Effect of the Macrolide Antibacterial Drug, Tylosin, on TNBS-Induced Colitis in the Rat

Menozzi, Alessandro; Pozzoli, Cristina; Poli, E.; Lazzaretti, Mirca; Cantoni, Anna Maria; Grandi, Daniela; Giovannini, Elena; Coruzzi, Gabriella

doi:10.1159/000084324

Cited by 14 publications

(11 citation statements)

References 75 publications

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“…However, at 1,000 mg/kg, AL-Na significantly ameliorated DSS-induced colitis in these mice. Moreover, 500 mg/kg AL-Na inhibited the progression of TNBS-induced colitis, as indicated by decreased MPO and serum amyloid A, which are produced in proportion to the severity of the colitis [27,28,29,30]. Therefore, it is proposed that oral AL-Na promotes mucosal healing after colonic inflammation in experimental colitis in mice.…”

Section: Discussionmentioning

confidence: 99%

Effect of Sodium Alginate on Dextran Sulfate Sodium- and 2,4,6-Trinitrobenzene Sulfonic Acid-Induced Experimental Colitis in Mice

et al. 2013

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We evaluated the effects of sodium alginate (AL-Na) on dextran sulfate sodium (DSS)- and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. DSS was added to the drinking water for 7 days. In another experiment, DSS was added to the drinking water for 5 days and DSS-free water was provided thereafter. In a separated study, colitis was induced by intrarectally administered TNBS. AL-Na, 5-aminosalicylic acid, or prednisolone was orally administered. These colitis models exhibited colonic damage and produced noticeable inflammatory responses and aggravated goblet cell damage. AL-Na significantly ameliorated DSS- and TNBS-induced experimental colitis and prevented goblet cell damage. Prednisolone also suppressed colitis but caused loss of body and spleen weight. In contrast, AL-Na did not provoke these symptoms. These data suggest that AL-Na may be a possible therapeutic agent for the treatment of inflammatory bowel disease.

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Section: Discussionmentioning

confidence: 99%

Effect of Sodium Alginate on Dextran Sulfate Sodium- and 2,4,6-Trinitrobenzene Sulfonic Acid-Induced Experimental Colitis in Mice

et al. 2013

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“…[193][194][195][196][197] Animal studies supported these observations, where pretreatment of mice with antibiotics showed significant alleviation of subsequent intestinal inflammation in several models. [198][199][200][201] In addition, knockout mice raised in conventional conditions developed spontaneous chronic colitis, while the mice did not develop intestinal inflammation if raised in germ-free conditions. 202 Recent studies have illustrated that Faecalibacterium prausnitzii, a prominent intestinal microorganism, was reduced in some patients with CD.…”

Section: Altered Mucosal Microbesmentioning

confidence: 99%

Importance of disrupted intestinal barrier in inflammatory bowel diseases

Salim

Söderholm

2011

Inflammatory Bowel Diseases

485

342

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The current paradigm of inflammatory bowel diseases (IBD), both Crohn's disease (CD) and ulcerative colitis (UC), involves the interaction between environmental factors in the intestinal lumen and inappropriate host immune responses in genetically predisposed individuals. The intestinal mucosal barrier has evolved to maintain a delicate balance between absorbing essential nutrients while preventing the entry and responding to harmful contents. In IBD, disruptions of essential elements of the intestinal barrier lead to permeability defects. These barrier defects exacerbate the underlying immune system, subsequently resulting in tissue damage. The epithelial phenotype in active IBD is very similar in CD and UC. It is characterized by increased secretion of chloride and water, leading to diarrhea, increased permeability via both the transcellular and paracellular routes, and increased apoptosis of epithelial cells. The main cytokine that seems to drive these changes is tumor necrosis factor alpha in CD, whereas interleukin (IL)-13 may be more important in UC. Therapeutic restoration of the mucosal barrier would provide protection and prevent antigenic overload due to intestinal "leakiness." Here we give an overview of the key players of the intestinal mucosal barrier and review the current literature from studies in humans and human systems on mechanisms underlying mucosal barrier dysfunction in IBD.

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“…However, this hypothesis has not been substantiated . Other hypotheses about tylosin's mode of action include promotion of beneficial commensal bacteria, decrease in total bacterial load in the small intestine, and suppression of aberrant mucosal immune responses …”

Section: Introductionmentioning

confidence: 99%

Long‐term impact of tylosin on fecal microbiota and fecal bile acids of healthy dogs

Manchester

Webb

Blake

et al. 2019

Veterinary Internal Medicne

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Background: Tylosin is commonly prescribed to dogs with diarrhea. Orally administered antibiotics may alter the intestinal microbiota, which is responsible for crucial key bile acid (BA) biotransformation reactions.Objectives: To prospectively evaluate the impact of tylosin administration on fecal microbiota and unconjugated bile acids (UBAs) over time.Animals: Sixteen healthy adult dogs.Methods: Prospective, randomized controlled clinical trial. Dogs were randomized to receive 20 mg/kg of tylosin or a placebo capsule PO q12h for 7 days while undergoing daily fecal scoring. Fecal samples were collected on days 0, 7, 21, and 63. The microbiota was assessed using quantitative PCR and 16S rRNA gene sequencing. Unconjugated BAs were assessed using gas chromatography-mass spectrometry (GC-MS).Results: Fecal scores were unchanged during placebo and tylosin administration.In the placebo group, no significant changes were observed in fecal microbiota or UBA concentrations. Day 7 samples from tylosin-exposed dogs exhibited decreased bacterial diversity (observed species, Chao1, Shannon, P < .001) characterized by decreases in anaerobes Fusobacteriaceae (linear discriminant analysis [LDA] score, 5.03) and Veillonellaceae (LDA score, 4.85). Primary UBA concentrations were increased at day 21 (median, [range]; 7.42, [0.67-18.77] μg/kg; P = .04) and day 63 (3.49 [0-28.43] μg/kg; P = .02) compared to day 0 (.14 [.03-1.19] μg/kg) in dogs receiving tylosin. At day 63, bacterial taxa were not significantly different compared to day 0, but the extent of microbial recovery was individualized.Conclusions and Clinical Importance: Tylosin causes fecal dysbiosis in healthy dogs with corresponding shifts in fecal UBAs. Changes did not uniformly resolve after discontinuation of tylosin.

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Effect of the Macrolide Antibacterial Drug, Tylosin, on TNBS-Induced Colitis in the Rat

Cited by 14 publications

References 75 publications

Effect of Sodium Alginate on Dextran Sulfate Sodium- and 2,4,6-Trinitrobenzene Sulfonic Acid-Induced Experimental Colitis in Mice

Effect of Sodium Alginate on Dextran Sulfate Sodium- and 2,4,6-Trinitrobenzene Sulfonic Acid-Induced Experimental Colitis in Mice

Importance of disrupted intestinal barrier in inflammatory bowel diseases

Long‐term impact of tylosin on fecal microbiota and fecal bile acids of healthy dogs

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