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The Role of Toll-Like Receptors (TLRs) in Infection and Inflammation: Third Edition

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: 31 January 2025 | Viewed by 2816

Special Issue Editors

Dr. Ralf Kircheis

E-Mail Website
Guest Editor
Syntacoll GmbH, Saal a.d.Donau, Bayern, Germany
Interests: toll-like receptors; NF-kappaB; COVID-19; cytokines; gene therapy; immune therapy
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Oliver Planz

E-Mail Website
Guest Editor
Institute of Cell Biology and Immunology, Eberhard Karls University, 72076 Tuebingen, Germany
Interests: immunology of viral infections; host cell targeted antivirals; virus cell interaction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Toll-like receptors (TLRs) represent a powerful system for the recognition and elimination of pathogen-associated molecular patterns (PAMPs) from bacteria, viruses, and other pathogens and of damage-associated molecular patterns (DAMPs) released from dying or lytic cells. TLRs are mainly expressed on immune cells but can also be present on some tissue-resident cell populations. Typical PAMPs are cell wall components of bacterial and viral pathogens, conserved proteins, or pathogenic nucleic acids, including viral RNA and DNA.

Activation of TLRs leads to the production of proinflammatory cytokines and type I interferons, which are important for induction of the host immune response against bacterial, fungal, and viral infections and malaria. However, dysregulation and overstimulation can be detrimental, leading to hyperinflammation, sepsis, and loss of tissue integrity. TLRs are involved in the pathogenesis of acute viral infections, including in the case of COVID-19. Altogether, activation of TLR plays a deciding role in both the induction of immunity and the pathophysiological effects associated with excessive activation, indicating TLRs are promising targets for pharmacological intervention and treatment.

Topics of interest include but are not limited to:

  • Activation of TLR and their downstream signaling pathways and their correlation with the immunology and pathophysiology of bacterial and viral infectious diseases.
  • Translational research, pharmacological and medical interventions with TLR activation and signaling, and their use as therapeutic targets for bacterial and viral infectious diseases, including COVID-19.
  • Clinical or model studies, though only in conjunction with biomolecular experiments.

Dr. Ralf Kircheis
Prof. Dr. Oliver Planz
Guest Editors

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

  • toll-like receptors (TLR)
  • pathogen associated molecular patterns (PAMPs)
  • sepsis
  • bacterial infections
  • viral infections
  • Myd88
  • TRIF
  • NF-kappaB
  • COVID-19
  • coagulopathies

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Published Papers (3 papers)

