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Special Issue "Immunomodulatory Compounds"

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: 30 September 2018

Special Issue Editor

Guest Editor
Prof. Dr. Günter Lochnit

Protein Analytics, Institute of Biochemistry, Faculty of Medicine, Justus-Liebig-University Giessen, Giessen, Germany
Website | E-Mail
Interests: protein analytics; mass spectrometry; C. Elegans; nematodes; parasitology

Special Issue Information

Dear Colleagues,

Nature has developed, during evolution, a broad variety of immunomodulatory compounds, e.g., to facilitate invasion and/or persistence of pathogens and parasites. The characterization of these compounds have provided new insights into immunology, parasitology and various diseases, such as autoimmune diseases. The development of chemical analogues of these naturally-occurring compounds has opened a new field of drug development and medical therapy.

The scope of this Special Issue is to give an overview of this field, comprising the detection and characterization of naturally-occurring immunomodulatory compounds, their application in medicine and veterinary medicine, and the development of chemical analogues and their therapeutic perspectives.

Prof. Dr. Günter Lochnit
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 papers will be 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. Molecules 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 1800 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

  • Immunology
  • Immunomodulation
  • Parasitology
  • autoimmune diseases
  • inflammation
  • pharmacology
  • immunotherapy
  • hepatic targeting

Published Papers (3 papers)

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Research

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Open AccessCommunication The Response of IL-17-Producing B Cells to ArtinM Is Independent of Its Interaction with TLR2 and CD14
Molecules 2018, 23(9), 2339; https://doi.org/10.3390/molecules23092339
Received: 30 July 2018 / Revised: 28 August 2018 / Accepted: 29 August 2018 / Published: 13 September 2018
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Abstract
ArtinM, a d-mannose-binding lectin from Artocarpus heterophyllus, activates antigen-presenting cells by recognizing Toll-like receptor (TLR)2 and cluster of differentiation (CD)14 N-glycans, induces cytokine production, and promotes type 1 T helper (Th1) immunity, a process that plays an assisting role in
[...] Read more.
ArtinM, a d-mannose-binding lectin from Artocarpus heterophyllus, activates antigen-presenting cells by recognizing Toll-like receptor (TLR)2 and cluster of differentiation (CD)14 N-glycans, induces cytokine production, and promotes type 1 T helper (Th1) immunity, a process that plays an assisting role in the combat against fungal infections. We recently demonstrated that ArtinM stimulates CD4+ T cells to produce interleukin (IL)-17 through direct interaction with CD3. Here, we further investigated the effects of ArtinM on the production of IL-17 by B cell activation. We showed that ArtinM activates murine B cells, increasing IL-17 and IL-12p40 production. The direct effect of ArtinM was sufficient to induce IL-17 production in B cells, and we did not find differences in the levels of IL-17 between the B cells purified from the wild-type (WT) and knockout (KO) mice for TLR2 or CD14 in the presence of ArtinM. Thus, the effects of ArtinM on splenic B cells through carbohydrate recognition may contribute to Th17 immunity; however, the mechanism involved is not associated with the interaction of ArtinM with TLR2 and CD14. The current work represents a pioneering effort in the understanding of the induction of IL-17 by lectins in B cells. Full article
(This article belongs to the Special Issue Immunomodulatory Compounds)
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Open AccessArticle Phosphocholine-Modified Lipooligosaccharides of Haemophilus influenzae Inhibit ATP-Induced IL-1β Release by Pulmonary Epithelial Cells
Molecules 2018, 23(8), 1979; https://doi.org/10.3390/molecules23081979
Received: 29 June 2018 / Revised: 19 July 2018 / Accepted: 27 July 2018 / Published: 8 August 2018
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Abstract
Phosphocholine-modified bacterial cell wall components are virulence factors enabling immune evasion and permanent colonization of the mammalian host, by mechanisms that are poorly understood. Recently, we demonstrated that free phosphocholine (PC) and PC-modified lipooligosaccharides (PC-LOS) from Haemophilus influenzae, an opportunistic pathogen of
[...] Read more.
Phosphocholine-modified bacterial cell wall components are virulence factors enabling immune evasion and permanent colonization of the mammalian host, by mechanisms that are poorly understood. Recently, we demonstrated that free phosphocholine (PC) and PC-modified lipooligosaccharides (PC-LOS) from Haemophilus influenzae, an opportunistic pathogen of the upper and lower airways, function as unconventional nicotinic agonists and efficiently inhibit the ATP-induced release of monocytic IL-1β. We hypothesize that H. influenzae PC-LOS exert similar effects on pulmonary epithelial cells and on the complex lung tissue. The human lung carcinoma-derived epithelial cell lines A549 and Calu-3 were primed with lipopolysaccharide from Escherichia coli followed by stimulation with ATP in the presence or absence of PC or PC-LOS or LOS devoid of PC. The involvement of nicotinic acetylcholine receptors was tested using specific antagonists. We demonstrate that PC and PC-LOS efficiently inhibit ATP-mediated IL-1β release by A549 and Calu-3 cells via nicotinic acetylcholine receptors containing subunits α7, α9, and/or α10. Primed precision-cut lung slices behaved similarly. We conclude that H. influenzae hijacked an endogenous anti-inflammatory cholinergic control mechanism of the lung to evade innate immune responses of the host. These findings may pave the way towards a host-centered antibiotic treatment of chronic airway infections with H. influenzae. Full article
(This article belongs to the Special Issue Immunomodulatory Compounds)
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Review

