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The Role of Toll-Like Receptors (TLR) in Infection and Inflammation

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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 (15 March 2023) | Viewed by 38207

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Dr. Ralf Kircheis

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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

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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

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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

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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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The Role of Toll-Like Receptors (TLRs) in Infection and Inflammation: Third Edition in International Journal of Molecular Sciences (3 articles)

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Editorial

Jump to: Research, Review

7 pages, 2647 KiB

Open AccessEditorial

The Role of Toll-like Receptors (TLRs) and Their Related Signaling Pathways in Viral Infection and Inflammation

by Ralf Kircheis and Oliver Planz

Int. J. Mol. Sci. 2023, 24(7), 6701; https://doi.org/10.3390/ijms24076701 - 4 Apr 2023

Cited by 15 | Viewed by 5923

Abstract

Toll-like receptors (TLRs) belong to a powerful system for the recognition and elimination of pathogen-associated molecular patterns (PAMPs) from bacteria, viruses, and other pathogens [...] Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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Research

Jump to: Editorial, Review

16 pages, 3690 KiB

Open AccessArticle

RAGE–TLR4 Crosstalk Is the Key Mechanism by Which High Glucose Enhances the Lipopolysaccharide-Induced Inflammatory Response in Primary Bovine Alveolar Macrophages

by Longfei Yan, Yanran Li, Tianyu Tan, Jiancheng Qi, Jing Fang, Hongrui Guo, Zhihua Ren, Liping Gou, Yi Geng, Hengmin Cui, Liuhong Shen, Shumin Yu, Zhisheng Wang and Zhicai Zuo

Int. J. Mol. Sci. 2023, 24(8), 7007; https://doi.org/10.3390/ijms24087007 - 10 Apr 2023

Cited by 6 | Viewed by 1937

Abstract

The receptor of advanced glycation end products (RAGE) and Toll-like receptor 4 (TLR4) are important receptors for inflammatory responses induced by high glucose (HG) and lipopolysaccharide (LPS) and show crosstalk phenomena in inflammatory responses. However, it is unknown whether RAGE and TLR4 can influence each other’s expression through a crosstalk mechanism and whether the RAGE–TLR4 crosstalk related to the molecular mechanism of HG enhances the LPS-induced inflammatory response. In this study, the implications of LPS with multiple concentrations (0, 1, 5, and 10 μg/mL) at various treatment times (0, 3, 6, 12, and 24 h) in primary bovine alveolar macrophages (BAMs) were explored. The results showed that a 5 μg/mL LPS treatment at 12 h had the most significant increment on the pro-inflammatory cytokine interleukin 1β (IL-1β), IL-6, and tumor necrosis factor (TNF)-α levels in BAMs (p < 0.05) and that the levels of TLR4, RAGE, MyD88, and NF-κB p65 mRNA and protein expression were upregulated (p < 0.05). Then, the effect of LPS (5 μg/mL) and HG (25.5 mM) co-treatment in BAMs was explored. The results further showed that HG significantly enhanced the release of IL-1β, IL-6, and TNF-α caused by LPS in the supernatant (p < 0.01) and significantly increased the levels of RAGE, TLR4, MyD88, and NF-κB p65 mRNA and protein expression (p < 0.01). Pretreatment with FPS-ZM1 and TAK-242, the inhibitors of RAGE and TLR4, significantly alleviated the HG + LPS-induced increment of RAGE, TLR4, MyD88, and NF-κB p65 mRNA and protein expression in the presence of HG and LPS (p < 0.01). This study showed that RAGE and TLR4 affect each other’s expression through crosstalk during the combined usage of HG and LPS and synergistically activate the MyD88/NF-κB signaling pathway to promote the release of pro-inflammatory cytokines in BAMs. Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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16 pages, 2677 KiB

Open AccessArticle

Advanced Glycation End Products and Activation of Toll-like Receptor-2 and -4 Induced Changes in Aquaporin-3 Expression in Mouse Keratinocytes

by Yonghong Luo, Rawipan Uaratanawong, Vivek Choudhary, Mary Hardin, Catherine Zhang, Samuel Melnyk, Xunsheng Chen and Wendy B. Bollag

