Zooming in on Inflammatory Bowel Disease: Microbial and Proteomic Features Associated With IBD in Colonic Microenvironments

Tamburini, Sabrina; Clemente, José C.

doi:10.1016/j.jcmgh.2016.07.001

Cited by 5 publications

(3 citation statements)

References 9 publications

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“…The increased proportion of Serratia after krill oil treatment led to the accumulation of the compound FR177391, which had an anti-hyperlipidemic effect (Sato et al, 2005 ). In addition to hyperlipidemia, krill oil supplementation was also beneficial for the treatment of inflammatory and neurological disorders, and inflammatory disease was positively correlated with the Ralstonia and Delftia abundance (Tyler et al, 2013 ; Chen et al, 2014c ; Bilgin et al, 2015 ; Tamburini and Clemente, 2016 ). In this study, krill oil treatment significantly decreased the proportion of Ralstonia , which might explain the anti-inflammatory effect.…”

Section: Discussionmentioning

confidence: 99%

Modulation of the Gut Microbiota by Krill Oil in Mice Fed a High-Sugar High-Fat Diet

Sun

et al. 2017

Front. Microbiol.

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Multiple lines of evidence suggest that the gut microbiota plays vital roles in metabolic diseases such as hyperlipidemia. Previous studies have confirmed that krill oil can alleviate hyperlipidemia, but the underlying mechanism remains unclear. To discern whether krill oil changes the structure of the gut microbiota during the hyperlipidemia treatment, 72 mice were acclimatized with a standard chow diet for 2 weeks and then randomly allocated to receive a standard chow diet (control group, n = 12) or a high-sugar-high-fat (HSHF) diet supplemented with a low (100 μg/g·d, HSHF+LD group, n = 12), moderate (200 μg/g·d, HSHF+MD group, n = 12) or high dosage of krill oil (600 μg/g·d, HSHF+HD group, n = 12), simvastatin (HSHF+S group, n = 12) or saline (HSHF group, n = 12) continuously for 12 weeks. The resulting weight gains were attenuated, the liver index and the low-density lipoprotein, total cholesterol and triglyceride concentrations showed a stepwise reduction in the treated groups compared with those of the control group. A dose-dependent modulation of the gut microbiota was observed after treatment with krill oil. Low- and moderate- doses of krill oil increased the similarity between the composition of the HSHF diet-induced gut microbiota and that of the control, whereas the mice fed the high-dose exhibited a unique gut microbiota structure that was different from that of the control and HSHF groups. Sixty-five key operational taxonomic units (OTUs) that responded to the krill oil treatment were identified using redundancy analysis, of which 26 OTUs were increased and 39 OTUs were decreased compared with those of the HSHF group. In conclusion, the results obtained in this study suggest that the structural alterations in the gut microbiota induced by krill oil treatment were dose-dependent and associated with the alleviation of hyperlipidemia. Additionally, the high-dose krill oil treatment showed combined effects on the alleviation of hyperlipidemia and obesity.

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Section: Discussionmentioning

confidence: 99%

Modulation of the Gut Microbiota by Krill Oil in Mice Fed a High-Sugar High-Fat Diet

Sun

et al. 2017

Front. Microbiol.

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“…Compared with specific pathogen‐free mice, germ‐free mice have reduced barrier function and remarkably lower lymphocyte counts in the mucosal epithelium 160 . In addition, studies aiming to map the web of associations between specific species and diseases have revealed even more diversity than ever imagined, with notable influences of the microbiota on the function of many organs and the progression of many diseases 163‐165 . In particular, lack of a healthy microbiota can affect the early growth of infants and harm the function of normal tissue, leading to disease 158 ; this altered state is called dysbiosis.…”

