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Role of NF-kappaB Pathway in Inflammation and Infection
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Role of NF-kappaB Pathway in Inflammation and Infection

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 (31 December 2022) | Viewed by 19492

Special Issue Editor

Dr. Ralf Kircheis

E-Mail Website
Guest Editor
Syntacoll GmbH, Saal a.d.Donau, Bayern, Germany
Interests: immunotherapy, gene therapy, gene delivery, non-viral vectors, innate immunity, cancer vaccines, COVID-19, NF-kappaB, cytokines, TNFalpha, collagen, drug
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The nuclear factor kappa B (NF-κB) pathway comprises a family of inducible transcription factors that serve as central regulators in essential physiological processes, such as cell growth, apoptosis, and innate and adaptive immune response by modulating the expression of hundreds of genes encoding multiple cytokines and chemokines, their receptors, molecules involved in immune recognition, antigen presentation, cell adhesion, and migration.

Chronical activation of the NF-κB pathway is involved in the pathogenesis of numerous chronic diseases, including rheumatoid arthritis, atherosclerosis, diabetes, and Alzheimer’s disease. Importantly, aging is also associated with increased NF-κB activation. In addition, NF-κB plays a pivotal role in the pathogenesis of various acute situations, such as sepsis, acute respiratory syndrome, and reactivity to CAR-T cell therapy triggering pro-inflammatory cytokine release and pro-coagulation activation.

Furthermore, NF-κB is known to play a central role in various highly pathogenic bacterial and viral infections, including Ebola, Dengue virus, highly pathogenic Influenza A, and SARS-CoV. Recent studies indicate that NF-κB may also be central to the immune hyper-activation and cytokine/chemokine storm observed during acute stage COVID-19.

Altogether, these data indicate that the NF-κB pathway may be highly relevant in the immune pathological mechanisms of infectious as well as non-infectious diseases and a promising target for pharmacological intervention and treatment.

The scope of this Special Issue is to summarize and enlarge knowledge in the NF-κB pathway and its involvement in inflammation and infection.

Topics include but are not limited to:

  • New aspects of NF-κB signaling pathways and their correlation to the pathophysiology of non-infectious diseases;
  • New aspects of NF-κB signaling pathways and their correlation to immunology and pathophysiology of bacterial and viral infectious diseases;
  • Translational research, pharmacological and medical interventions with the NF-κB pathway as a therapeutic target for bacterial and viral infectious diseases, including COVID-19.

Dr. Ralf Kircheis
Guest Editor

Manuscript Submission Information

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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.

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Keywords

  • Inflammation
  • Innate and adaptive immune response
  • Cytokine and chemokine
  • Complement and coagulation
  • Obesity and diabetes
  • Aging
  • Sepsis
  • Viral disease
  • Influenza
  • COVID-19

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Published Papers (5 papers)

