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6.4
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Microorganisms
Special Issues
IgA and Microbiota
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IgA and Microbiota

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Medical Microbiology".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 11863

Special Issue Editor

Dr. Laureline Berthelot

E-Mail Website
Guest Editor
Center of Research in Transplantation and Translational Immunology, University of Nantes, Nantes, France
Interests: transplant immunology; transplantation; pathologies in neurology, nephrology and pneumology; IgA nephropathy; T lymphocytes; cytokines; flow cytometry; immunity; inflammation; cellular immunology; innate immunity; autoimmunity; cell culture; macrophage; immunoglobulin A nephropathy; proteinuria; kidney diseases; vasculitis; petechia; nephritis

Special Issue Information

Dear Colleagues,

On the front line against pathogens at the mucosal surface, IgAs play an important role in the regulation and exclusion of bacteria, viruses, and fungi. The IgA class switch in B cells is induced following the immune activation of host mucosa by microbiota organisms, leading to IgA floods in the external fluid secretions of the body (intestines, lungs, uro-genital mucosa, saliva, tears, milk, etc.).

This Special Issue will be devoted to the close interactions between IgAs and the microbiota in physiology, infections, and diseases. As the Guest Editor of this Special Issue, I invite you to submit research articles, review articles, and short communications related to IgAs and the microbiota.

Dr. Laureline Berthelot
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. Microorganisms is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • IgA
  • microbiota
  • microbiota colonization
  • mucosal immunity
  • B cells
  • plasmocytes
  • IgA receptors

Published Papers (3 papers)

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Review

12 pages, 636 KiB  
Review
Is There a Role for Gut Microbiome Dysbiosis in IgA Nephropathy?
by Renato C. Monteiro, Dina Rafeh and Patrick J. Gleeson
Microorganisms 2022, 10(4), 683; https://0-doi-org.brum.beds.ac.uk/10.3390/microorganisms10040683 - 22 Mar 2022
Cited by 6 | Viewed by 3215
Abstract
Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis and one of the leading causes of renal failure worldwide. The pathophysiology of IgAN involves nephrotoxic IgA1-immune complexes. These complexes are formed by galactose-deficient (Gd) IgA1 with autoantibodies against the hinge region of [...] Read more.
Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis and one of the leading causes of renal failure worldwide. The pathophysiology of IgAN involves nephrotoxic IgA1-immune complexes. These complexes are formed by galactose-deficient (Gd) IgA1 with autoantibodies against the hinge region of Gd-IgA1 as well as soluble CD89, an immune complex amplifier with an affinity for mesangial cells. These multiple molecular interactions result in the induction of the mesangial IgA receptor, CD71, injuring the kidney and causing disease. This review features recent immunological and microbiome studies that bring new microbiota-dependent mechanisms developing the disease based on data from IgAN patients and a humanized mouse model of IgAN. Dysbiosis of the microbiota in IgAN patients is also discussed in detail. Highlights of this review underscore that nephrotoxic IgA1 in the humanized mice originates from mucosal surfaces. Fecal microbiota transplantation (FMT) experiments in mice using stools from patients reveal a possible microbiota dysbiosis in IgAN with the capacity to induce progression of the disease whereas FMT from healthy hosts has beneficial effects in mice. The continual growth of knowledge in IgAN patients and models can lead to the development of new therapeutic strategies targeting the microbiota to treat this disease. Full article
(This article belongs to the Special Issue IgA and Microbiota)
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23 pages, 1519 KiB  
Review
Microbiota, IgA and Multiple Sclerosis
by Léo Boussamet, Muhammad Shahid Riaz Rajoka and Laureline Berthelot
Microorganisms 2022, 10(3), 617; https://0-doi-org.brum.beds.ac.uk/10.3390/microorganisms10030617 - 14 Mar 2022
Cited by 10 | Viewed by 4244
Abstract
Multiple sclerosis (MS) is a neuroinflammatory disease characterized by immune cell infiltration in the central nervous system and destruction of myelin sheaths. Alterations of gut bacteria abundances are present in MS patients. In mouse models of neuroinflammation, depletion of microbiota results in amelioration [...] Read more.
Multiple sclerosis (MS) is a neuroinflammatory disease characterized by immune cell infiltration in the central nervous system and destruction of myelin sheaths. Alterations of gut bacteria abundances are present in MS patients. In mouse models of neuroinflammation, depletion of microbiota results in amelioration of symptoms, and gavage with MS patient microbiota exacerbates the disease and inflammation via Th17 cells. On the other hand, depletion of B cells using anti-CD20 is an efficient therapy in MS, and growing evidence shows an important deleterious role of B cells in MS pathology. However, the failure of TACI-Ig treatment in MS highlighted the potential regulatory role of plasma cells. The mechanism was recently demonstrated involving IgA+ plasma cells, specific for gut microbiota and producing IL-10. IgA-coated bacteria in MS patient gut exhibit also modifications. We will focus our review on IgA interactions with gut microbiota and IgA+ B cells in MS. These recent data emphasize new pathways of neuroinflammation regulation in MS. Full article
(This article belongs to the Special Issue IgA and Microbiota)
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31 pages, 1367 KiB  
Review
Immunoglobulin A, an Active Liaison for Host-Microbiota Homeostasis
by Ahmed A. Abokor, Grant H. McDaniel, Rachel M. Golonka, Connor Campbell, Sreya Brahmandam, Beng San Yeoh, Bina Joe, Matam Vijay-Kumar and Piu Saha
Microorganisms 2021, 9(10), 2117; https://0-doi-org.brum.beds.ac.uk/10.3390/microorganisms9102117 - 08 Oct 2021
Cited by 20 | Viewed by 3720
Abstract
Mucosal surfaces in the gastrointestinal tract are continually exposed to native, commensal antigens and susceptible to foreign, infectious antigens. Immunoglobulin A (IgA) provides dual humoral responses that create a symbiotic environment for the resident gut microbiota and prevent the invasion of enteric pathogens. [...] Read more.
Mucosal surfaces in the gastrointestinal tract are continually exposed to native, commensal antigens and susceptible to foreign, infectious antigens. Immunoglobulin A (IgA) provides dual humoral responses that create a symbiotic environment for the resident gut microbiota and prevent the invasion of enteric pathogens. This review features recent immunological and microbial studies that elucidate the underlying IgA and microbiota-dependent mechanisms for mutualism at physiological conditions. IgA derailment and concurrent microbiota instability in pathological diseases are also discussed in detail. Highlights of this review underscore that the source of IgA and its structural form can dictate microbiota reactivity to sustain a diverse niche where both host and bacteria benefit. Other important studies emphasize IgA insufficiency can result in the bloom of opportunistic pathogens that encroach the intestinal epithelia and disseminate into circulation. The continual growth of knowledge in these subjects can lead to the development of therapeutics targeting IgA and/or the microbiota to treat life threatening diseases. Full article
(This article belongs to the Special Issue IgA and Microbiota)
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