Bacterial adaptation in patients with short bowel and colon in continuity

Briet, F.; Flourié, Bernard; Achour, Lotfi; Maurel, M.; Rambaud, Jean–Claude; Messing, Bernard

doi:10.1016/0016-5085(95)90629-0

Cited by 94 publications

(44 citation statements)

References 38 publications

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“…Such abnormal microbial flora may be a risk factor for gut-derived systemic infection, as suggested in animal models and some clinical studies (2,14,35,36). We did not test for the presence of SBBO in our study subjects, but our data raise the possibility that stimulation of local innate cytokine-mediated inflammatory responses by flagellin or LPS (Fig.…”

Section: Discussionmentioning

confidence: 76%

“…SBS is characterized by chronic diarrhea and malabsorption, dehydration and malnutrition, and, in patients requiring parenteral nutrition (PN), frequent infections (13,36). Unfortunately, SBS and PN administration are each associated with infection by enteric gramnegative bacteria, suggesting that failure of the gut barrier occurs (2,4,5,18,20,22,24,25,33,34). …”

mentioning

confidence: 99%

“…Based on evidence derived largely from animal models (36) and limited human studies (2,4,14,18,20,33,35,38), common events that occur in human SBS may contribute to gut barrier dysfunction. These include small bowel bacterial overgrowth (SBBO), systemic or local infection, splanchnic hypoperfusion, gut mucosal inflammation, use of PN, lack of enteral feeding, and malnutrition, all of which may cause erosion of mucosal anatomic and immune barriers (36).…”

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confidence: 99%

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Detectable serum flagellin and lipopolysaccharide and upregulated anti-flagellin and lipopolysaccharide immunoglobulins in human short bowel syndrome

Ziegler

Luo²,

Estívariz³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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DP, Gewirtz AT. Detectable serum flagellin and lipopolysaccharide and upregulated anti-flagellin and lipopolysaccharide immunoglobulins in human short bowel syndrome. Am J Physiol Regul Integr Comp Physiol 294: R402-R410, 2008. First published November 14, 2007 doi:10.1152/ajpregu.00650.2007.-Gut barrier dysfunction may occur in short bowel syndrome (SBS). We hypothesized that systemic exposure to flagellin and lipopolysaccharide (LPS) in SBS might regulate specific immune responses. We analyzed serial serum samples obtained from parenteral nutrition (PN)-dependent patients with SBS versus non-SBS control serum. Serum from 23 adult SBS patients was obtained at baseline and 4, 8, 12, 16, 20, and 24 wk 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 an ELISA recognizing an array of gram-negative flagellins, and LPS was detected by limulus assay. Serum flagellin-and LPS-specific immunoglobulin levels (IgM, IgA, and IgG) were determined by ELISA. Serum flagellin and LPS were undetectable in control subjects. In contrast, serum flagellin, LPS, or both were detected in 14 SBS patients (61%) during one or more time points [flagellin alone, 5/23 (22%); LPS alone, 6/23 (26%); or flagellin ϩ LPS, 3/23 (13%)]. Flagellin-specific serum IgM, IgA, and IgG levels were markedly increased in SBS patients compared with both control populations and remained elevated during the 6-mo study period. LPS-specific IgA was significantly higher in SBS patients compared with healthy controls; LPS-specific IgM, IgA, and IgG levels each decreased over time in association with PN weaning. We conclude that 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. parenteral nutrition; intestinal barrier function SHORT BOWEL SYNDROME (SBS) occurs after massive small bowel resection and is an important clinical entity, with significant morbidity and mortality (13,36). SBS is characterized by chronic diarrhea and malabsorption, dehydration and malnutrition, and, in patients requiring parenteral nutrition (PN), frequent infections (13,36). Unfortunately, SBS and PN administration are each associated with infection by enteric gramnegative bacteria, suggesting that failure of the gut barrier occurs (2,4,5,18,20,22,24,25,33,34).

