| 1. |
- Buey, B., et al.
(författare)
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Potential role of milk bioactive peptides on the serotonergic system and the gut-brain axis
- 2023
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Ingår i: International Dairy Journal. - : Elsevier BV. - 0958-6946. ; 137
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Tidskriftsartikel (refereegranskat)abstract
- Dairy-derived bioactive components have health-promoting effects due to their large number of bio-logical properties. Although the physiological significance of several of these substances is not yet fully understood, both proteins and bioactive peptides are now believed to be health-enhancing components. Serotonin is a key signalling neurotransmitter for the gut-brain axis that controls a wide range of physiological functions, highlighting its regulation of neurobiological and intestinal physiology. Here, we discuss the roles and pathways whereby these milk-derived bioactive peptides could modulate seroto-nergic functions as they are an emerging and potential therapeutic adjuvant for the dietary modulation of gut-brain axis disorders mediated by serotonin.(c) 2022 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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| 2. |
- Garcia-Bonete, Maria-Jose, 1989, et al.
(författare)
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The Underrated Gut Microbiota Helminths, Bacteriophages, Fungi, and Archaea
- 2023
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Ingår i: Life-Basel. ; 13:8
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Tidskriftsartikel (refereegranskat)abstract
- The microbiota inhabits the gastrointestinal tract, providing essential capacities to the host. The microbiota is a crucial factor in intestinal health and regulates intestinal physiology. However, microbiota disturbances, named dysbiosis, can disrupt intestinal homeostasis, leading to the development of diseases. Classically, the microbiota has been referred to as bacteria, though other organisms form this complex group, including viruses, archaea, and eukaryotes such as fungi and protozoa. This review aims to clarify the role of helminths, bacteriophages, fungi, and archaea in intestinal homeostasis and diseases, their interaction with bacteria, and their use as therapeutic targets in intestinal maladies.
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| 3. |
- Grasa, L., et al.
(författare)
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TLR2 and TLR4 interact with sulfide system in the modulation of mouse colonic motility
- 2019
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Ingår i: Neurogastroenterology and Motility. - : Wiley. - 1350-1925 .- 1365-2982. ; 31:9
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Tidskriftsartikel (refereegranskat)abstract
- Background: H2S is a neuromodulator that may inhibit intestinal motility. H2S production in colon is yielded by cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE) enzymes and sulfate-reducing bacteria (SRB). Toll-like receptors (TLRs) recognize intestinal microbiota. The aim of this work was to evaluate the influence of TLR2 and TLR4 on the endogenous and SRB-mediated synthesis of H2S and its consequences on the colonic motility of mouse. Methods: Muscle contractility studies were performed in colon from WT, Tlr2-/-, and Tlr4-/- mice. The mRNA levels of TLR2, TLR4, CBS, CSE, and SRB were measured by real-time PCR. Free sulfide levels in colon and feces were determined by colorimetric assays. Results: NaHS and GYY4137, donors of H2S, reduced the contractility of colon. Aminooxyacetic acid (AOAA), inhibitor of CBS, and D-L propargylglycine (PAG), inhibitor of CSE, increased the contractility of colon. In vivo treatment with NaHS or GYY4137 inhibited the spontaneous contractions and upregulated TLR2 expression. The in vivo activation of TLR4 with lipopolysaccharide increased the contractile response to PAG, mRNA levels of CSE, and the free sulfide levels of H2S in colon. In Tlr2-/- and Tlr4-/-mice, the contractions induced by AOAA and PAG and mRNA levels of CBS and CSE were lower with respect to WT mice. Deficiency of TLR2 or TLR4 provokes alterations in free sulfide levels and SRB of colon. Conclusions and Inferences: Our study demonstrates interaction between TLR2 and TLR4 and the sulfide system in the regulation of colonic motility and contributes to the pathophysiology knowledge of intestinal motility disorders. © 2019 John Wiley & Sons Ltd
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| 4. |
- Layunta, Elena, et al.
(författare)
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Crosstalk Between Intestinal Serotonergic System and Pattern Recognition Receptors on the Microbiota-Gut-Brain Axis
- 2021
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Ingår i: Frontiers in Endocrinology. - : Frontiers Media SA. - 1664-2392. ; 12
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Forskningsöversikt (refereegranskat)abstract
- Disruption of the microbiota-gut-brain axis results in a wide range of pathologies that are affected, from the brain to the intestine. Gut hormones released by enteroendocrine cells to the gastrointestinal (GI) tract are important signaling molecules within this axis. In the search for the language that allows microbiota to communicate with the gut and the brain, serotonin seems to be the most important mediator. In recent years, serotonin has emerged as a key neurotransmitter in the gut-brain axis because it largely contributes to both GI and brain physiology. In addition, intestinal microbiota are crucial in serotonin signaling, which gives more relevance to the role of the serotonin as an important mediator in microbiota-host interactions. Despite the numerous investigations focused on the gut-brain axis and the pathologies associated, little is known regarding how serotonin can mediate in the microbiota-gut-brain axis. In this review, we will mainly discuss serotonergic system modulation by microbiota as a pathway of communication between intestinal microbes and the body on the microbiota-gut-brain axis, and we explore novel therapeutic approaches for GI diseases and mental disorders.
