Lactobacillus johnsonii ameliorates intestinal, extra-intestinal and systemic pro-inflammatory immune responses following murine Campylobacter jejuni infection

Bereswill, Stefan; Ekmekciu, Ira; Escher, Ulrike; Fiebiger, Ulrike; Stingl, Kerstin; Heimesaat, Markus M.

doi:10.1038/s41598-017-02436-2

Cited by 49 publications

(48 citation statements)

References 44 publications

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“…This may suggest that a critical population level of attached bifidobacteria is required to result in the competitive exclusion of a pathogen. In contrast to the results demonstrated here, a previous study in mice with L. johnsonii indicated no reduction in lower intestinal C. jejuni colonisation; however, a suppressed intestinal and systemic pro-inflammatory and enhanced anti-inflammatory immune response were both observed, indicating other potential benefits of the use of probiotics on C. jejuni infection [45]. Notably, no statistically significant increase in C. jejuni growth in the presence of GMO was observed under anti-infective and exclusion assay conditions.…”

Section: Combined Effect Of Gmo and B Infantis On C Jejuni Adhesioncontrasting

confidence: 99%

Bifidobacterium longum subsp. infantis ATCC 15697 and Goat Milk Oligosaccharides Show Synergism In Vitro as Anti-Infectives against Campylobacter jejuni

Quinn

Slattery

Walsh

et al. 2020

Foods

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Bifidobacteria are known to inhibit, compete with and displace the adhesion of pathogens to human intestinal cells. Previously, we demonstrated that goat milk oligosaccharides (GMO) increased the attachment of Bifidobacterium longum subsp. infantis ATCC 15697 to intestinal cells in vitro. In this study, we aimed to exploit this effect as a mechanism for inhibiting pathogen association with intestinal cells. We examined the synergistic effect of GMO-treated B. infantis on preventing the attachment of a highly invasive strain of Campylobacter jejuni to intestinal HT-29 cells. The combination decreased the adherence of C. jejuni to the HT-29 cells by an average of 42% compared to the control (non-GMO treated B. infantis). Increasing the incubation time of the GMO with the Bifidobacterium strain resulted in the strain metabolizing the GMO, correlating with a subsequent 104% increase in growth over a 24 h period when compared to the control. Metabolite analysis in the 24 h period also revealed increased production of acetate, lactate, formate and ethanol by GMO-treated B. infantis. Statistically significant changes in the GMO profile were also demonstrated over the 24 h period, indicating that the strain was digesting certain structures within the pool such as lactose, lacto-N-neotetraose, lacto-N-neohexaose 3 -sialyllactose, 6 -sialyllactose, sialyllacto-N-neotetraose c and disialyllactose. It may be that early exposure to GMO modulates the adhesion of B. infantis while carbohydrate utilisation becomes more important after the bacteria have transiently colonised the host cells in adequate numbers. This study builds a strong case for the use of synbiotics that incorporate oligosaccharides sourced from goat s milk and probiotic bifidobacteria in functional foods, particularly considering the growing popularity of formulas based on goat milk. Foods 2020, 9, 348 2 of 15Listeria monocytogenes, and Clostridium difficile [4][5][6]. Microbe-associated molecular patterns (MAMPs) are recognized by the host s intestinal pattern recognition receptors (PRRs), and these interactions play key roles in the association of pathogens with the intestinal epithelia. Probiotics also express molecular patterns which can recognize the same trans-membrane receptors as the pathogens, thus blocking the sites for pathogenic contact by competitive exclusion and, in some cases, displacing already-attached pathogens [7]. However, the health benefits associated with bifidobacteria are reliant on such strains colonising the host in sufficient numbers [8]. The important step in microbial colonisation of the intestinal epithelium is the attachment of bacterial surface lectins to intestinal sugar structures. Recent studies have suggested that milk oligosaccharides may enhance the specific ability of bifidobacteria to attach to the GI epithelium [9][10][11]. Indeed, our group investigated the ability of goat milk oligosaccharides (GMO) to increase the attachment of Bifidobacterium longum subsp. infantis ATCC 15697 to HT-29 cells. Exposure of the strain ...

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Section: Combined Effect Of Gmo and B Infantis On C Jejuni Adhesioncontrasting

confidence: 99%

Bifidobacterium longum subsp. infantis ATCC 15697 and Goat Milk Oligosaccharides Show Synergism In Vitro as Anti-Infectives against Campylobacter jejuni

Quinn

Slattery

Walsh

et al. 2020

Foods

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“…Clinical treatment with probiotic bacteria has been found to efficiency protect against pathogens invasion or intestinal inflammation . However, the mechanism underlying the anti‐inflammatory effect of probiotics has not yet been fully understood due in part to the complex intestine environment in vivo.…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus Protects Against S. Typhimurium–Induced Intestinal Inflammation by Determining the Fate of Epithelial Proliferation and Differentiation