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Section: Discussionmentioning

confidence: 76%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Detectable serum flagellin and lipopolysaccharide and upregulated anti-flagellin and lipopolysaccharide immunoglobulins in human short bowel syndrome

Ziegler

Luo²,

Estívariz³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Many factors that may promote the adaptation of the remaining bowel functions have been reported, such as pancreatico-biliary secretions, hormones, luminal nutrients (1-4) such as dietary fiber, short-chain fatty acid, and glutamine (GLN) (5,6). However, there have been limited reports concerned about the relations between nutrients and floral changes in the gut (7,8).…”

Section: Introductionmentioning

confidence: 99%

“…Discontinuation of the oral nutrient changes normal bacterial flora (7) and weakens the barrier function of the mucosa (8). GLN is also known to maintain the structure and function of the intestine (9), especially the intestinal permeability (10).…”

Section: Introductionmentioning

confidence: 99%

Glutamine on the Luminal Microbial Environment After Massive Small Bowel Resection

Choi

Lee

2002

J Korean Med Sci

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To evaluate the oral glutamine (GLN) on the luminal microbes and bacterial translocation (BT) in short bowel, 45 Wistar rats were utilized in three groups; A (control), and B and C (short bowel, 85% of small bowel resected). The group A was fed with elemental diet (EmD), B with EmD+2% glycine, and C with EmD+2% GLN. The groups B and C were isocaloric and isonitrogenous. Wet weight, DNA, protein, and histomorphometry of the mucosa and parallel microbial culture from cecal contents, caval blood, and tissue blocks of the liver, spleen, and mesenteric lymph nodes were performed on the 5th, 10th, and 15th day. Mucosal growth was higher in group C than B. Colony forming units (CFU) from cecal contents increased more in group B than in C. BTs in A, B, and C were 7/15, 8/15, and 2/15, respectively. Total CFUs in blood and tissues were 5.8×10 4 /g, 5.5×106 /g, and 1.8×10 4 /g, respectively. As for BT, the most frequent organism was Klebsiella in A (79.3%), but E. coli in B and C (94.2% and 55.6%). GLN seems to suppress luminal microbes, and reduces BT in short bowel due to enforced barrier function and proliferation of the mucosa.

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Irreversible Intestinal Failure

Goulet,

Ruemmele,

Lacaille

et al. 2004

J. pediatr. gastroenterol. nutr.

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Intestinal failure (IF) can be defined as the reduction of functional gut mass below the minimal amount necessary for digestion and absorption adequate to satisfy the nutrient and fluid requirements for maintenance in adults or growth in children. In developed countries, IF mainly includes individuals with the congenital or early onset of conditions requiring protracted or indefinite parenteral nutrition (PN). Short bowel syndrome was the first commonly recognized cause of protracted IF. The normal physiologic process of intestinal adaptation after extensive resection usually allows for recovery of sufficient intestinal function within weeks to months. During this time, patients can be sustained on parenteral nutrition. Only a few children have permanent intestinal insufficiency and life‐long dependency on PN. Non‐transplant surgery including small bowel tapering and lengthening may allow weaning from PN in some cases. Hormonal therapy with recombinant human growth hormone has produced poor results while therapy with glucagon‐like peptide‐2 holds promise. Congenital diseases of enterocyte development such as microvillus inclusion disease or intestinal epithelial dysplasia cause permanent IF for which no curative medical treatment is currently available. Severe and extensive motility disorders such as total or subtotal intestinal aganglionosis (long segment Hirschsprung disease) or chronic intestinal pseudo‐obstruction syndrome may also cause permanent IF. PN and home‐PN remain are the mainstays of therapy regardless of the cause of IF. Some patients develop complications while receiving long‐term PN for IF especially catheter related complications (thrombosis, sepsis) and liver disease. These patients may be candidates for intestinal transplantation. This review discusses the causes of irreversible IF and emphasizes the specific medico‐surgical strategies for prevention and treatment of these conditions at several stages of IF.

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Bacterial adaptation in patients with short bowel and colon in continuity

Cited by 94 publications

References 38 publications

Detectable serum flagellin and lipopolysaccharide and upregulated anti-flagellin and lipopolysaccharide immunoglobulins in human short bowel syndrome

Detectable serum flagellin and lipopolysaccharide and upregulated anti-flagellin and lipopolysaccharide immunoglobulins in human short bowel syndrome

Glutamine on the Luminal Microbial Environment After Massive Small Bowel Resection

Irreversible Intestinal Failure

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