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Research

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20 pages, 4295 KiB  
Article
Simulated Microgravity Disrupts Nuclear Factor κB Signaling and Impairs Murine Dendritic Cell Phenotype and Function
by Gaetano Calcagno, Jeremy Jeandel, Jean-Pol Frippiat and Sandra Kaminski
Int. J. Mol. Sci. 2023, 24(2), 1720; https://doi.org/10.3390/ijms24021720 - 15 Jan 2023
Cited by 4 | Viewed by 1758
Abstract
During spaceflights, astronauts face different forms of stress (e.g., socio-environmental and gravity stresses) that impact physiological functions and particularly the immune system. In this context, little is known about the effect of such stress on dendritic cells (DCs). First, we showed that hypergravity, [...] Read more.
During spaceflights, astronauts face different forms of stress (e.g., socio-environmental and gravity stresses) that impact physiological functions and particularly the immune system. In this context, little is known about the effect of such stress on dendritic cells (DCs). First, we showed that hypergravity, but not chronic ultra-mild stress, a socio-environmental stress, induced a less mature phenotype characterized by a decreased expression of MHCII and co-stimulatory molecules. Next, using the random positioning machine (RPM), we studied the direct effects of simulated microgravity on either splenic DCs or Flt-3L-differentiated bone marrow dendritic cells (BMDCs). Simulated microgravity was found to reduce the BM-conventional DC (cDC) and splenic cDC activation/maturation phenotype. Consistent with this, BMDCs displayed a decreased production of pro-inflammatory cytokines when exposed to microgravity compared to the normogravity condition. The induction of a more immature phenotype in microgravity than in control DCs correlated with an alteration of the NFκB signaling pathway. Since the DC phenotype is closely linked to their function, we studied the effects of microgravity on DCs and found that microgravity impaired their ability to induce naïve CD4 T cell survival, proliferation, and polarization. Thus, a deregulation of DC function is likely to induce immune deregulation, which could explain the reduced efficiency of astronauts’ immune response. Full article
(This article belongs to the Special Issue Role of NF-kappaB Pathway in Inflammation and Infection)
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17 pages, 4221 KiB  
Article
Keratocyte Differentiation Is Regulated by NF-κB and TGFβ Signaling Crosstalk
by Xin Zhou, Junhong Li, Ludvig J. Backman and Patrik Danielson
Int. J. Mol. Sci. 2022, 23(19), 11073; https://doi.org/10.3390/ijms231911073 - 21 Sep 2022
Cited by 3 | Viewed by 1732
Abstract
Interleukin-1 (IL-1) and transforming growth factor-beta (TGFβ) are important cytokines involved in corneal wound healing. Here, we studied the effect of these cytokines on corneal stromal cell (keratocyte) differentiation. IL-1β treatment resulted in reduced keratocyte phenotype, as evident by morphological changes and decreased [...] Read more.
Interleukin-1 (IL-1) and transforming growth factor-beta (TGFβ) are important cytokines involved in corneal wound healing. Here, we studied the effect of these cytokines on corneal stromal cell (keratocyte) differentiation. IL-1β treatment resulted in reduced keratocyte phenotype, as evident by morphological changes and decreased expression of keratocyte markers, including keratocan, lumican, ALDH3A1, and CD34. TGFβ1 treatment induced keratocyte differentiation towards the myofibroblast phenotype. This was inhibited by simultaneous treatment with IL-1β, as seen by inhibition of α-SMA expression, morphological changes, and reduced contractibility. We found that the mechanism of crosstalk between IL-1β and TGFβ1 occurred via regulation of the NF-κB signaling pathway, since the IL-1β induced inhibition of TGFβ1 stimulated keratocyte-myofibroblast differentiation was abolished by a specific NF-κB inhibitor, TPCA-1. We further found that Smad7 participated in the downstream signaling. Smad7 expression level was negatively regulated by IL-1β and positively regulated by TGFβ1. TPCA-1 treatment led to an overall upregulation of Smad7 at mRNA and protein level, suggesting that NF-κB signaling downregulates Smad7 expression levels in keratocytes. All in all, we propose that regulation of cell differentiation from keratocyte to fibroblast, and eventually myofibroblast, is closely related to the opposing effects of IL-1β and TGFβ1, and that the mechanism of this is governed by the crosstalk of NF-κB signaling. Full article
(This article belongs to the Special Issue Role of NF-kappaB Pathway in Inflammation and Infection)
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15 pages, 5904 KiB  
Article
Ultramicronized Palmitoylethanolamide in the Management of Sepsis-Induced Coagulopathy and Disseminated Intravascular Coagulation
by Ramona D’Amico, Francesco Monaco, Rosalba Siracusa, Marika Cordaro, Roberta Fusco, Alessio Filippo Peritore, Enrico Gugliandolo, Rosalia Crupi, Salvatore Cuzzocrea, Rosanna Di Paola, Daniela Impellizzeri and Tiziana Genovese
Int. J. Mol. Sci. 2021, 22(21), 11388; https://doi.org/10.3390/ijms222111388 - 21 Oct 2021
Cited by 7 | Viewed by 2807
Abstract
Disseminated intravascular coagulation (DIC) is a severe condition characterized by the systemic formation of microthrombi complicated with bleeding tendency and organ dysfunction. In the last years, it represents one of the most frequent consequences of coronavirus disease 2019 (COVID-19). The pathogenesis of DIC [...] Read more.
Disseminated intravascular coagulation (DIC) is a severe condition characterized by the systemic formation of microthrombi complicated with bleeding tendency and organ dysfunction. In the last years, it represents one of the most frequent consequences of coronavirus disease 2019 (COVID-19). The pathogenesis of DIC is complex, with cross-talk between the coagulant and inflammatory pathways. The objective of this study is to investigate the anti-inflammatory action of ultramicronized palmitoylethanolamide (um-PEA) in a lipopolysaccharide (LPS)-induced DIC model in rats. Experimental DIC was induced by continual infusion of LPS (30 mg/kg) for 4 h through the tail vein. Um-PEA (30 mg/kg) was given orally 30 min before and 1 h after the start of intravenous infusion of LPS. Results showed that um-PEA reduced alteration of coagulation markers, as well as proinflammatory cytokine release in plasma and lung samples, induced by LPS infusion. Furthermore, um-PEA also has the effect of preventing the formation of fibrin deposition and lung damage. Moreover, um-PEA was able to reduce the number of mast cells (MCs) and the release of its serine proteases, which are also necessary for SARS-CoV-2 infection. These results suggest that um-PEA could be considered as a potential therapeutic approach in the management of DIC and in clinical implications associated to coagulopathy and lung dysfunction, such as COVID-19. Full article
(This article belongs to the Special Issue Role of NF-kappaB Pathway in Inflammation and Infection)
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Review

