In vivo efficacy of microbiota-sensitive coatings for colon targeting: A promising tool for IBD therapy

Karrout, Youness; Dubuquoy, Laurent; Piveteau, Catherine; Siepmann, Florence; Moussa, Eman A.; Wils, Daniel; Beghyn, Terence; Neut, Christel; Flament, Marie‐Pierre; Guérin‐Deremaux, Laetitia; Dubreuil, L.; Deprez, Benoı̂t; Desreumaux, Pierre; Siepmann, Juergen

doi:10.1016/j.jconrel.2014.11.006

Cited by 38 publications

(19 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is produced by various cell types including monocytes, neutrophils, and endothelial cells [ 20 , 21 ]. In TNBS-treated rats, colonic mRNA levels of TNF- α and IL-1 β are increased significantly [ 22 ]. Similarly, in the current study, TNBS-treated rats displayed the same tendency with an increase in serum TNF- α and IL-1 β levels, as well as colon IL-1 β mRNA levels, all of which were decreased following allicin treatment and in particular following treatment with allicin combined with mesalazine.…”

Section: Discussionmentioning

confidence: 99%

Allicin Alleviates Inflammation of Trinitrobenzenesulfonic Acid‐Induced Rats and Suppresses P38 and JNK Pathways in Caco‐2 Cells

Lun

Zhao

et al. 2015

Mediators of Inflammation

View full text Add to dashboard Cite

Background. Allicin has anti-inflammatory, antioxidative and proapoptotic properties. Aims. To evaluate the effects and investigate the mechanism of allicin on trinitrobenzenesulfonic acid-induced colitis, specifically with mesalazine or sulfasalazine. Methods. 80 rats were divided equally into 8 groups: control; trinitrobenzenesulfonic acid; allicin prevention; allicin; mesalazine; sulfasalazine; allicin + sulfasalazine, and mesalazine + allicin. Systemic and colonic inflammation parameters were analysed. In addition, protein and culture medium of Caco-2 cells treated with various concentrations of IL-1β or allicin were collected for investigation of IL-8, NF-κB p65 P38, ERK, and JNK. One-way ANOVA and Kruskal-Wallis H test were used for parametric and nonparametric tests, respectively. Results. Allicin reduced the body weight loss of trinitrobenzenesulfonic acid-induced rats, histological score, serum TNF-α and IL-1β levels, and colon IL-1β mRNA level and induced serum IL-4 level, particularly in combination with mesalazine. In addition, 1 ng/mL IL-1β stimulated the P38, ERK, and JNK pathways, whereas pretreatment with allicin depressed this phenomenon, except for the ERK pathway. Conclusions. The inflammation induced by trinitrobenzenesulfonic acid is mitigated significantly by allicin treatment, particularly combined with mesalazine. Allicin inhibits the P38 and JNK pathways and the expression of NF-κB which explained the potential anti-inflammatory mechanisms of allicin.

show abstract

Section: Discussionmentioning

confidence: 99%

Allicin Alleviates Inflammation of Trinitrobenzenesulfonic Acid‐Induced Rats and Suppresses P38 and JNK Pathways in Caco‐2 Cells

Lun

Zhao

et al. 2015

Mediators of Inflammation

View full text Add to dashboard Cite

show abstract

“…Therapeutic advantages of bioresponsive delivery systems in IBD therapy have also been demonstrated by other studies. Siepmann et al fabricated microbiota-sensitive 5-aminosalicylic acid pellets [ 322 ]. The resulting pellets notably mitigated manifestations relevant to TNBS-induced colitis in rats and significantly decreased inflammatory markers.…”

Section: Treatment Of Inflammatory Diseases By Bioresponsive Drug Delmentioning

confidence: 99%

Bioresponsive drug delivery systems for the treatment of inflammatory diseases

Ding

et al. 2020

Journal of Controlled Release

121

View full text Add to dashboard Cite

Inflammation is intimately related to the pathogenesis of numerous acute and chronic diseases like cardiovascular disease, inflammatory bowel disease, rheumatoid arthritis, and neurodegenerative diseases. Therefore anti-inflammatory therapy is a very promising strategy for the prevention and treatment of these inflammatory diseases. To overcome the shortcomings of existing anti-inflammatory agents and their traditional formulations, such as nonspecific tissue distribution and uncontrolled drug release, bioresponsive drug delivery systems have received much attention in recent years. In this review, we first provide a brief introduction of the pathogenesis of inflammation, with an emphasis on representative inflammatory cells and mediators in inflammatory microenvironments that serve as pathological fundamentals for rational design of bioresponsive carriers. Then we discuss different materials and delivery systems responsive to inflammation-associated biochemical signals, such as pH, reactive oxygen species, and specific enzymes. Also, applications of various bioresponsive drug delivery systems in the treatment of typical acute and chronic inflammatory diseases are described. Finally, crucial challenges in the future development and clinical translation of bioresponsive anti-inflammatory drug delivery systems are highlighted.

show abstract

“…Salicylic acid is, for example, formulated for fast or sustained systemic absorption using different formulation principles. Different cellulose coatings have been used to deliver the drug to distal parts of the gut for local IBD therapy [ 81 , 82 ]. Basically, the microbiota ferments the coating material and releases the drug distally for sustained release (or local treatment).…”

Section: The Plant Cell Wall Viewed As a “Pharmaceutical-nutrient mentioning

confidence: 99%

The Microbiotic Highway to Health—New Perspective on Food Structure, Gut Microbiota, and Host Inflammation

Hansen

Sams

2018

Nutrients

View full text Add to dashboard Cite

This review provides evidence that not only the content of nutrients but indeed the structural organization of nutrients is a major determinant of human health. The gut microbiota provides nutrients for the host by digesting food structures otherwise indigestible by human enzymes, thereby simultaneously harvesting energy and delivering nutrients and metabolites for the nutritional and biological benefit of the host. Microbiota-derived nutrients, metabolites, and antigens promote the development and function of the host immune system both directly by activating cells of the adaptive and innate immune system and indirectly by sustaining release of monosaccharides, stimulating intestinal receptors and secreting gut hormones. Multiple indirect microbiota-dependent biological responses contribute to glucose homeostasis, which prevents hyperglycemia-induced inflammatory conditions. The composition and function of the gut microbiota vary between individuals and whereas dietary habits influence the gut microbiota, the gut microbiota influences both the nutritional and biological homeostasis of the host. A healthy gut microbiota requires the presence of beneficial microbiotic species as well as vital food structures to ensure appropriate feeding of the microbiota. This review focuses on the impact of plant-based food structures, the “fiber-encapsulated nutrient formulation”, and on the direct and indirect mechanisms by which the gut microbiota participate in host immune function.

show abstract

In vivo efficacy of microbiota-sensitive coatings for colon targeting: A promising tool for IBD therapy

Cited by 38 publications

References 31 publications

Allicin Alleviates Inflammation of Trinitrobenzenesulfonic Acid‐Induced Rats and Suppresses P38 and JNK Pathways in Caco‐2 Cells

Allicin Alleviates Inflammation of Trinitrobenzenesulfonic Acid‐Induced Rats and Suppresses P38 and JNK Pathways in Caco‐2 Cells

Bioresponsive drug delivery systems for the treatment of inflammatory diseases

The Microbiotic Highway to Health—New Perspective on Food Structure, Gut Microbiota, and Host Inflammation

Contact Info

Product

Resources

About