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Gut Microbiota and Immunity 2.0
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Gut Microbiota and Immunity 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 23102

Special Issue Editor

Dr. Maria Pascual

E-Mail Website
Guest Editor
Department of Physiology, School of Medicine and Dentistry, University of Valencia, 15 Avda. Blasco Ibanez, 46010 Valencia, Spain
Interests: effects of ethanol on TLR4 immune response; extracellular vesicles; effect of binge drinking in adolescent brain; microbiome; inflammatory response; glial cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous special issue "Gut Microbiota and Immunity".

The human gut hosts a wide and diverse ecosystem of microorganisms termed the microbiota or the novel name “holobiota”. The microbiota is involved in both health and disease, contributing to prevent illness by facilitating the metabolism, the immune system, cancer resistance, endocrine signaling and brain function. However, dysfunctions of the microbiota could lead to gut dysbiosis, leading to alterations of the intestinal permeability and in the immune system. Innate and adaptive immunity plays an important role in the containment and clearance of microbial pathogens, and new mechanisms have been discovered that can cause or influence systemic immunity alterations in different disorders, such as cancer, autoimmune or neurodegenerative diseases, among others. In this Special Issue, a particular emphasis will be given to the role of the microbiota–gut–brain axis, to deepen the knowledge of the mechanisms of gut microbiota–brain communication, including immune signaling and neural–enteroendocrine pathways. We will also review important advances in techniques associated with microbial research, such as DNA sequencing, metabolomics, and proteomics combined with computation-based bioinformatics. Finally, this Special Issue of IJMS will also focus on advances in therapeutic applications, for instance, the usefulness of microbial or chemobiotic applications as promising therapeutic choices to palliate immune-mediated diseases, neurodegenerative disorders, and other syndromes.

Dr. Maria Pascual
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • gut
  • microbiota
  • immune response
  • infectious disease
  • cancer
  • brain function
  • metabolism
  • endocrine signaling
  • pathological conditions 
  • therapy

Published Papers (6 papers)

