The Molecular Mechanism of the Interplay between Toxins Driven Microbiota Dysbiosis and Innate Immunity

A special issue of Toxins (ISSN 2072-6651).

Deadline for manuscript submissions: closed (1 December 2018) | Viewed by 8553

Special Issue Editors

E-Mail Website
Guest Editor
Department of Clinical Sciences, College of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates
Interests: cancer; oncology; multiple sclerosis; autoimmune diseases; immunology; chemokines; hematology; drug mechanisms of action (MOA)
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
1.Department of Clinical Sciences, College of Medicine, University of Sharjah, Sharjah, UAE
2.Computational and Molecular Surgical Pathology. Division of Surgery & Interventional Science, University College London, London WC1E 6BT, UK
Interests: Computational Medicine; Oncology; Pathology; Bioinformatics; Mathematical Modelling of non-linear processes; Molecular and Cellular Immunology; Haematology; Personalised Medicine

E-Mail Website
Guest Editor
Center for Gender-Specific Medicine, Istituto Superiore di Sanità, 00161 Rome, Italy
Interests: diet; inflammation; colorectal cancer; adipose tissue; obesity; immune regulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Gut microbiota is a key node that integrates a variety of signaling pathways, activated through environmental stimuli, such as diet, genetic, and epigenetic inputs that profoundly affect host metabolism, toxicity, and disease pathogenesis. There is considerable evidence suggesting that a complex interplay between microbiota and innate immunity may mediate development of chronic inflammation that precedes the development of numerous types of diseases. Inflammation and toxicity have been linked with increased DNA methylation in healthy tissues and chronic inflammation has been defined as “a truly epigenetic phenomenon”. Distinct epigenetic changes in various types of immune cells are frequently observed in obesity and type 2 diabetes mellitus, and these are associated with alterations in the phenotype, function, and trafficking patterns of these cells. Many of them, at least in the context of metabolic disorders, are linked to toxicity. Epigenetics alterations related to food components, metabolites and environmental factors have also been recognized as important mediators of inflammation and toxicity, with a role in the pathogenesis of inflammatory diseases. An epigenetic dynamic drives gene transcription during the different phases of inflammation enabling to co-ordinately regulate the activity of toxic mediators at both molecular and cellular level. In this respect, the novel epigenetics and transcriptomics molecular technologies have provided unprecedented opportunity to achieve a wider picture, at multiple levels, allowing concrete advancements in the field. It cannot be denied that the study of transcriptomics and epigenetics provided important insights on the cellular pathways by which toxicity and pathology progress in several disorders, as well as highlighted novel therapeutic options.

Potential topics include but are not limited to the followings:

  • Role of microbiota toxins in epigenetic switches leading to complex immune diseases
  • The role of microbiota dysbiosis in innate immunity regulation.
  • Epigenetics and transcriptomics regulation of innate immune cells mediating the release of toxic mediators.
  • Classification and potential functions of innate lymphoid cells (ILCs) as mediators of toxicity and inflammation.
Dr. Azzam A. Maghazachi
Dr. Rifat Akram Hamoudi
Dr. Sandra Gessani
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at 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 double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins 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.


  • Toxins
  • Microbiota, Dysbiosis
  • Inflammatory Mediators
  • Epigenetic
  • Innate Lymphoid Cells
  • Cancer
  • Metabolic Disorders
  • Autoimmunity

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:


751 KiB  
Innate Lymphoid Cells (ILCs) as Mediators of Inflammation, Release of Cytokines and Lytic Molecules
by Noha Mousaad Elemam, Suad Hannawi and Azzam A. Maghazachi
Toxins 2017, 9(12), 398; - 10 Dec 2017
Cited by 31 | Viewed by 8113
Innate lymphoid cells (ILCs) are an emerging group of immune cells that provide the first line of defense against various pathogens as well as contributing to tissue repair and inflammation. ILCs have been classically divided into three subgroups based on their cytokine secretion [...] Read more.
Innate lymphoid cells (ILCs) are an emerging group of immune cells that provide the first line of defense against various pathogens as well as contributing to tissue repair and inflammation. ILCs have been classically divided into three subgroups based on their cytokine secretion and transcription factor profiles. ILC nomenclature is analogous to that of T helper cells. Group 1 ILCs composed of natural killer (NK) cells as well as IFN-γ secreting ILC1s. ILC2s have the capability to produce TH2 cytokines while ILC3s and lymphoid tissue inducer (LTis) are subsets of cells that are able to secrete IL-17 and/or IL-22. A recent subset of ILC known as ILC4 was discovered, and the cells of this subset were designated as NK17/NK1 due to their release of IL-17 and IFN-γ. In this review, we sought to explain the subclasses of ILCs and their roles as mediators of lytic enzymes and inflammation. Full article
Show Figures

Figure 1

Back to TopTop