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| 5. |
- Layunta, Elena, et al.
(författare)
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IL-22 promotes the formation of a MUC17 glycocalyx barrier in the postnatal small intestine during weaning
- 2021
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Ingår i: Cell Reports. - : Elsevier BV. - 2211-1247. ; 34:7
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Tidskriftsartikel (refereegranskat)abstract
- The intestine is under constant exposure to chemicals, antigens, and microorganisms from the external environment. Apical aspects of transporting epithelial cells (enterocytes) form a brush-border membrane (BBM), shaped by packed microvilli coated with a dense glycocalyx. We present evidence showing that the glycocalyx forms an epithelial barrier that prevents exogenous molecules and live bacteria from gaining access to BBM. We use a multi-omics approach to investigate the function and regulation of membrane mucins exposed on the BBM during postnatal development of the mouse small intestine. Muc17 is identified as a major membrane mucin in the glycocalyx that is specifically upregulated by IL-22 as part of an epithelial defense repertoire during weaning. High levels of IL-22 at time of weaning reprogram neonatal postmitotic progenitor enterocytes to differentiate into Muc17-expressing enterocytes, as found in the adult intestine during homeostasis. Our findings propose a role for Muc17 in epithelial barrier function in the small intestine.
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| 6. |
- Layunta, Elena, et al.
(författare)
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Intestinal serotonergic system is modulated by Toll-like receptor 9
- 2022
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Ingår i: Journal of Physiology and Biochemistry. - : Springer Science and Business Media LLC. - 1138-7548 .- 1877-8755. ; 78, s. 689-701
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Tidskriftsartikel (refereegranskat)abstract
- Intestinal serotonergic system is a key modulator of intestinal homeostasis; however, its regulation is still unclear. Toll-like receptor 9 (TLR9), an innate immune receptor, detects different external agents in the intestine, preserving intestinal integrity. Since little is known about TLR9 role in the intestine, our aim was to address the potential regulation between TLR9 and intestinal serotonergic system. Caco-2/TC7 cell line and intestinal tract of Tlr9(-/-) mice were used in this study. Serotonin uptake studies were performed, and molecular expression of different serotonergic components was analyzed by western blot and real-time PCR. Our results show that TLR9 activation inhibits serotonin transporter activity and expression, involving p38/MAPK and ERK/MAPK intracellular pathways, and reciprocally, serotonin increases TLR9 expression. Supporting this interaction, serotonin transporter, serotonin receptors and serotonin producer enzymes were found altered in intestinal tract of Tlr9(-/-) mice. We conclude that TLR9 could contribute to intestinal homeostasis by modulation of intestinal serotonergic system.
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| 7. |
- Layunta, Elena, et al.
(författare)
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TLR2 and TLR4 Modulate Mouse Ileal Motility by the Interaction with Muscarinic and Nicotinic Receptors
- 2022
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Ingår i: Cells. - : MDPI AG. - 2073-4409. ; 11:11
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Tidskriftsartikel (refereegranskat)abstract
- Irritable bowel syndrome (IBS) is a chronic functional bowel disorder characterized by intestinal dysmotility. Changes in intestinal microbiota (dysbiosis) can lead to alterations in neuro-muscular functions in the gut. Toll-like receptors (TLRs) 2 and 4 recognize intestinal bacteria and are involved in the motor response induced by gastrointestinal (GI) neurotransmitters. Acetylcholine (ACh) is a well-known neurotransmitter involved in the regulation of GI motility. This study aimed to evaluate the role of TLR2 and TLR4 in the intestinal motor-response induced by ACh in the mouse ileum, as well as the expression and function of the muscarinic and nicotinic ACh receptors. Muscle contractility studies showed that the contractions induced by ACh were significantly lower in TLR2(-/-) and TLR4(-/-) with respect to WT mice. In WT mice, the contractions induced by ACh were reduced in the presence of AF-DX AF-DX 116 (a muscarinic ACh receptor (mAChR) M2 antagonist), 4-DAMP (a mAChR M3 antagonist), mecamylamine (a nicotinic AChR receptor (nAChR) alpha 3 beta 4 antagonist) and alpha-bungarotoxin (a nAChR alpha 7 antagonist). In TLR2(-/-) mice, the contractions induced by ACh were increased by AF-DX 116 and mecamylamine. In TLR4(-/-) mice, the contractions induced by ACh were reduced by alpha-bungarotoxin and 4-DAMP. The mRNA and protein expressions of M3 and alpha 3 receptors were diminished in the ileum from TLR2(-/-) and TLR4(-/-) with respect to WT mice. However, the levels of mRNA and protein of beta 4 were diminished only in TLR4(-/-) but not in TLR2(-/-) mice. In conclusion, our results show that TLR2 and TLR4 modulates the motor responses to ACh in the mouse ileum. TLR2 acts on muscarinic M2 and M3 and nicotinic alpha 3 beta 4 ACh receptors, while TLR4 acts on muscarinic M3 and nicotinic alpha 3 beta 4 and alpha 7 ACh receptors.
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