Journal article
Novel Model To Study Combined Effects of Microorganisms and Oxidants on Development of Intestinal Necrosis
Surgical infections, Vol.13(4), pp.238-244
08/01/2012
DOI: 10.1089/sur.2011.055
PMID: 22789034
Abstract
Background:
Although the cause of intestinal necrosis in diseases such as necrotizing enterocolitis (NEC) is multi-factorial, oxidants and bacteria likely are key factors. Many animal models of NEC generate histologic necrosis, but it is rare to see the gross necrosis that is observed in infants. Here, we present a novel model that produces full-thickness intestinal necrosis when chloramine-T, an oxidizing agent, is introduced directly into isolated intestinal loops. The aim of this study was to determine the role of bacteria in this model.
Methods:
Three-week-old mice underwent isolated ileal loop construction by suture ligation, and either chloramine-T or saline was injected into the loop. Intestines were then returned to the abdominal cavity, and the incision was closed for 24 h, after which the intestinal loops were analyzed histologically and microbiologically. To determine if bacteria home to the site of injury, some mice had intracecal injection of luminescent
Pseudomonas aeruginosa
(PA). These mice were sacrificed 2, 6, 8, and 24 h later, and luminescent bacteria were localized via photon camera imaging.
Results:
No gross necrosis was observed in the saline-treated group, but 59% of the animals in the chloramine-T-treated group had necrosis (p<0.001). Relative bacterial species numbers were calculated for untreated control animals and those with saline-treated loops and chloramine-T-treated loops without and with necrosis.
Lactobacillus
was detected in 60% of the control animals but was absent in all animals that underwent surgery. Methicillin-sensitive
Staphylococcus aureus
, PA, and
Enterococcus faecium
were present only in animals that underwent loop construction; however, bacterial communities did not differ according to loop treatment or the presence or absence of necrosis. After intracecal injection of PA, bacteria homed to the loop and proximal bowel even though the loop was discontinuous with the remaining bowel.
Conclusions:
Intraluminal chloramine-T causes full-thickness necrosis in three-week-old mice and is characterized by a loss of probiotic bacteria such as
Lactobacillus
. Necrotic loops of bowel become colonized rapidly with pathogenic bacteria by unconventional mechanisms. Oxidant stress and colonization by pathogenic bacteria may play important roles in intestinal necrosis across a wide spectrum of pathologic states, including NEC.
Details
- Title: Subtitle
- Novel Model To Study Combined Effects of Microorganisms and Oxidants on Development of Intestinal Necrosis
- Creators
- Erica M Carlisle - 1Department of Surgery, University of Chicago Medical Center, Chicago, IllinoisDonald Liu - 2Department of Pediatrics, University of Chicago Medical Center, Chicago, IllinoisOlga Zaborina - 1Department of Surgery, University of Chicago Medical Center, Chicago, IllinoisJohn C Alverdy - 1Department of Surgery, University of Chicago Medical Center, Chicago, Illinois
- Resource Type
- Journal article
- Publication Details
- Surgical infections, Vol.13(4), pp.238-244
- Publisher
- Mary Ann Liebert, Inc
- DOI
- 10.1089/sur.2011.055
- PMID
- 22789034
- ISSN
- 1096-2964
- eISSN
- 1557-8674
- Language
- English
- Date published
- 08/01/2012
- Academic Unit
- Stead Family Department of Pediatrics; Surgery
- Record Identifier
- 9984051785002771
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