<i>Helicobacter hepaticus</i>increases intestinal injury in a rat model of necrotizing enterocolitis

Dvorak, Katerina; Coursodon-Boyiddle, Christine F.; Snarrenberg, Chelsea L.; Kananurak, Anchasa; Underwood, Mark A.; Dvořák, Bohuslav

doi:10.1152/ajpgi.00483.2012

Cited by 9 publications

(11 citation statements)

References 58 publications

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“…Necrotizing enterocolitis (NEC) is the second most common cause of morbidity in premature infants, and dysbiosis is thought to play an important role in disease onset. H. hepaticus infection of premature formulafed rats (model of NEC) induced inflammation, increased levels of TLR4 receptor, altered activation of autophagy, and increased the incidence and severity of NEC in rats exposed to asphyxia and cold stress [69]. These results are consistent with observations in neonates of blooms of proinflammatory microbes just before the onset of NEC and support dysbiosis in the incidence of NEC.…”

Section: Experimental Infection With Non-h Pylori Helicobacterssupporting

confidence: 86%

Gastric and Enterohepatic Helicobacters other than Helicobacter pylori

et al. 2014

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During the past year, research on non-Helicobacter pylori species has intensified. H. valdiviensis was isolated from wild birds, and putative novel species have been isolated from Bengal tigers and Australian marsupials. Various genomes have been sequenced: H. bilis, H. canis, H. macacae, H. fennelliae, H. cetorum, and H. suis. Several studies highlighted the virulence of non-H. pylori species including H. cinaedi in humans and hyperlipidemic mice or H. macacae in geriatric rhesus monkeys with intestinal adenocarcinoma. Not surprisingly, increased attention has been paid to the position of Helicobacter species in the microbiota of children and animal species (mice, chickens, penguins, and migrating birds). A large number of experimental studies have been performed in animal models of Helicobacter induced typhlocolitis, showing that the gastrointestinal microbial community is involved in modulation of host pathways leading to chronic inflammation. Animal models of H. suis, H. heilmannii, and H. felis infection have been used to study the development of severe inflammation-related pathologies, including gastric MALT lymphoma and adenocarcinoma.

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Section: Experimental Infection With Non-h Pylori Helicobacterssupporting

confidence: 86%

Gastric and Enterohepatic Helicobacters other than Helicobacter pylori

et al. 2014

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“…So far, only a few strains of bacteria have been proven in this rigorous manner to be true NEC pathogens. They include strains of Clostridium butyricum and Clostridium perfringens [69] , Helicobacter hepaticus MU 94-1 [70] , and C. muytjensii 51329 [71] .…”

Section: Identification Of Nec Pathogensmentioning

confidence: 99%

Roles of nitric oxide and intestinal microbiota in the pathogenesis of necrotizing enterocolitis

Grishin

Bowling

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et al. 2016

Journal of Pediatric Surgery

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Necrotizing enterocolitis remains one of the most vexing problems in the neonatal intensive care unit. Risk factors for NEC2 include prematurity, formula feeding, and inappropriate microbial colonization of the GI tract. The pathogenesis of NEC is believed to involve weakening of the intestinal barrier by perinatal insults, translocation of luminal bacteria across the weakened barrier, an exuberant inflammatory response, and exacerbation of the barrier damage by inflammatory factors, leading to a vicious circle of inflammation-inflicted epithelial damage. Nitric oxide (NO), produced by inducible NO synthase (iNOS) and reactive NO oxidation intermediates play a prominent role in the intestinal barrier damage by inducing enterocyte apoptosis and inhibiting the epithelial restitution processes, namely enterocyte proliferation and migration. The factors that govern iNOS upregulation in the intestine are not well understood, which hampers efforts in developing NO/iNOS-targeted therapies. Similarly, efforts to identify bacteria or bacterial colonization patterns associated with NEC have met with limited success, because the same bacterial species can be found in NEC and in non-NEC subjects. However, microbiome studies have identified the three important characteristics of early bacterial populations of the GI tract: high diversity, low complexity, and fluidity. Whether NEC is caused by specific bacteria remains a matter of debate, but data from hospital outbreaks of NEC strongly argue in favor of the infectious nature of this disease. Studies in Cronobacter muytjensii have established that the ability to induce NEC is the property of specific strains rather than the species as a whole. Progress in our understanding of the roles of bacteria in NEC will require microbiological experiments and genome-wide analysis of virulence factors.

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“…In the rat model, the stressors include separation from the dam, tube feeding, hypoxia, hypothermia, and enteral nourishment with bovine-based rat milk substitute. ( 11 )…”

Section: Introductionmentioning

confidence: 99%

Bifidobacterium longum subsp. infantis in experimental necrotizing enterocolitis: alterations in inflammation, innate immune response, and the microbiota

et al. 2014

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Background Probiotics decrease the risk of necrotizing enterocolits (NEC). We sought to determine the impact of Bifidobacterium longum subsp. infantis (B. infantis) in the established rat model of NEC. Methods Rat pups delivered one day prior to term gestation were assigned to one of three groups: dam-fed (DF), formula-fed (FF), or fed with formula supplemented with 5 × 106 CFU B. infantis per day (FF+Binf). Experimental pups were exposed to hypoxia and cold stress. Ileal tissue was examined for pathology and expression of inflammatory mediators, antimicrobial peptides, and goblet-cell products. Ceca were assessed for bacterial composition by analysis of 16S rRNA sequence. Results Administration of B. infantis significantly reduced the incidence of NEC, decreased expression of Il6, Cxcl1, Tnfa, Il23, and iNOS, and decreased expression of the antimicrobial peptides Reg3b and Reg3g. There was significant microbial heterogeneity both within groups and between experiments. The cecal microbiota was not significantly different between the FF and FF+Binf groups. Bifidobacteria were not detected in the cecum in significant numbers. Conclusions In the rat model, the inflammation associated with NEC was attenuated by administration of probiotic B. infantis. Dysbiosis was highly variable precluding determination of the precise role of the microbiota in experimental NEC.

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Helicobacter hepaticusincreases intestinal injury in a rat model of necrotizing enterocolitis

Cited by 9 publications

References 58 publications

Gastric and Enterohepatic Helicobacters other than Helicobacter pylori

Gastric and Enterohepatic Helicobacters other than Helicobacter pylori

Roles of nitric oxide and intestinal microbiota in the pathogenesis of necrotizing enterocolitis

Bifidobacterium longum subsp. infantis in experimental necrotizing enterocolitis: alterations in inflammation, innate immune response, and the microbiota

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