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Immune Modulation of Mucosal Inflammation 2.0
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Immune Modulation of Mucosal Inflammation 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 (30 September 2022) | Viewed by 13010

Special Issue Editor

Dr. José Luis Subiza

E-Mail Website
Guest Editor
Inmunotek, SL, Madrid, Spain
Interests: allergy; immunology; vaccines; dendritic cells; regulatory T cells; allergens
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mucous membranes are lined by an epithelial layer that covers the respiratory, gastrointestinal and genitourinary tracts from the external environment.  Although it is an effective barrier against external insults, the mucosal tissues are continuously challenged by a plethora of microorganisms, allergens and other substances that can access to the mucosal surface. As a consequence, the mucosal immune system has evolved to discriminate when to respond, when to tolerate, and to what extent. To this end, there is interplay among microbiota, epithelial cells, innate immune cells and resident and circulating lymphocytes.

In situations derived from infections, epithelia disruption, disbiosis, allergy, autoimmune phenomena and others, an inflammatory response may occur altering the mucosal homeostasis. This gives rises to a number of acute or chronic conditions, from rhinosinusitis or allergic asthma in airways to different inflammatory disorders in intestinal and other mucosal tissues.

Down-regulating mucosal inflammation and restoring mucosal homeostasis by inducing tolerance is a topic of great interest. Different approaches are being considered, from targeting tolerogenic dendritic cells to modulating regulatory T cells.

Therefore, authors are invited to submit original research and review articles which address the progress and current standing of immunomodulation of mucosal inflammation.

Topics include, but are not limited to:

  • Epithelial cells and triggers of mucosal inflammation
  • Induction of tolerogenic dendritic cells
  • Induction of regulatory T cells
  • Immunomodulation by mucosal microbiota

Dr. José Luis Subiza
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

  • mucosal
  • inflammation
  • dendritic cells
  • regulatory T cells
  • mucosal epithelial cells
  • gut microbiota
  • bronchial microbiota
  • tolerance
  • allergens
  • infections

Related Special Issue

Published Papers (4 papers)

