In contrast, serum flagellin, LPS, or both was detected in 14 SBS patients (61%) during one or more time points [flagellin alone, 5/23 (22%); LPS alone, 6/23 (26%); or flagellin + LPS, 3/23 (13%)]. Flagellin-specific serum IgM, IgA and IgG levels were markedly increased in SBS patients compared to both control populations and remained elevated during the 6-month study period. LPS-specific IgA was significantly higher in SBS patients versus healthy controls; LPS-specific IgM, IgA and IgG each decreased over time in association with PN weaning. Conclusions: Adults with PN-dependent SBS are systemically exposed to flagellin and LPS, presumably from the gut lumen. This likely regulates innate and adaptive immune responses to these specific bacterial products.
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