Xiao

Xie

et al. 2020

Molecular Nutrition Food Res

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Scope The influence of the intestinal microbiota, such as Lactobacillus, on the intestinal mucosa, particularly intestinal stem cells, remains incompletely understood. In this study, mice and intestinal organoids are used to explore the regulatory effect of Lactobacillus on the proliferation and differentiation of intestinal epithelial cells. Methods and results This study demonstrates that S. typhimurium causes intestinal epithelial damage and affected growth of intestinal organoids. S. typhimurium also colonizes the intestine and then causes pathological changes to the intestinal epithelium, intestinal inflammation, and even death. However, L. acidophilus alleviates damage to intestinal organoids, increases the survival ratio of mice infected with S. typhimurium, and reduces tumor necrosis factor‐α (TNF‐α) secretion. Moreover, L. acidophilus affects the differentiation of epithelial cells through inhibition of the excessive expansion of goblet cells and Paneth cells induced by S. typhimurium to avoid over‐exhaustion. Finally, it is also demonstrated that L. acidophilus ameliorates overactivation of Wnt/β‐catenin pathway by Salmonella, depending on the contact with toll‐like receptor 2 (TLR2), to affect the proliferation of the intestinal epithelium. Conclusions This study demonstrates that L. acidophilus protects the intestinal mucosa against S. typhimurium infection through not only the inhibition of pathogen invasion but also determination of the fate of the intestinal epithelium.

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“…Lactobacillus johnsonii is a lactic acid‐producing probiotic bacterium, and certain strains exhibit anti‐inflammatory properties and attenuate systemic proinflammatory immune responses . A recent study indicated that L. johnsonii strongly inhibits the growth of S .…”

Section: Introductionmentioning

confidence: 99%

“…8 Lactobacillus johnsonii is a lactic acid-producing probiotic bacterium, and certain strains exhibit anti-inflammatory properties and attenuate systemic proinflammatory immune responses. 9,10 A recent study indicated that L. johnsonii strongly inhibits the growth of S. Enteritidis, Escherichia coli, and Staphylococcus aureus. 11 We recently showed that L. johnsonii L531 reduces pathogen load and helps maintain short-chain fatty acid levels in the intestines of pigs challenged with S. infantis.…”

Section: Introductionmentioning

confidence: 99%

Lactobacillus johnsonii L531 ameliorates enteritis via elimination of damaged mitochondria and suppression of SQSTM1‐dependent mitophagy in a Salmonella infantis model of piglet diarrhea

Xia

et al. 2019

FASEB j.

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Newly weaned piglets challenged with Salmonella infantis were particularly susceptible, whereas oral preadministration of Lactobacillus johnsonii L531 alleviated enteritis and promoted intestinal secretory IgA production. Salmonella infantisinduced activation of NLRC4 and NLRP3 inflammasomes and (nuclear factor kappa B) NF-κB signaling in the small intestine was also inhibited by L. johnsonii L531 pretreatment, thus limiting inflammation. An IPEC-J2 cell model of S. infantis infection yielded similar results. Salmonella infantis infection also resulted in mitochondrial damage and impaired mitophagy in the ileum and IPEC-J2 cells, as demonstrated by immunofluorescence colocalization of mitochondria with microtubule-binding protein light chain 3 (LC3) and high expression of autophagy-related proteins PTEN-induced putative kinase 1 (PINK1), sequestosome 1 (SQSTM1/p62), optineurin (OPTN), and LC3 by Western blotting analysis. However, L. johnsonii L531 pretreatment reduced both the extent of mitochondrial damage and autophagyrelated protein expression. Our findings suggest that the amelioration of S. infantisassociated enteritis by L. johnsonii L531 is associated with regulation of NLRC4 and NLRP3 inflammasomes and NF-κB signaling pathway activation and suppression of mitochondrial damage. Amelioration of impaired mitophagy by L. johnsonii L531 could involve eliminating damaged mitochondria and regulating S. infantis-induced activation of the NF-κB-SQSTM1mitophagy signaling pathway in host cells to prevent the further mitochondrial damage and S. infantis dissemination. K E Y W O R D S autophagy, inflammasome, IPEC-J2, pig, probiotic 2822 |

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Lactobacillus johnsonii ameliorates intestinal, extra-intestinal and systemic pro-inflammatory immune responses following murine Campylobacter jejuni infection

Cited by 49 publications

References 44 publications

Bifidobacterium longum subsp. infantis ATCC 15697 and Goat Milk Oligosaccharides Show Synergism In Vitro as Anti-Infectives against Campylobacter jejuni

Bifidobacterium longum subsp. infantis ATCC 15697 and Goat Milk Oligosaccharides Show Synergism In Vitro as Anti-Infectives against Campylobacter jejuni

Lactobacillus Protects Against S. Typhimurium–Induced Intestinal Inflammation by Determining the Fate of Epithelial Proliferation and Differentiation

Lactobacillus johnsonii L531 ameliorates enteritis via elimination of damaged mitochondria and suppression of SQSTM1‐dependent mitophagy in a Salmonella infantis model of piglet diarrhea

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