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12 pages, 1463 KiB  
Review
Role of NF-κB during Mycobacterium tuberculosis Infection
by Nicole Poladian, Davit Orujyan, William Narinyan, Armani K. Oganyan, Inesa Navasardyan, Prathosh Velpuri, Abraham Chorbajian and Vishwanath Venketaraman
Int. J. Mol. Sci. 2023, 24(2), 1772; https://doi.org/10.3390/ijms24021772 - 16 Jan 2023
Cited by 12 | Viewed by 3108
Abstract
Mycobacterium tuberculosis (M. tb) causes tuberculosis infection in humans worldwide, especially among immunocompromised populations and areas of the world with insufficient funding for tuberculosis treatment. Specifically, M. tb is predominantly exhibited as a latent infection, which poses a greater risk of [...] Read more.
Mycobacterium tuberculosis (M. tb) causes tuberculosis infection in humans worldwide, especially among immunocompromised populations and areas of the world with insufficient funding for tuberculosis treatment. Specifically, M. tb is predominantly exhibited as a latent infection, which poses a greater risk of reactivation for infected individuals. It has been previously shown that M. tb infection requires pro-inflammatory and anti-inflammatory mediators to manage its associated granuloma formation via tumor necrosis factor-α (TNF-α), interleukin-12 (IL-12), interferon-γ (IFN-γ), and caseum formation via IL-10, respectively. Nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) has been found to play a unique mediator role in providing a pro-inflammatory response to chronic inflammatory disease processes by promoting the activation of macrophages and the release of various cytokines such as IL-1, IL-6, IL-12, and TNF-α. NF-κB’s role is especially interesting in its mechanism of assisting the immune system’s defense against M. tb, wherein NF-κB induces IL-2 receptors (IL-2R) to decrease the immune response, but has also been shown to crucially assist in keeping a granuloma and bacterial load contained. In order to understand NF-κB’s role in reducing M. tb infection, within this literature review we will discuss the dynamic interaction between M. tb and NF-κB, with a focus on the intracellular signaling pathways and the possible side effects of NF-κB inactivation on M. tb infection. Through a thorough review of these interactions, this review aims to highlight the role of NF-κB in M. tb infection for the purpose of better understanding the complex immune response to M. tb infection and to uncover further potential therapeutic methods. Full article
(This article belongs to the Special Issue Role of NF-kappaB Pathway in Inflammation and Infection)
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25 pages, 1071 KiB  
Review
Coagulopathies after Vaccination against SARS-CoV-2 May Be Derived from a Combined Effect of SARS-CoV-2 Spike Protein and Adenovirus Vector-Triggered Signaling Pathways
by Ralf Kircheis
Int. J. Mol. Sci. 2021, 22(19), 10791; https://doi.org/10.3390/ijms221910791 - 6 Oct 2021
Cited by 25 | Viewed by 8618
Abstract
Novel coronavirus SARS-CoV-2 has resulted in a global pandemic with worldwide 6-digit infection rates and thousands of death tolls daily. Enormous efforts are undertaken to achieve high coverage of immunization to reach herd immunity in order to stop the spread of SARS-CoV-2 infection. [...] Read more.
Novel coronavirus SARS-CoV-2 has resulted in a global pandemic with worldwide 6-digit infection rates and thousands of death tolls daily. Enormous efforts are undertaken to achieve high coverage of immunization to reach herd immunity in order to stop the spread of SARS-CoV-2 infection. Several SARS-CoV-2 vaccines based on mRNA, viral vectors, or inactivated SARS-CoV-2 virus have been approved and are being applied worldwide. However, the recent increased numbers of normally very rare types of thromboses associated with thrombocytopenia have been reported, particularly in the context of the adenoviral vector vaccine ChAdOx1 nCoV-19 from Astra Zeneca. The statistical prevalence of these side effects seems to correlate with this particular vaccine type, i.e., adenoviral vector-based vaccines, but the exact molecular mechanisms are still not clear. The present review summarizes current data and hypotheses for molecular and cellular mechanisms into one integrated hypothesis indicating that coagulopathies, including thromboses, thrombocytopenia, and other related side effects, are correlated to an interplay of the two components in the vaccine, i.e., the spike antigen and the adenoviral vector, with the innate and immune systems, which under certain circumstances can imitate the picture of a limited COVID-19 pathological picture. Full article
(This article belongs to the Special Issue Role of NF-kappaB Pathway in Inflammation and Infection)
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