Int. J. Mol. Sci. 2023, 24(2), 1376; https://doi.org/10.3390/ijms24021376 - 10 Jan 2023

Cited by 4 | Viewed by 2338

Abstract

Prolonged inflammation and impaired re-epithelization are major contributing factors to chronic non-healing diabetic wounds; diabetes is also characterized by xerosis. Advanced glycation end products (AGEs), and the activation of toll-like receptors (TLRs), can trigger inflammatory responses. Aquaporin-3 (AQP3) plays essential roles in keratinocyte function and skin wound re-epithelialization/re-generation and hydration. Suberanilohydroxamic acid (SAHA), a histone deacetylase inhibitor, mimics the increased acetylation observed in diabetes. We investigated the effects of TLR2/TLR4 activators and AGEs on keratinocyte AQP3 expression in the presence and absence of SAHA. Primary mouse keratinocytes were treated with or without TLR2 agonist Pam₃Cys-Ser-(Lys)₄ (PAM), TLR4 agonist lipopolysaccharide (LPS), or AGEs, with or without SAHA. We found that (1) PAM and LPS significantly upregulated AQP3 protein basally (without SAHA) and PAM downregulated AQP3 protein with SAHA; and (2) AGEs (100 µg/mL) increased AQP3 protein expression basally and decreased AQP3 levels with SAHA. PAM and AGEs produced similar changes in AQP3 expression, suggesting a common pathway or potential crosstalk between TLR2 and AGEs signaling. Our findings suggest that TLR2 activation and AGEs may be beneficial for wound healing and skin hydration under normal conditions via AQP3 upregulation, but that these pathways are likely deleterious in diabetes chronically through decreased AQP3 expression. Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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17 pages, 3977 KiB

Open AccessArticle

Breast Cancer Vaccine Containing a Novel Toll-like Receptor 7 Agonist and an Aluminum Adjuvant Exerts Antitumor Effects

by Shuquan Zhang, Yu Liu, Ji Zhou, Jiaxin Wang, Guangyi Jin and Xiaodong Wang

Int. J. Mol. Sci. 2022, 23(23), 15130; https://doi.org/10.3390/ijms232315130 - 1 Dec 2022

Cited by 11 | Viewed by 2190

Abstract

Mucin 1 (MUC1) has received increasing attention due to its high expression in breast cancer, in which MUC1 acts as a cancer antigen. Our group has been committed to the development of small-molecule TLR7 (Toll-like receptor 7) agonists, which have been widely investigated in the field of tumor immunotherapy. In the present study, we constructed a novel tumor vaccine (SZU251 + MUC1 + Al) containing MUC1 and two types of adjuvants: a TLR7 agonist (SZU251) and an aluminum adjuvant (Al). Immunostimulatory responses were first verified in vitro, where the vaccine promoted the release of cytokines and the expression of costimulatory molecules in mouse BMDCs (bone marrow dendritic cells) and spleen lymphocytes. Then, we demonstrated that SZU251 + MUC1 + Al was effective and safe against a tumor expressing the MUC1 antigen in both prophylactic and therapeutic schedules in vivo. The immune responses in vivo were attributed to the increase in specific humoral and cellular immunity, including antibody titers, CD4⁺, CD8⁺ and activated CD8⁺ T cells. Therefore, our vaccine candidate may have beneficial effects in the prevention and treatment of breast cancer patients. Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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13 pages, 2923 KiB

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A Xanthohumol-Rich Hop Extract Diminishes Endotoxin-Induced Activation of TLR4 Signaling in Human Peripheral Blood Mononuclear Cells: A Study in Healthy Women

by Finn Jung, Raphaela Staltner, Anja Baumann, Katharina Burger, Emina Halilbasic, Claus Hellerbrand and Ina Bergheim

Int. J. Mol. Sci. 2022, 23(20), 12702; https://doi.org/10.3390/ijms232012702 - 21 Oct 2022