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Research

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20 pages, 5781 KiB  
Article
The Cysteine Protease Giardipain-1 from Giardia duodenalis Contributes to a Disruption of Intestinal Homeostasis
by Rodrigo Quezada-Lázaro, Yessica Vázquez-Cobix, Rocío Fonseca-Liñán, Porfirio Nava, Daniel Dimitri Hernández-Cueto, Carlos Cedillo-Peláez, Yolanda López-Vidal, Sara Huerta-Yepez and M. Guadalupe Ortega-Pierres
Int. J. Mol. Sci. 2022, 23(21), 13649; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232113649 - 07 Nov 2022
Cited by 2 | Viewed by 1843
Abstract
In giardiasis, diarrhoea, dehydration, malabsorption, weight loss and/or chronic inflammation are indicative of epithelial barrier dysfunction. However, the pathogenesis of giardiasis is still enigmatic in many aspects. Here, we show evidence that a cysteine protease of Giardia duodenalis called giardipain-1, contributes to the [...] Read more.
In giardiasis, diarrhoea, dehydration, malabsorption, weight loss and/or chronic inflammation are indicative of epithelial barrier dysfunction. However, the pathogenesis of giardiasis is still enigmatic in many aspects. Here, we show evidence that a cysteine protease of Giardia duodenalis called giardipain-1, contributes to the pathogenesis of giardiasis induced by trophozoites of the WB strain. In an experimental system, we demonstrate that purified giardipain-1 induces apoptosis and extrusion of epithelial cells at the tips of the villi in infected jirds (Meriones unguiculatus). Moreover, jird infection with trophozoites expressing giardipain-1 resulted in intestinal epithelial damage, cellular infiltration, crypt hyperplasia, goblet cell hypertrophy and oedema. Pathological alterations were more pronounced when jirds were infected intragastrically with Giardia trophozoites that stably overexpress giardipain-1. Furthermore, Giardia colonization in jirds results in a chronic inflammation that could relate to the dysbiosis triggered by the protist. Taken together, these results reveal that giardipain-1 plays a key role in the pathogenesis of giardiasis. Full article
(This article belongs to the Special Issue Gut Microbiota and Immunity 2.0)
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19 pages, 6524 KiB  
Article
The Phagocytosis of Lacticaseibacillus casei and Its Immunomodulatory Properties on Human Monocyte-Derived Dendritic Cells Depend on the Expression of Lc-p75, a Bacterial Peptidoglycan Hydrolase
by Márta Tóth, Szabolcs Muzsai, Krzysztof Regulski, Tímea Szendi-Szatmári, Zsolt Czimmerer, Éva Rajnavölgyi, Marie-Pierre Chapot-Chartier and Attila Bácsi
Int. J. Mol. Sci. 2022, 23(14), 7620; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23147620 - 10 Jul 2022
Cited by 1 | Viewed by 1586
Abstract
The human gut symbiont Lacticaseibacillus (L.) casei (previously Lactobacillus casei) is under intense research due to its wide range of immunomodulatory effects on the human host. Dendritic cells (DCs) are crucial players in the direct and indirect communication with lactobacilli in the [...] Read more.
The human gut symbiont Lacticaseibacillus (L.) casei (previously Lactobacillus casei) is under intense research due to its wide range of immunomodulatory effects on the human host. Dendritic cells (DCs) are crucial players in the direct and indirect communication with lactobacilli in the gastrointestinal tract. Here, we demonstrate that human monocyte-derived DCs (moDCs) are able to engulf L. casei BL23, in which the intact bacterial cell wall and morphology have a key role. The absence of the bacterial cell-wall-degrading enzyme, Lc-p75, in L. casei cells causes remarkable morphological changes, which have important consequences in the phagocytosis of L. casei by moDCs. Our results showed that the Lc-p75 mutation induced defective internalization and impaired proinflammatory and T-cell-polarizing cytokine secretion by bacteria-exposed moDCs. The T helper (Th) 1 and Th17 cell activating capacity of moDCs induced by the mutant L. casei was consequently reduced. Moreover, inhibition of the phagocytosis of wild-type bacteria showed similar results. Taken together, these data suggested that formation of short bacterial chains helps to exert the potent immunomodulatory properties of L. casei BL23. Full article
(This article belongs to the Special Issue Gut Microbiota and Immunity 2.0)
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19 pages, 2973 KiB  
Article
A High-Fat Diet Induces Low-Grade Cochlear Inflammation in CD-1 Mice
by Jeffrey Chan, Ravi Telang, Dagmara Kociszewska, Peter R. Thorne and Srdjan M. Vlajkovic
Int. J. Mol. Sci. 2022, 23(9), 5179; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23095179 - 06 May 2022
Cited by 5 | Viewed by 2734
Abstract
There is growing evidence for a relationship between gut dysbiosis and hearing loss. Inflammatory bowel disease, diet-induced obesity (DIO), and type 2 diabetes have all been linked to hearing loss. Here, we investigated the effect of a chronic high-fat diet (HFD) on the [...] Read more.
There is growing evidence for a relationship between gut dysbiosis and hearing loss. Inflammatory bowel disease, diet-induced obesity (DIO), and type 2 diabetes have all been linked to hearing loss. Here, we investigated the effect of a chronic high-fat diet (HFD) on the development of inner ear inflammation using a rodent model. Three-week-old CD-1 (Swiss) mice were fed an HFD or a control diet for ten weeks. After ten weeks, mouse cochleae were harvested, and markers of cochlear inflammation were assessed at the protein level using immunohistochemistry and at the gene expression level using quantitative real-time RT-PCR. We identified increased immunoexpression of pro-inflammatory biomarkers in animals on an HFD, including intracellular adhesion molecule 1 (ICAM1), interleukin 6 receptor α (IL6Rα), and toll-like-receptor 2 (TLR2). In addition, increased numbers of ionized calcium-binding adapter molecule 1 (Iba1) positive macrophages were found in the cochlear lateral wall in mice on an HFD. In contrast, gene expression levels of inflammatory markers were not affected by an HFD. The recruitment of macrophages to the cochlea and increased immunoexpression of inflammatory markers in mice fed an HFD provide direct evidence for the association between HFD and cochlear inflammation. Full article
(This article belongs to the Special Issue Gut Microbiota and Immunity 2.0)
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20 pages, 3788 KiB  
Article
TLR4 Deficiency Affects the Microbiome and Reduces Intestinal Dysfunctions and Inflammation in Chronic Alcohol-Fed Mice
by Carlos M. Cuesta, María Pascual, Raúl Pérez-Moraga, Irene Rodríguez-Navarro, Francisco García-García, Juan R. Ureña-Peralta and Consuelo Guerri
Int. J. Mol. Sci. 2021, 22(23), 12830; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222312830 - 27 Nov 2021
Cited by 13 | Viewed by 2407
Abstract
Chronic alcohol abuse causes an inflammatory response in the intestinal tract with damage to the integrity of the mucosa and epithelium, as well as dysbiosis in the gut microbiome. However, the role of gut bacteria in ethanol effects and how these microorganisms interact [...] Read more.
Chronic alcohol abuse causes an inflammatory response in the intestinal tract with damage to the integrity of the mucosa and epithelium, as well as dysbiosis in the gut microbiome. However, the role of gut bacteria in ethanol effects and how these microorganisms interact with the immune system are not well understood. The aim of the present study was to evaluate if TLR4 alters the ethanol-induced intestinal inflammatory response, and whether the response of this receptor affects the gut microbiota profile. We analyzed the 16S rRNA sequence of the fecal samples from wild-type (WT) and TLR4-knockout (TLR4-KO) mice with and without ethanol intake for 3 months. The results demonstrated that chronic ethanol consumption reduces microbiota diversity and causes dysbiosis in WT mice. Likewise, ethanol upregulates several inflammatory genes (IL-1β, iNOS, TNF-α) and miRNAs (miR-155-5p, miR-146a-5p) and alters structural and permeability genes (INTL1, CDH1, CFTR) in the colon of WT mice. Our results further demonstrated that TLR4-KO mice exhibit a different microbiota that can protect against the ethanol-induced activation of the immune system and colon integrity dysfunctions. In short, our results reveal that TLR4 is a key factor for determining the gut microbiota, which can participate in dysbiosis and the inflammatory response induced by alcohol consumption. Full article
(This article belongs to the Special Issue Gut Microbiota and Immunity 2.0)
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Review