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Research

11 pages, 2054 KiB  
Article
Variants rs3804099 and rs3804100 in the TLR2 Gene Induce Different Profiles of TLR-2 Expression and Cytokines in Response to Spike of SARS-CoV-2
by Julio Flores-González, Zurisadai Monroy-Rodríguez, Ramcés Falfán-Valencia, Ivette Buendía-Roldán, Ingrid Fricke-Galindo, Rafael Hernández-Zenteno, Ricardo Herrera-Sicairos, Leslie Chávez-Galán and Gloria Pérez-Rubio
Int. J. Mol. Sci. 2024, 25(20), 11063; https://doi.org/10.3390/ijms252011063 - 15 Oct 2024
Viewed by 797
Abstract
The present study aimed to identify in patients with severe COVID-19 and acute respiratory distress syndrome (ARDS) the association between rs3804099 and rs3804100 (TLR2) and evaluate the expression of TLR-2 on the cell surface of innate and adaptive cells of patients’ [...] Read more.
The present study aimed to identify in patients with severe COVID-19 and acute respiratory distress syndrome (ARDS) the association between rs3804099 and rs3804100 (TLR2) and evaluate the expression of TLR-2 on the cell surface of innate and adaptive cells of patients’ carriers of C allele in at least one genetic variant. We genotyped 1018 patients with COVID-19 and ARDS. According to genotype, a subgroup of 12 patients was selected to stimulate peripheral blood mononuclear cells (PBMCs) with spike and LPS + spike. We evaluated soluble molecules in cell culture supernatants. The C allele in TLR2 (rs3804099, rs3804100) is not associated with a risk of severe COVID-19; however, the presence of the C allele (rs3804099 or rs3804100) affects the TLR-2 ability to respond to a spike of SARS-CoV-2 correctly. The reference group (genotype TT) downregulated the frequency of non-switched TLR-2+ B cells in response to spike stimulus; however, the allele’s C carriers group is unable to induce this regulation, but they produce high levels of IL-10, IL-6, and TNF-α by an independent pathway of TLR-2. Findings showed that TT genotypes (rs3804099 and rs3804100) affect the non-switched TLR-2+ B cell distribution. Genotype TT (rs3804099 and rs3804100) affects the TLR-2’s ability to respond to a spike of SARS-CoV-2. However, the C allele had increased IL-10, IL-6, and TNF-α by stimulation with spike and LPS. Full article
(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLRs) in Infection and Inflammation: Third Edition)
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19 pages, 8284 KiB  
Article
Impact of Mygalin on Inflammatory Response Induced by Toll-like Receptor 2 Agonists and IFN-γ Activation
by Nayara Del Santos, Ricardo Vázquez-Ramírez, Elizabeth Mendes, Pedro Ismael Silva Júnior and Monamaris Marques Borges
Int. J. Mol. Sci. 2024, 25(19), 10555; https://doi.org/10.3390/ijms251910555 - 30 Sep 2024
Viewed by 702
Abstract
Several natural products are being studied to identify new bioactive molecules with therapeutic potential for infections, immune modulation, and other pathologies. TLRs are a family of receptors that play a crucial role in the immune system, constituting the first line of immune defense. [...] Read more.
Several natural products are being studied to identify new bioactive molecules with therapeutic potential for infections, immune modulation, and other pathologies. TLRs are a family of receptors that play a crucial role in the immune system, constituting the first line of immune defense. They recognize specific products derived from microorganisms that activate multiple pathways and transcription factors in target cells, which are vital for producing immune mediators. Mygalin is a synthetic acylpolyamine derived from hemocytes of the spider Acanthoscurria gomesiana. This molecule negatively regulates macrophage response to LPS stimulation by interacting with MD2 in the TLR4/MD2 complex. Here, we investigated the activity of Mygalin mediated by TLR2 agonists in cells treated with Pam3CSK4 (TLR2/1), Pam2CSK4, Zymosan (TLR2/6), and IFN-γ. Our data showed that Mygalin significantly inhibited stimulation with agonists and IFN-γ, reducing NO and IL-6 synthesis, regardless of the stimulation. There was also a significant reduction in the phosphorylation of proteins NF-κB p65 and STAT-1 in cells treated with Pam3CSK4. Molecular docking assays determined the molecular structure of Mygalin and agonists Pam3CSK4, Pam2CSK4, and Zymosan, as well as their interaction and free energy with the heterodimeric complexes TLR2/1 and TLR2/6. Mygalin interacted with the TLR1 and TLR2 dimer pathway through direct interaction with the agonists, and the ligand-binding domain was similar in both complexes. However, the binding of Mygalin was different from that of the agonists, since the interaction energy with the receptors was lower than with the agonists for their receptors. In conclusion, this study showed the great potential of Mygalin as a potent natural inhibitor of TLR2/1 and TLR2/6 and a suppressor of the inflammatory response induced by TLR2 agonists, in part due to its ability to interact with the heterodimeric complexes. Full article
(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLRs) in Infection and Inflammation: Third Edition)
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23 pages, 2417 KiB  
Article
Effects of Omega-3 Polyunsaturated Fatty Acids on the Formation of Adipokines, Cytokines, and Oxylipins in Retroperitoneal Adi-Pose Tissue of Mice
by Tatjana Wenderoth, Martin Feldotto, Jessica Hernandez, Julia Schäffer, Stephan Leisengang, Fabian Johannes Pflieger, Janne Bredehöft, Konstantin Mayer, Jing X. Kang, Jens Bier, Friedrich Grimminger, Nadine Paßlack and Christoph Rummel
Int. J. Mol. Sci. 2024, 25(18), 9904; https://doi.org/10.3390/ijms25189904 - 13 Sep 2024
Viewed by 1002
Abstract
Oxylipins and specialized pro-resolving lipid mediators (SPMs) derived from polyunsaturated fatty acids (PUFAs) are mediators that coordinate an active process of inflammation resolution. While these mediators have potential as circulating biomarkers for several disease states with inflammatory components, the source of plasma oxylipins/SPMs [...] Read more.
Oxylipins and specialized pro-resolving lipid mediators (SPMs) derived from polyunsaturated fatty acids (PUFAs) are mediators that coordinate an active process of inflammation resolution. While these mediators have potential as circulating biomarkers for several disease states with inflammatory components, the source of plasma oxylipins/SPMs remains a matter of debate but may involve white adipose tissue (WAT). Here, we aimed to investigate to what extent high or low omega (n)-3 PUFA enrichment affects the production of cytokines and adipokines (RT-PCR), as well as oxylipins/SPMs (liquid chromatography–tandem mass spectrometry) in the WAT of mice during lipopolysaccharide (LPS)-induced systemic inflammation (intraperitoneal injection, 2.5 mg/kg, 24 h). For this purpose, n-3 PUFA genetically enriched mice (FAT-1), which endogenously synthesize n-3 PUFAs, were compared to wild-type mice (WT) and combined with n-3 PUFA-sufficient or deficient diets. LPS-induced systemic inflammation resulted in the decreased expression of most adipokines and interleukin-6 in WAT, whereas the n-3-sufficient diet increased them compared to the deficient diet. The n-6 PUFA arachidonic acid was decreased in WAT of FAT-1 mice, while n-3 derived PUFAs (eicosapentaenoic acid, docosahexaenoic acid) and their metabolites (oxylipins/SPMs) were increased in WAT by genetic and nutritional n-3 enrichment. Several oxylipins/SPMs were increased by LPS treatment in WAT compared to PBS-treated controls in genetically n-3 enriched FAT-1 mice. Overall, we show that WAT may significantly contribute to circulating oxylipin production. Moreover, n-3-sufficient or n-3-deficient diets alter adipokine production. The precise interplay between cytokines, adipokines, and oxylipins remains to be further investigated. Full article
(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLRs) in Infection and Inflammation: Third Edition)
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