Cited by 6 | Viewed by 2173

Abstract

Infections with Gram-negative bacteria are still among the leading causes of infection-related deaths. Several studies suggest that the chalcone xanthohumol (XN) found in hop (Humulus lupulus) possesses anti-inflammatory effects. In a single-blinded, placebo controlled randomized cross-over design study we assessed if the oral intake of a single low dose of 0.125 mg of a XN derived through a XN-rich hop extract (75% XN) affects lipopolysaccharide (LPS)-induced immune responses in peripheral blood mononuclear cells (PBMCs) ex vivo in normal weight healthy women (n = 9) (clinicaltrials.gov: NCT04847193) and determined associated molecular mechanisms. LPS-stimulation of PBMCs isolated from participants 1 h after the intake of the placebo for 2 h resulted in a significant induction of pro-inflammatory cytokine release which was significantly attenuated when participants had consumed XN. The XN-dependent attenuation of proinflammatory cytokine release was less pronounced 6 h after the LPS stimulation while the release of sCD14 was significantly reduced at this timepoint. The LPS-dependent activation of hTLR4 transfected HEK293 cells was significantly and dose-dependently suppressed by the XN-rich hop extract which was attenuated when cells were co-challenged with sCD14. Taken together, our results suggest even a one-time intake of low doses of XN consumed in a XN-rich hop extract can suppress LPS-dependent stimulation of PBMCs and that this is related to the interaction of the hop compound with the CD14/TLR4 signaling cascade. Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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14 pages, 5200 KiB

Open AccessArticle

Identification of an Optimal TLR8 Ligand by Alternating the Position of 2′-O-Ribose Methylation

by Marina Nicolai, Julia Steinberg, Hannah-Lena Obermann, Francisco Venegas Solis, Eva Bartok, Stefan Bauer and Stephanie Jung

Int. J. Mol. Sci. 2022, 23(19), 11139; https://doi.org/10.3390/ijms231911139 - 22 Sep 2022

Cited by 3 | Viewed by 2347

Abstract

Recognition of RNA by receptors of the innate immune system is regulated by various posttranslational modifications. Different single 2′-O-ribose (2′-O-) methylations have been shown to convert TLR7/TLR8 ligands into specific TLR8 ligands, so we investigated whether the position of 2′-O-methylation is crucial for its function. To this end, we designed different 2′-O-methylated RNA oligoribonucleotides (ORN), investigating their immune activity in various cell systems and analyzing degradation under RNase T2 treatment. We found that the 18S rRNA-derived TLR7/8 ligand, RNA63, was differentially digested as a result of 2′-O-methylation, leading to variations in TLR8 and TLR7 inhibition. The suitability of certain 2′-O-methylated RNA63 derivatives as TLR8 agonists was further demonstrated by the fact that other RNA sequences were only weak TLR8 agonists. We were thus able to identify specific 2′-O-methylated RNA derivatives as optimal TLR8 ligands. Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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23 pages, 3331 KiB

Open AccessArticle

Investigation of TLR2 and TLR4 Polymorphisms and Sepsis Susceptibility: Computational and Experimental Approaches

by Mohammed Y. Behairy, Ali A. Abdelrahman, Eman A. Toraih, Emad El-Deen A. Ibrahim, Marwa M. Azab, Anwar A. Sayed and Hany R. Hashem

Int. J. Mol. Sci. 2022, 23(18), 10982; https://doi.org/10.3390/ijms231810982 - 19 Sep 2022

Cited by 12 | Viewed by 2526

Abstract

Toll-like receptors (TLR) play an eminent role in the regulation of immune responses to invading pathogens during sepsis. TLR genetic variants might influence individual susceptibility to developing sepsis. The current study aimed to investigate the association of genetic polymorphisms of the TLR2 and TLR4 with the risk of developing sepsis with both a pilot study and in silico tools. Different in silico tools were used to predict the impact of our SNPs on protein structure, stability, and function. Furthermore, in our prospective study, all patients matching the inclusion criteria in the intensive care units (ICU) were included and followed up, and DNA samples were genotyped using real-time polymerase chain reaction (RT-PCR) technology. There was a significant association between TLR2 Arg753Gln polymorphisms and sepsis under the over-dominant model (p = 0.043). In contrast, we did not find a significant difference with the TLR4 Asp299Gly polymorphism with sepsis. However, there was a significant association between TLR4 Asp299Gly polymorphisms and Acinetobacter baumannii infection which is quite a virulent organism in ICU (p = 0.001) and post-surgical cohorts (p = 0.033). Our results conclude that the TLR2 genotype may be a risk factor for sepsis in adult patients. Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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18 pages, 2923 KiB

