Energy Taxis toward Host-Derived Nitrate Supports a
            <i>Salmonella</i>
            Pathogenicity Island 1-Independent Mechanism of Invasion

Rivera-Chávez, Fabian; Lopez, Christopher A.; Zhang, Lillian F.; García-Pastor, Lucía; Chávez‐Arroyo, Alfredo; Lokken, Kristen L.; Tsolis, Renée M.; Winter, Sebastian; Bäumler, Andreas J.

doi:10.1128/mbio.00960-16

Cited by 57 publications

(50 citation statements)

References 62 publications

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“…In addition to the role of the bacterial flagellum as a rotational motility organelle, a variety of other flagella‐mediated mechanisms contribute to the outcome of a successful infection of the host: adhesion to cell surfaces (Crawford, Reeve, & Gunn, ; Erdem, Avelino, Xicohtencatl‐Cortes, & Girón, ; Girón, Torres, Freer, & Kaper, ) and invasion of the epithelial cell barrier (Elhadad, Desai, Rahav, McClelland, & Gal‐Mor, ; Rivera‐Chávez et al . , ), as well as immune recognition and evasion (Finlay & McFadden, ; Schreiber et al . , ).…”

Section: Discussionmentioning

confidence: 99%

Flagellin phase-dependent swimming on epithelial cell surfaces contributes to productiveSalmonellagut colonisation

Horstmann

Zschieschang

Truschel³

et al. 2017

Cellular Microbiology

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The flagellum is a sophisticated nanomachine and an important virulence factor of many pathogenic bacteria. Flagellar motility enables directed movements towards host cells in a chemotactic process, and near-surface swimming on cell surfaces is crucial for selection of permissive entry sites. The long external flagellar filament is made of tens of thousands subunits of a single protein, flagellin, and many Salmonella serovars alternate expression of antigenically distinct flagellin proteins, FliC and FljB. However, the role of the different flagellin variants during gut colonisation and host cell invasion remains elusive. Here, we demonstrate that flagella made of different flagellin variants display structural differences and affect Salmonella's swimming behaviour on host cell surfaces. We observed a distinct advantage of bacteria expressing FliC-flagella to identify target sites on host cell surfaces and to invade epithelial cells. FliC-expressing bacteria outcompeted FljB-expressing bacteria for intestinal tissue colonisation in the gastroenteritis and typhoid murine infection models. Intracellular survival and responses of the host immune system were not altered. We conclude that structural properties of flagella modulate the swimming behaviour on host cell surfaces, which facilitates the search for invasion sites and might constitute a general mechanism for productive host cell invasion of flagellated bacteria.

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Section: Discussionmentioning

confidence: 99%

Flagellin phase-dependent swimming on epithelial cell surfaces contributes to productiveSalmonellagut colonisation

Horstmann

Zschieschang

Truschel³

et al. 2017

Cellular Microbiology

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“…At 8 or 20 hours after treatments, cells were collected for gene expression or protein analysis by Western Blot, as described below. For nitrate measurement experiments, a trans well plate model of polarized intestinal cells was used as previously described (30). Briefly, Caco-2 cells were maintained on minimum essential medium (MEM) containing 10% fetal bovine serum (FBS).…”

Section: Methodsmentioning

confidence: 99%

“…Intestinal nitrate measurements were performed as described previously (30). Briefly, uninfected mice were euthanized, and the intestine was removed and divided along its sagittal plane.…”

Section: Methodsmentioning

confidence: 99%

Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion

Byndloss

Olsan

Rivera-Chávez

et al. 2017

Science

Self Cite

853

696

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Perturbation of the gut-associated microbial community may underlie many human illnesses, but the mechanisms that maintain homeostasis are poorly understood. We found depletion of butyrate-producing microbes by antibiotic treatment reduced epithelial signaling through the intracellular butyrate sensor PPAR-γ. Nitrate levels increased in the colonic lumen because epithelial expression of Nos2, the gene encoding inducible nitric oxide synthase (iNOS) was elevated in the absence of PPAR-γ-signaling. Microbiota-induced PPAR-γ-signaling also limits the luminal bioavailability of oxygen by driving the energy metabolism of colonic epithelial cells (colonocytes) towards β-oxidation. Therefore, microbiota-activated PPAR-γ-signaling is a homeostatic pathway that prevents a dysbiotic expansion of potentially pathogenic Escherichia and Salmonella by reducing the bioavailability of respiratory electron acceptors to Enterobacteriaceae in the lumen of the colon.

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“…Nitrate measurement was performed as previously described (36). Briefly, the mucus layer of intestine was scraped, homogenized in PBS, and filter sterilized.…”

Section: Methodsmentioning

confidence: 99%

The gut microbiota modulator berberine ameliorates collagen‐induced arthritis in rats by facilitating the generation of butyrate and adjusting the intestinal hypoxia and nitrate supply

Yue

Yu²,

Fang³

et al. 2019

The FASEB Journal

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The commensal microbiota is one of the environmental triggers of rheumatoid arthritis (RA). Recent studies have identified the characteristics of the gut microbiota in patients with RA. However, it is still unclear how the microbiota can be modulated to slow down disease progression. In the present study, berberine, a modulator of gut microbiota with substantial anti‐RA effect, was chosen to explore the mechanisms by which the microbiota modulators ameliorate RA. The results showed that oral administration of berberine alleviated collagen‐induced arthritis (CIA) in rats in a gut microbiota‐dependent manner. Berberine down‐regulated the diversity and richness of the gut bacteria, reduced the abundance of Prevotella, and elevated the abundance of butyrate‐producing bacteria in CIA rats as determined by the 16S rRNA gene sequence, which might function through limiting the generation of nitrate and stabilizing the physiologic hypoxia in the intestine. Moreover, berberine treatment significantly increased the intestinal butyrate level and promoted the expression and activity of butyryl‐CoA:acetate‐CoA transferase (BUT). The coadministration of a BUT inhibitor largely diminished the adjustment of intestinal environment and the antiarthritic effect of berberine. In conclusion, modulators of the gut microbiota might serve as therapeutic agents for RA by inducing the butyrate generation through promoting the expression and activity of BUT.—Yue, M., Tao, Y., Fang, Y., Lian, X., Zhang, Q., Xia, Y., Wei, Z., Dai, Y. The gut microbiota modulator berberine ameliorates collagen‐induced arthritis in rats by facilitating the generation of butyrate and adjusting the intestinal hypoxia and nitrate supply. FASEB J. 33,12311‐12323 (2019). http://www.fasebj.org

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Energy Taxis toward Host-Derived Nitrate Supports a Salmonella Pathogenicity Island 1-Independent Mechanism of Invasion

Cited by 57 publications

References 62 publications

Flagellin phase-dependent swimming on epithelial cell surfaces contributes to productiveSalmonellagut colonisation

Flagellin phase-dependent swimming on epithelial cell surfaces contributes to productiveSalmonellagut colonisation

Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion

The gut microbiota modulator berberine ameliorates collagen‐induced arthritis in rats by facilitating the generation of butyrate and adjusting the intestinal hypoxia and nitrate supply

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