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20 pages, 1284 KiB  
Review
The Link between Gut Dysbiosis Caused by a High-Fat Diet and Hearing Loss
by Dagmara Kociszewska, Jeffrey Chan, Peter R. Thorne and Srdjan M. Vlajkovic
Int. J. Mol. Sci. 2021, 22(24), 13177; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222413177 - 07 Dec 2021
Cited by 16 | Viewed by 5142
Abstract
This review aims to provide a conceptual and theoretical overview of the association between gut dysbiosis and hearing loss. Hearing loss is a global health issue; the World Health Organisation (WHO) estimates that 2.5 billion people will be living with some degree of [...] Read more.
This review aims to provide a conceptual and theoretical overview of the association between gut dysbiosis and hearing loss. Hearing loss is a global health issue; the World Health Organisation (WHO) estimates that 2.5 billion people will be living with some degree of hearing loss by 2050. The aetiology of sensorineural hearing loss (SNHL) is complex and multifactorial, arising from congenital and acquired causes. Recent evidence suggests that impaired gut health may also be a risk factor for SNHL. Inflammatory bowel disease (IBD), type 2 diabetes, diet-induced obesity (DIO), and high-fat diet (HFD) all show links to hearing loss. Previous studies have shown that a HFD can result in microangiopathy, impaired insulin signalling, and oxidative stress in the inner ear. A HFD can also induce pathological shifts in gut microbiota and affect intestinal barrier (IB) integrity, leading to a leaky gut. A leaky gut can result in chronic systemic inflammation, which may affect extraintestinal organs. Here, we postulate that changes in gut microbiota resulting from a chronic HFD and DIO may cause a systemic inflammatory response that can compromise the permeability of the blood–labyrinth barrier (BLB) in the inner ear, thus inducing cochlear inflammation and hearing deficits. Full article
(This article belongs to the Special Issue Gut Microbiota and Immunity 2.0)
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15 pages, 1673 KiB  
Review
The Immune System through the Lens of Alcohol Intake and Gut Microbiota
by Javier Calleja-Conde, Victor Echeverry-Alzate, Kora-Mareen Bühler, Pedro Durán-González, Jose Ángel Morales-García, Lucía Segovia-Rodríguez, Fernando Rodríguez de Fonseca, Elena Giné and Jose Antonio López-Moreno
Int. J. Mol. Sci. 2021, 22(14), 7485; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147485 - 13 Jul 2021
Cited by 15 | Viewed by 8133
Abstract
The human gut is the largest organ with immune function in our body, responsible for regulating the homeostasis of the intestinal barrier. A diverse, complex and dynamic population of microorganisms, called microbiota, which exert a significant impact on the host during homeostasis and [...] Read more.
The human gut is the largest organ with immune function in our body, responsible for regulating the homeostasis of the intestinal barrier. A diverse, complex and dynamic population of microorganisms, called microbiota, which exert a significant impact on the host during homeostasis and disease, supports this role. In fact, intestinal bacteria maintain immune and metabolic homeostasis, protecting our organism against pathogens. The development of numerous inflammatory disorders and infections has been linked to altered gut bacterial composition or dysbiosis. Multiple factors contribute to the establishment of the human gut microbiota. For instance, diet is considered as one of the many drivers in shaping the gut microbiota across the lifetime. By contrast, alcohol is one of the many factors that disrupt the proper functioning of the gut, leading to a disruption of the intestinal barrier integrity that increases the permeability of the mucosa, with the final result of a disrupted mucosal immunity. This damage to the permeability of the intestinal membrane allows bacteria and their components to enter the blood tissue, reaching other organs such as the liver or the brain. Although chronic heavy drinking has harmful effects on the immune system cells at the systemic level, this review focuses on the effect produced on gut, brain and liver, because of their significance in the link between alcohol consumption, gut microbiota and the immune system. Full article
(This article belongs to the Special Issue Gut Microbiota and Immunity 2.0)
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