Open AccessArticle

Mechanical Compression by Simulating Orthodontic Tooth Movement in an In Vitro Model Modulates Phosphorylation of AKT and MAPKs via TLR4 in Human Periodontal Ligament Cells

by Charlotte E. Roth, Rogerio B. Craveiro, Christian Niederau, Hanna Malyaran, Sabine Neuss, Joachim Jankowski and Michael Wolf

Int. J. Mol. Sci. 2022, 23(15), 8062; https://doi.org/10.3390/ijms23158062 - 22 Jul 2022

Cited by 8 | Viewed by 3163

Abstract

Mechanical compression simulating orthodontic tooth movement in in vitro models induces pro-inflammatory cytokine expression in periodontal ligament (PDL) cells. Our previous work shows that TLR4 is involved in this process. Here, primary PDL cells are isolated and characterized to better understand the cell signaling downstream of key molecules involved in the process of sterile inflammation via TLR4. The TLR4 monoclonal blocking antibody significantly reverses the upregulation of phospho-AKT, caused by compressive force, to levels comparable to controls by inhibition of TLR4. Phospho-ERK and phospho-p38 are also modulated in the short term via TLR4. Additionally, moderate compressive forces of 2 g/cm², a gold standard for static compressive mechanical stimulation, are not able to induce translocation of Nf-kB and phospho-ERK into the nucleus. Accordingly, we demonstrated for the first time that TLR4 is also one of the triggers for signal transduction under compressive force. The TLR4, one of the pattern recognition receptors, is involved through its specific molecular structures on damaged cells during mechanical stress. Our findings provide the basis for further research on TLR4 in the modulation of sterile inflammation during orthodontic therapy and periodontal remodeling. Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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Review

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20 pages, 1549 KiB

Open AccessReview

Is There a Role for Immunoregulatory and Antiviral Oligonucleotides Acting in the Extracellular Space? A Review and Hypothesis

by Aleksandra Dondalska, Sandra Axberg Pålsson and Anna-Lena Spetz

Int. J. Mol. Sci. 2022, 23(23), 14593; https://doi.org/10.3390/ijms232314593 - 23 Nov 2022

Cited by 2 | Viewed by 2013

Abstract

Here, we link approved and emerging nucleic acid-based therapies with the expanding universe of small non-coding RNAs (sncRNAs) and the innate immune responses that sense oligonucleotides taken up into endosomes. The Toll-like receptors (TLRs) 3, 7, 8, and 9 are located in endosomes and can detect nucleic acids taken up through endocytic routes. These receptors are key triggers in the defense against viruses and/or bacterial infections, yet they also constitute an Achilles heel towards the discrimination between self- and pathogenic nucleic acids. The compartmentalization of nucleic acids and the activity of nucleases are key components in avoiding autoimmune reactions against nucleic acids, but we still lack knowledge on the plethora of nucleic acids that might be released into the extracellular space upon infections, inflammation, and other stress responses involving increased cell death. We review recent findings that a set of single-stranded oligonucleotides (length of 25–40 nucleotides (nt)) can temporarily block ligands destined for endosomes expressing TLRs in human monocyte-derived dendritic cells. We discuss knowledge gaps and highlight the existence of a pool of RNA with an approximate length of 30–40 nt that may still have unappreciated regulatory functions in physiology and in the defense against viruses as gatekeepers of endosomal uptake through certain routes. Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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25 pages, 1993 KiB

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Toll-like Receptor Mediation in SARS-CoV-2: A Therapeutic Approach

by Abdul Manan, Rameez Hassan Pirzada, Muhammad Haseeb and Sangdun Choi

Int. J. Mol. Sci. 2022, 23(18), 10716; https://doi.org/10.3390/ijms231810716 - 14 Sep 2022