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Research

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18 pages, 2695 KiB  
Article
Antibody Conjugates Bispecific for Pollen Allergens and ICAM-1 with Potential to Prevent Epithelial Allergen Transmigration and Rhinovirus Infection
by Christina Weichwald, Ines Zettl, Isabella Ellinger, Katarzyna Niespodziana, Eva E. Waltl, Sergio Villazala-Merino, Daniel Ivanov, Julia Eckl-Dorna, Verena Niederberger-Leppin, Rudolf Valenta and Sabine Flicker
Int. J. Mol. Sci. 2023, 24(3), 2725; https://doi.org/10.3390/ijms24032725 - 01 Feb 2023
Viewed by 4014
Abstract
Allergy and rhinovirus (RV) infections are major triggers for rhinitis and asthma, causing a socioeconomic burden. As RVs and allergens may act synergistically to promote airway inflammation, simultaneous treatment strategies for both causative agents would be innovative. We have previously identified the transmembrane [...] Read more.
Allergy and rhinovirus (RV) infections are major triggers for rhinitis and asthma, causing a socioeconomic burden. As RVs and allergens may act synergistically to promote airway inflammation, simultaneous treatment strategies for both causative agents would be innovative. We have previously identified the transmembrane glycoprotein intercellular adhesion molecule 1 (ICAM-1) as an anchor for antibody conjugates bispecific for ICAM-1 and Phleum pratense (Phl p) 2, a major grass pollen allergen, to block allergen transmigration through the epithelial barrier. Since ICAM-1 is a receptor for the major group RVs, we speculated that our bispecific antibody conjugates may protect against RV infection. Therefore, we created antibody conjugates bispecific for ICAM-1 and the major grass pollen allergen Phl p 5 and analyzed their capacity to affect allergen penetration and RV infection. Bispecific antibody conjugates significantly reduced the trans-epithelial migration of Phl p 5 and thus the basolateral Phl p 5 concentration and allergenic activity as determined by humanized rat basophilic leukemia cells and inhibited RV infection of cultured epithelial cells. A reduction in allergenic activity was obtained only through the prevention of allergen transmigration because the Phl p 5-specific IgG antibody did not block the allergen–IgE interaction. Our results indicate the potential of allergen/ICAM-1-specific antibody conjugates as a topical treatment strategy for allergy and RV infections. Full article
(This article belongs to the Special Issue Immune Modulation of Mucosal Inflammation 2.0)
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18 pages, 4685 KiB  
Article
ZnT2 Is Critical for TLR4-Mediated Cytokine Expression in Colonocytes and Modulates Mucosal Inflammation in Mice
by Katherine McGourty, Ramya Vijayakumar, Tong Wu, Annie Gagnon and Shannon L. Kelleher
Int. J. Mol. Sci. 2022, 23(19), 11467; https://doi.org/10.3390/ijms231911467 - 28 Sep 2022
Cited by 1 | Viewed by 2197
Abstract
A wide range of microbial pathogens can enter the gastrointestinal tract, causing mucosal inflammation and infectious colitis and accounting for most cases of acute diarrhea. Severe cases of infectious colitis can persist for weeks, and if untreated, may lead to major complications and [...] Read more.
A wide range of microbial pathogens can enter the gastrointestinal tract, causing mucosal inflammation and infectious colitis and accounting for most cases of acute diarrhea. Severe cases of infectious colitis can persist for weeks, and if untreated, may lead to major complications and death. While the molecular pathogenesis of microbial infections is often well-characterized, host-associated epithelial factors that affect risk and severity of infectious colitis are less well-understood. The current study characterized functions of the zinc (Zn) transporter ZnT2 (SLC30A2) in cultured HT29 colonocytes and determined consequences of ZnT2 deletion in mice on the colonic response to enteric infection with Citrobacter rodentium. ZnT2 in colonocytes transported Zn into vesicles buffering cytoplasmic Zn pools, which was important for Toll-like receptor 4 (TLR4) expression, activation of pathogen-stimulated NF-κβ translocation and cytokine expression. Additionally, ZnT2 was critical for lysosome biogenesis and bacterial-induced autophagy, both promoting robust host defense and resolution mechanisms in response to enteric pathogens. These findings reveal that ZnT2 is a novel regulator of mucosal inflammation in colonocytes and is critical to the response to infectious colitis, suggesting that manipulating the function of ZnT2 may offer new therapeutic strategies to treat specific intestinal infections. Full article
(This article belongs to the Special Issue Immune Modulation of Mucosal Inflammation 2.0)
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16 pages, 2354 KiB  
Article
Human Milk Oligosaccharide 2′-Fucosyllactose Modulates Local Viral Immune Defense by Supporting the Regulatory Functions of Intestinal Epithelial and Immune Cells
by Veronica Ayechu-Muruzabal, Bente Poelmann, Alinda J. Berends, Nienke Kettelarij, Johan Garssen, Belinda van’t Land and Linette E. M. Willemsen
Int. J. Mol. Sci. 2022, 23(18), 10958; https://doi.org/10.3390/ijms231810958 - 19 Sep 2022
Cited by 3 | Viewed by 2044
Abstract
Human milk contains bioactive components that provide protection against viral infections in early life. In particular, intestinal epithelial cells (IEC) have key regulatory roles in the prevention of enteric viral infections. Here we established an in vitro model to study the modulation of [...] Read more.
Human milk contains bioactive components that provide protection against viral infections in early life. In particular, intestinal epithelial cells (IEC) have key regulatory roles in the prevention of enteric viral infections. Here we established an in vitro model to study the modulation of host responses against enteric viruses mimicked by poly I:C (pIC). The effects of 2′-fucosyllactose (2′FL), abundantly present in human milk, were studied on IEC and/or innate immune cells, and the subsequent functional response of the adaptive immune cells. IEC were pre-incubated with 2′FL and stimulated with naked or Lyovec™-complexed pIC (LV-pIC). Additionally, monocyte-derived dendritic cells (moDC) alone or in co-culture with IEC were stimulated with LV-pIC. Then, conditioned-moDC were co-cultured with naïve CD4+ T helper (Th)-cells. IEC stimulation with naked or LV-pIC promoted pro-inflammatory IL-8, CCL20, GROα and CXCL10 cytokine secretion. However, only exposure to LV-pIC additionally induced IFNβ, IFNλ1 and CCL5 secretion. Pre-incubation with 2′FL further increased pIC induced CCL20 secretion and LV-pIC induced CXCL10 secretion. LV-pIC-exposed IEC/moDC and moDC cultures showed increased secretion of IL-8, GROα, IFNλ1 and CXCL10, and in the presence of 2′FL galectin-4 and -9 were increased. The LV-pIC-exposed moDC showed a more pronounced secretion of CCL20, CXCL10 and CCL5. The moDC from IEC/moDC cultures did not drive T-cell development in moDC/T-cell cultures, while moDC directly exposed to LV-pIC secreted Th1 driving IL-12p70 and promoted IFNγ secretion by Th-cells. Hereby, a novel intestinal model was established to study mucosal host-defense upon a viral trigger. IEC may support intestinal homeostasis, regulating local viral defense which may be modulated by 2′FL. These results provide insights regarding the protective capacity of human milk components in early life. Full article
(This article belongs to the Special Issue Immune Modulation of Mucosal Inflammation 2.0)
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Review

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18 pages, 1650 KiB  
Review
Enhancing Regulatory T Cells to Treat Inflammatory and Autoimmune Diseases
by Tara Fiyouzi, Hector F. Pelaez-Prestel, Raquel Reyes-Manzanas, Esther M. Lafuente and Pedro A. Reche
Int. J. Mol. Sci. 2023, 24(9), 7797; https://doi.org/10.3390/ijms24097797 - 25 Apr 2023
Cited by 6 | Viewed by 4174
Abstract
Regulatory T cells (Tregs) control immune responses and are essential to maintain immune homeostasis and self-tolerance. Hence, it is no coincidence that autoimmune and chronic inflammatory disorders are associated with defects in Tregs. These diseases have currently no cure and are treated with [...] Read more.
Regulatory T cells (Tregs) control immune responses and are essential to maintain immune homeostasis and self-tolerance. Hence, it is no coincidence that autoimmune and chronic inflammatory disorders are associated with defects in Tregs. These diseases have currently no cure and are treated with palliative drugs such as immunosuppressant and immunomodulatory agents. Thereby, there is a great interest in developing medical interventions against these diseases based on enhancing Treg cell function and numbers. Here, we give an overview of Treg cell ontogeny and function, paying particular attention to mucosal Tregs. We review some notable approaches to enhance immunomodulation by Tregs with therapeutic purposes including adoptive Treg cell transfer therapy and discuss relevant clinical trials for inflammatory bowel disease. We next introduce ways to expand mucosal Tregs in vivo using microbiota and dietary products that have been the focus of clinical trials in various autoimmune and chronic-inflammatory diseases. Full article
(This article belongs to the Special Issue Immune Modulation of Mucosal Inflammation 2.0)
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