Section: Immune System and Commensal Bacterial Floramentioning

confidence: 99%

Maintaining a protective state for human periodontal tissue

Yamamoto

Aizawa

2021

Periodontology 2000

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In the 20th century, dentists largely classified periodontal diseases according to patient age at onset, rate of progression, and pathology. Accordingly, the main concepts of periodontitis were "adult," "early-onset," and "refractory"; however, these names did not correspond to the specific bacterial species identified, in such cases, using bacteriological approaches. Therefore, in 1999, the American Academy of Periodontology reorganized this tripartite classification into 2 broad groups: severe, rapid destruction of periodontal tissue not attributable to systemic diseases; and periodontitis as a manifestation of systemic diseases. 1 The former group is considered to be "aggressive periodontitis" (class III in the American Academy of Periodontology Periodontal Disease Classification System), while the latter can be grouped under periodontitis associated with hematological or genetic disorders (classes IVa and IVb in the American Academy of Periodontology Periodontal Disease Classification System), often presenting with comorbid immune (neutrophil) dysfunction. 1,2 However, researchers could not identify specific bacteria or pathologies unique to any of these classes. Subsequently, the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions led to a series of changes in periodontal disease taxonomy, transforming classification into a stage-and grade-based system. 3 | Periodontitis as a multifactorial diseaseClinical manifestations of incipient periodontitis vary considerably across individuals, depending on where the tissue damage originates and how it progresses; thus, it is impossible to explain the symptomatology in terms of bacterial infection alone. We now know that destruction of the periodontal tissue does not progress continuously and linearly, but is rather a result of repeated switches between dormant and active stages of resident bacteria. 4,5 Simplistically describing periodontitis as an infection with certain bacteria cannot completely explain the diverse patterns observed. The fact that periodontitis is a multifactorial disease lies at the heart of this complexity. The tissue damage is thought to be driven by a variety of factors, 6,7 which have started to be illuminated in recent years, and these risk factors have now been conceptually organized into 3 main groups: bacterial, host, and environmental. A host factor can include an underlying metabolic disease that affects the whole body, while smoking is an archetypal environmental factor. Changes in the biological properties of host cells can have an enormous influence on defense mechanisms in the periodontal tissue. In vitro analyses can be used to chronicle the detailed changes in immunocytes and resident cell populations; however, physiological samples are more useful for investigating systemic shifts in host defense mechanisms. Data from analyses of the gingival crevicular fluid have provided intriguing insights into how the protective state evolves and changes as humans grow and age. For example, by comp...

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“…A gyulladásos bélbetegségek (IBD: inflammatory bowel diseases) lehetséges kiváltó okai között több genetikai és környezeti tényező felmerült [1]. Az elmúlt évek kutatásai során a mikrobiom tanulmányozása hozott ígéretes eredményeket az IBD kialakulásával kapcsolatban [2][3][4]. Egy japán munkacsoport egy colitis ulcerosás beteg érintett bélszakasz-nyálkahártyájából vett szövettani mintában Staphylococcus aureust izolált [5].…”

Section: First Description Of An Association Of Symptomsunclassified

Staphylococcus által kiváltott, immunglobulin-E-alapú anafilaxiás reakciók Crohn-betegségben. Egy tünetegyüttes első leírása

et al. 2019

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Immunglobulin E (IgE)-based, irregularly recurring, severe anaphylactic reactions occurred in a 50-year-old European white male patient suffering also from Crohn’s disease. On the base of immunologic laboratory tests concerning the mechanism of the phenomenon, the idea arose whether molecules derived for certain microbial derivatives could enter the blood circulation via the damaged bowel walls in the patient with Crohn’s disease and they might act as allergens. The microbial analysis diagnosed atypical Staphylococcus in the stool. The serum level of IgE was very high. The concomitant use of targeted antibiotics and anti-allergy and immunosuppressive agents resulted in a complete remission during a couple of months. Not only Crohn’s disease has improved, but also the total serum IgE level has decreased significantly, and the unpredictable anaphylactic attacks have been completely eliminated. In Crohn’s disease, the anaphylactic complications induced by atypical microbial allergens (e.g., derivatives of Staphylococcus) can be effectively treated after the recognition of this pathological mechanism. This is the first description of such a pathologic state. Orv Hetil. 2019; 160(38): 1514–1518.

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Zooming in on Inflammatory Bowel Disease: Microbial and Proteomic Features Associated With IBD in Colonic Microenvironments

Cited by 5 publications

References 9 publications

Modulation of the Gut Microbiota by Krill Oil in Mice Fed a High-Sugar High-Fat Diet

Modulation of the Gut Microbiota by Krill Oil in Mice Fed a High-Sugar High-Fat Diet

Maintaining a protective state for human periodontal tissue

Staphylococcus által kiváltott, immunglobulin-E-alapú anafilaxiás reakciók Crohn-betegségben. Egy tünetegyüttes első leírása

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