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Spisani, Susanna; Traniello, Serena; Onori, Alberto Mochi; Rizzuti, Olivia; Martuccio, Concetta; Cellai, Luciano

doi:10.1023/a:1022341909396

Cited by 13 publications

(4 citation statements)

References 10 publications

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“…Drugs belonging to the rifamycin class exert anti-inflammatory activity, which seems to be independent from the anti-microbial properties. Rifamycins indeed inhibit human neutrophil functions ( Spisani et al, 1997 , 1998 ) and intra-articular rifamycin SV was shown to be effective in patients with chronic arthritides, like juvenile rheumatoid arthritis and ankylosing spondylitis ( Caruso, 1997 ).…”

Section: Discussionmentioning

confidence: 99%

Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention

et al. 2018

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Non-steroidal anti-inflammatory drugs (NSAIDs) can damage the small intestine, mainly through an involvement of enteric bacteria. This study examined the pathophysiology of NSAID-associated intestinal lesions in a rat model of diclofenac-enteropathy and evaluated the effect of rifaximin on small bowel damage. Enteropathy was induced in 40-week old male rats by intragastric diclofenac (4 mg/kg BID, 14 days). Rifaximin (delayed release formulation) was administered (50 mg/kg BID) 1 h before the NSAID. At the end of treatments, parameters dealing with ileal damage, inflammation, barrier integrity, microbiota composition, and TLR-NF-κB-inflammasome pathway were evaluated. In addition, the modulating effect of rifaximin on NLRP3 inflammasome was tested in an in vitro cell system. Diclofenac induced intestinal damage and inflammation, triggering an increase in tissue concentrations of tumor necrosis factor and interleukin-1β, higher expression of TLR-2 and TLR-4, MyD88, NF-κB and activation of caspase-1. In addition, the NSAID decreased ileal occludin expression and provoked a shift of bacterial phyla toward an increase in Proteobacteria and Bacteroidetes abundance. All these changes were counterbalanced by rifaximin co-administration. This drug was also capable of increasing the proportion of Lactobacilli, a genus depleted by the NSAID. In LPS-primed THP-1 cells stimulated by nigericin (a model to study the NLRP3 inflammasome), rifaximin reduced IL-1β production in a concentration-dependent fashion, this effect being associated with inhibition of the up-stream caspase-1 activation. In conclusion, diclofenac induced ileal mucosal lesions, driving inflammatory pathways and microbiota changes. In conclusion, rifaximin prevents diclofenac-induced enteropathy through both anti-bacterial and anti-inflammatory activities.

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Section: Discussionmentioning

confidence: 99%

Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention

et al. 2018

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“…It is worth mentioning that rifamycins inhibit human neutrophil functions and may therefore display an anti-inflammatory action [93, 94]. And indeed, intra-articular rifamycin has been successfully used in chronic arthritides, like juvenile rheumatoid arthritis and ankylosing spondylitis [95].…”

Section: General Pharmacologymentioning

confidence: 99%

Experimental and Clinical Pharmacology of Rifaximin, a Gastrointestinal Selective Antibiotic

Scarpignato

Pelosini²

2006

Digestion

100

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Rifaximin (4-deoxy-4′-methylpyrido[1′,2′-1,2]imidazo [5,4-c]rifamycin SV) is a product of synthesis experiments designed to modify the parent compound, rifamycin, in order to achieve low gastrointestinal (GI) absorption while retaining good antibacterial activity. Both experimental and clinical pharmacology clearly show that this compound is a non-systemic antibiotic with a broad spectrum of antibacterial action covering Gram-positive and Gram-negative organisms, both aerobes and anaerobes. Being virtually non-absorbed, its bioavailability within the GI tract is rather high with intraluminal and fecal drug concentrations that largely exceed the minimum inhibitory concentration values observed in vitro against a wide range of pathogenic organisms. The GI tract represents therefore the primary therapeutic target and GI infections the main indication. This antibiotic has therefore little value outside the enteric area and this will minimize both antimicrobial resistance and systemic adverse events. Indeed, the drug proved to be safe in all patient populations, including young children. The appreciation of the pathogenic role of gut bacteria in several organic and functional GI diseases has increasingly broadened its clinical use, which is now extended to hepatic encephalopathy, small intestine bacterial overgrowth, inflammatory bowel disease and colonic diverticular disease.

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“…[26][27][28] In addition, rifamycin SV has a strong inhibitory effect on polymerase enzymes. 29) A few studies have investigated effects of some medical drugs on human serum PON1 enzyme in vitro. Most of these, on the modulation of PON1 by pharmaceutical compounds, have focused on lipid-lowering compounds.…”

Section: Resultsmentioning

confidence: 99%

Effects of Some Antibiotics on Paraoxonase from Human Serum in Vitro and from Mouse Serum and Liver in Vivo

Sinan

Köçkar

Gençer³

et al. 2006

Biological & Pharmaceutical Bulletin

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Untitled

Cited by 13 publications

References 10 publications

Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention

Pathophysiology of NSAID-Associated Intestinal Lesions in the Rat: Luminal Bacteria and Mucosal Inflammation as Targets for Prevention

Experimental and Clinical Pharmacology of Rifaximin, a Gastrointestinal Selective Antibiotic

Effects of Some Antibiotics on Paraoxonase from Human Serum in Vitro and from Mouse Serum and Liver in Vivo

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