Mouse model of Colonization of the Digestive Tract with
            <i>Acinetobacter Baumannii</i>
            and Subsequent Pneumonia

Coron, Noémie; Pavlíčková, Silvie; Godefroy, A.; Pailhoriès, Hélène; Kempf, Marie; Cassisa, Viviane; Marsollier, Laurent; Marion, Estelle; Joly-Guillou, Marie-Laure; Eveillard, Matthieu

doi:10.2217/fmb-2016-0203

Cited by 3 publications

(5 citation statements)

References 36 publications

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“…Acinetobacter species have been identified in the human fecal microbiota and it has been speculated that the gut could serve as a potential reservoir for Acinetobacter infection ( Timsit et al, 1993 ; Xavier et al, 1996 ; Ayats et al, 1997 ; Dijkshoorn et al, 2005 ; Roy et al, 2010 ; Pandey et al, 2012 ; Aljindan et al, 2015 ; Cheng et al, 2015 ; Li et al, 2015 ; Braun et al, 2017 ; Li et al, 2019 ). Consistent with this hypothesis, A. baumannii can bind to rabbit small intestinal glycosphingolipids ( Madar Johansson et al, 2020 ) and colonize the mouse gastrointestinal tract in a secretory IgA dependent manner ( Coron et al, 2017 ; Ketter et al, 2018 ). Moreover, ampicillin treatment of mice has been shown to elevate A. baumannii and A. calcoaceticus fecal levels, suggesting that antibiotic selection could allow the outgrowth of endogenous strains ( Raplee et al, 2021 ).…”

Section: Introductionmentioning

confidence: 71%

“…Entry of Acinetobacter spp. into the gut has recently been examined by Coron et al (2017) . The authors found that intranasal administration of A. baumannii in mice, which mimicked the major method by which ventilated patients in ICUs commonly become infected with Acinetobacter , resulted in digestive-tract colonization.…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, Medina et al found that A. baumannii gut colonization was an independent risk factor for the development of A. baumannii respiratory infections ( Medina-Presentado et al, 2013 ). Wisplinghof et al reported that the portal of entry was not identified in 48.6% of the A. baumannii bloodstream infections, suggesting that a significant proportion of these infections could be due to intestinal carriage ( Wisplinghoff et al, 2000 ; Coron et al, 2017 ). Our work complements these findings by demonstrating that Acinetobacter species are equipped to colonize the gastrointestinal tract, where they could serve as a reservoir for infection.…”

Section: Discussionmentioning

confidence: 99%

“…In animal models, A. baumannii colonized both the small and large intestine ( Coron et al, 2017 ; Ketter et al, 2018 ). In these models, intestinal inflammation was not specifically examined.…”

Section: Discussionmentioning

confidence: 99%

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Acinetobacter calcoaceticus is Well Adapted to Withstand Intestinal Stressors and Modulate the Gut Epithelium

et al. 2022

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Background: The gastrointestinal tract has been speculated to serve as a reservoir for Acinetobacter, however little is known about the ecological fitness of Acinetobacter strains in the gut. Likewise, not much is known about the ability of Acinetobacter to consume dietary, or host derived nutrients or their capacity to modulate host gene expression. Given the increasing prevalence of Acinetobacter in the clinical setting, we sought to characterize how A. calcoaceticus responds to gut-related stressors and identify potential microbe-host interactions.Materials and Methods: To accomplish these aims, we grew clinical isolates and commercially available strains of A. calcoaceticus in minimal media with different levels of pH, osmolarity, ethanol and hydrogen peroxide. Utilization of nutrients was examined using Biolog phenotypic microarrays. To examine the interactions of A. calcoaceticus with the host, inverted murine organoids where the apical membrane is exposed to bacteria, were incubated with live A. calcoaceticus, and gene expression was examined by qPCR.Results: All strains grew modestly at pH 6, 5 and 4; indicating that these strains could tolerate passage through the gastrointestinal tract. All strains had robust growth in 0.1 and 0.5 M NaCl concentrations which mirror the small intestine, but differences were observed between strains in response to 1 M NaCl. Additionally, all strains tolerated up to 5% ethanol and 0.1% hydrogen peroxide. Biolog phenotypic microarrays revealed that A. calcoaceticus strains could use a range of nutrient sources, including monosaccharides, disaccharides, polymers, glycosides, acids, and amino acids. Interestingly, the commercially available A. calcoaceticus strains and one clinical isolate stimulated the pro-inflammatory cytokines Tnf, Kc, and Mcp-1 while all strains suppressed Muc13 and Muc2.Conclusion: Collectively, these data demonstrate that A. calcoaceticus is well adapted to dealing with environmental stressors of the gastrointestinal system. This data also points to the potential for Acinetobacter to influence the gut epithelium.

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Section: Introductionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Acinetobacter calcoaceticus is Well Adapted to Withstand Intestinal Stressors and Modulate the Gut Epithelium

et al. 2022

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“…We identified that A. calcoaceticus strains are fairly resistant to changing pH, osmolarity, ethanol and hydrogen Entry of Acinetobacter spp. into the gut has recently been examined by Coron et al (2017). The authors found that intranasal administration of A. baumannii in mice, which mimicked the major method by which ventilated patients in ICUs commonly become infected with Acinetobacter, resulted in digestive-tract colonization.…”

Section: Discussionmentioning

confidence: 99%

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Amino acid competition shapesAcinetobacter baumanniigut carriage

Ren,

Clark,

Bansah

et al. 2024

Preprint

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Antimicrobial resistance is an urgent threat to human health. Asymptomatic colonization is often critical for persistence of antimicrobial-resistant pathogens. Gut colonization by the antimicrobial-resistant priority pathogenAcinetobacter baumanniiis associated with increased risk of clinical infection. Ecological factors shapingA. baumanniigut colonization remain unclear. Here we show thatA. baumanniiand other pathogenicAcinetobacterevolved to utilize the amino acid ornithine, a non-preferred carbon source.A. baumanniiutilizes ornithine to compete with the resident microbiota and persist in the gut in mice. Supplemental dietary ornithine promotes long-term fecal shedding ofA. baumannii. By contrast, supplementation of a preferred carbon source--monosodium glutamate (MSG)--abolishes the requirement forA. baumanniiornithine catabolism. Additionally, we report evidence for diet promotingA. baumanniigut carriage in humans. Together, these results highlight that evolution of ornithine catabolism allowsA. baumanniito compete with the microbiota in the gut, a reservoir for pathogen spread.

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Mouse model of Colonization of the Digestive Tract with Acinetobacter Baumannii and Subsequent Pneumonia

Cited by 3 publications

References 36 publications

Acinetobacter calcoaceticus is Well Adapted to Withstand Intestinal Stressors and Modulate the Gut Epithelium

Acinetobacter calcoaceticus is Well Adapted to Withstand Intestinal Stressors and Modulate the Gut Epithelium

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Amino acid competition shapesAcinetobacter baumanniigut carriage

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