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Open AccessReview Immunomodulatory Action of Substituted 1,3,4-Thiadiazines on the Course of Myocardial Infarction
Molecules 2018, 23(7), 1611; https://doi.org/10.3390/molecules23071611
Received: 11 June 2018 / Revised: 29 June 2018 / Accepted: 30 June 2018 / Published: 2 July 2018
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Abstract
This review focuses on the biological action of the compounds from the group of substituted 1,3,4-thiadiazines on stress response and myocardial infarction. The aim of this review is to propose the possible mechanisms of action of 1,3,4-thiadiazines and offer prospectives in the development
[...] Read more.
This review focuses on the biological action of the compounds from the group of substituted 1,3,4-thiadiazines on stress response and myocardial infarction. The aim of this review is to propose the possible mechanisms of action of 1,3,4-thiadiazines and offer prospectives in the development of new derivatives as therapeutic agents. It is known, that compounds that have biological effects similar to those used as antidepressants can down-regulate the secretion of proinflammatory cytokines, up-regulate the release of anti-inflammatory ones and affect cell recruitment, which allows them to be considered immunomodulators as well. The results of pharmacological evaluation, in silico studies, and in vivo experiments of several compounds from the group of substituted 1,3,4-thiadiazines with antidepressant properties are presented. It is proposed that the cardioprotective effects of substituted 1,3,4-thiadiazines might be explained by the peculiarities of their multi-target action: the ability of the compounds to interact with various types of receptors and transporters of dopaminergic, serotonergic and acetylcholinergic systems and to block the kinase signal pathway PI3K-AKT. The described effects of substituted 1,3,4-thiadiazines suggest that it is necessary to search for a new agents for limiting the peripheral inflammatory/ischemic damage through the entral mechanisms of stress reaction and modifying pro-inflammatory cytokine signaling pathways in the brain. Full article
(This article belongs to the Special Issue Immunomodulatory Compounds)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Type of the paper: Short Communication
Tentative title: Effect of the ArtinM lectin in the IL-17 production by B cells 
Authors: Patrícia Kellen Oliveira-Brito, Maria Cristina Roque-Barreira, Thiago A da Silva
Affiliations: University of São Paulo-FMRP; Ribeirão Preto, São Paulo, Brazil 
 
Tentative title: Haemophilus influenzae lipooligosaccharides inhibit ATP-induced IL-1b release by pulmonary epithelial cells
Authors: Katrin Richter1,*, Christian Koch1,*, Elke K.H. Schweda2, Sven Wichmann1, Sigrid Wilker1, Ilona Magel1, Michael Sander1, J. Michael McIntosh3, Winfried Padberg1, Veronika Grau1
Affiliations: 1Justus-Liebig University, Giessen, Germany; 2Linköping University, Linköping, Sweden; 3University of Utah, Salt Lake City, Utah, USA
Abstract: Phosphocholine (PC)-modified cell wall components of Gram-negative and Gram-positive bacteria are known virulence factors that enable immune evasion and permanent colonization of the mammalian host, via mechanisms that are poorly understood. Recently, our group demonstrated that high concentrations of free PC as well as PC-modified lipooligosaccharides from Haemophilus influenzae function as unconventional nicotinic agonists and efficiently inhibit the ATP-induced release of monocytic IL-1β. This pro-inflammatory cytokine plays a central role in host defense against bacteria. Here, we test the hypothesis that H. influenzae lipooligosaccharides exert similar effect on pulmonary epithelial cells.
The human adenocarcinoma-derived cell lines A549 and Calu-3 were primed with lipopolysaccharide from Echerichia coli followed by stimulation with ATP in the presence or absence of PC or PC-modified H. influenzae lipooligosaccharides. As a negative control, we included lipooligosaccharides devoid of PC that were purified from corresponding H. influenzae lic1 mutants. The involvement of nicotinic acetylcholine receptors was tested using specific nicotinic antagonists.
We demonstrate that PC and PC-modified lipooligosaccharides efficiently inhibit ATP-mediated IL-1β release of human pulmonary adenocarcinoma cell lines A-549 and Calu-3 via nicotinic acetylcholine receptors containing subunit α7, α9, and/or α10. Our data suggest that H. influenzae hijacked an endogenous anti-inflammatory cholinergic control mechanism of the lung to evade innate immune responses of the host. These findings may pave the way towards a host-centered antibiotic treatment of chronic airway infections with H. influenzae.
 
 
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