Cited by 7 | Viewed by 3598

Abstract

The innate immune system facilitates defense mechanisms against pathogen invasion and cell damage. Toll-like receptors (TLRs) assist in the activation of the innate immune system by binding to pathogenic ligands. This leads to the generation of intracellular signaling cascades including the biosynthesis of molecular mediators. TLRs on cell membranes are adept at recognizing viral components. Viruses can modulate the innate immune response with the help of proteins and RNAs that downregulate or upregulate the expression of various TLRs. In the case of COVID-19, molecular modulators such as type 1 interferons interfere with signaling pathways in the host cells, leading to an inflammatory response. Coronaviruses are responsible for an enhanced immune signature of inflammatory chemokines and cytokines. TLRs have been employed as therapeutic agents in viral infections as numerous antiviral Food and Drug Administration-approved drugs are TLR agonists. This review highlights the therapeutic approaches associated with SARS-CoV-2 and the TLRs involved in COVID-19 infection. Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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35 pages, 2854 KiB

Open AccessReview

Could a Lower Toll-like Receptor (TLR) and NF-κB Activation Due to a Changed Charge Distribution in the Spike Protein Be the Reason for the Lower Pathogenicity of Omicron?

by Ralf Kircheis and Oliver Planz

Int. J. Mol. Sci. 2022, 23(11), 5966; https://doi.org/10.3390/ijms23115966 - 25 May 2022

Cited by 16 | Viewed by 4368

Abstract

The novel SARS-CoV-2 Omicron variant B.1.1.529, which emerged in late 2021, is currently active worldwide, replacing other variants, including the Delta variant, due to an enormously increased infectivity. Multiple substitutions and deletions in the N-terminal domain (NTD) and the receptor binding domain (RBD) in the spike protein collaborate with the observed increased infectivity and evasion from therapeutic monoclonal antibodies and vaccine-induced neutralizing antibodies after primary/secondary immunization. In contrast, although three mutations near the S1/S2 furin cleavage site were predicted to favor cleavage, observed cleavage efficacy is substantially lower than in the Delta variant and also lower compared to the wild-type virus correlating with significantly lower TMPRSS2-dependent replication in the lungs, and lower cellular syncytium formation. In contrast, the Omicron variant shows high TMPRSS2-independent replication in the upper airway organs, but lower pathogenicity in animal studies and clinics. Based on recent data, we present here a hypothesis proposing that the changed charge distribution in the Omicron’s spike protein could lead to lower activation of Toll-like receptors (TLRs) in innate immune cells, resulting in lower NF-κB activation, furin expression, and viral replication in the lungs, and lower immune hyper-activation. Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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13 pages, 848 KiB

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Toll-like Receptor Response to Hepatitis C Virus Infection: A Recent Overview

by Mohammad Enamul Hoque Kayesh, Michinori Kohara and Kyoko Tsukiyama-Kohara

Int. J. Mol. Sci. 2022, 23(10), 5475; https://doi.org/10.3390/ijms23105475 - 13 May 2022

Cited by 11 | Viewed by 3112

Abstract

Hepatitis C virus (HCV) infection remains a major global health burden, causing chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Toll-like receptors (TLRs) are evolutionarily conserved pattern recognition receptors that detect pathogen-associated molecular patterns and activate downstream signaling to induce proinflammatory cytokine and chemokine production. An increasing number of studies have suggested the importance of TLR responses in the outcome of HCV infection. However, the exact role of innate immune responses, including TLR response, in controlling chronic HCV infection remains to be established. A proper understanding of the TLR response in HCV infection is essential for devising new therapeutic approaches against HCV infection. In this review, we discuss the progress made in our understanding of the host innate immune response to HCV infection, with a particular focus on the TLR response. In addition, we discuss the mechanisms adopted by HCV to avoid immune surveillance mediated by TLRs. Full article

(This article belongs to the Special Issue The Role of Toll-Like Receptors (TLR) in Infection and Inflammation)

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