Regulating Immune Responses Induced by PEGylated Messenger RNA–Lipid Nanoparticle Vaccine DOI Creative Commons

Hyein Jo,

Jaewhoon Jeoung,

Won‐Ho Kim

et al.

Vaccines, Journal Year: 2024, Volume and Issue: 13(1), P. 14 - 14

Published: Dec. 27, 2024

Messenger RNA (mRNA)-based therapeutics have shown remarkable progress in the treatment and prevention of diseases. Lipid nanoparticles (LNPs) great successes delivering mRNAs. After an mRNA-LNP vaccine enters a cell via endosome, mRNA is translated into antigen, which can activate adaptive immunity. mRNAs bind to various pattern recognition receptors (PRRs), including toll-like (TLRs), increase production inflammatory cytokines. This review summarizes mechanisms innate immunity induced by Polyethylene glycol (PEG) has been employed as component vaccine. PEGylated display enhanced stability preventing aggregation particles. However, PEGylation cause adverse reactions, blood clearance (ABC) complement activation anaphylaxis. Mechanisms PEG-induced ABC phenomenon anaphylaxis are presented discussed. There studies aimed at reducing immune responses associated with PEG make safe effective vaccines. Effects modifying or replacing also Modifying induce tolerance, prevent hypersensitivity reactions Current tolerance induction association summarized. might be helpful for developing

Language: Английский

Mechanisms of endothelial activation, hypercoagulation and thrombosis in COVID-19: a link with diabetes mellitus DOI Creative Commons
Inés Valencia, Jairo Lumpuy‐Castillo, Giselle Santos Magalhães

et al.

Cardiovascular Diabetology, Journal Year: 2024, Volume and Issue: 23(1)

Published: Feb. 20, 2024

Abstract Early since the onset of COVID-19 pandemic, medical and scientific community were aware extra respiratory actions SARS-CoV-2 infection. Endothelitis, hypercoagulation, hypofibrinolysis identified in patients as subsequent responses endothelial dysfunction. Activation barrier may increase severity disease contribute to long-COVID syndrome post-COVID sequelae. Besides, it cause alterations primary, secondary, tertiary hemostasis. Importantly, these have been highly decisive evolution infected also diagnosed with diabetes mellitus (DM), who showed previous In this review, we provide an overview potential triggers activation related under diabetic milieu. Several mechanisms are induced by both viral particle itself immune-defensive response (i.e., NF-κB/NLRP3 inflammasome pathway, vasoactive peptides, cytokine storm, NETosis, complement system). Alterations coagulation mediators such factor VIII, fibrin, tissue factor, von Willebrand factor: ADAMST-13 ratio, kallikrein-kinin or plasminogen-plasmin systems reported. Moreover, imbalance thrombotic thrombolytic (tPA, PAI-I, fibrinogen) factors favors hypercoagulation hypofibrinolysis. context DM, can be exacerbated leading higher loss However, a series therapeutic strategies targeting activated endothelium specific antibodies inhibitors against thrombin, key cytokines, X, system, system might represent new opportunities address hypercoagulable state present DM. Antidiabetics ameliorate dysfunction, inflammation, platelet aggregation. By improving microvascular pathology subjects, associated comorbidities risk mortality could reduced.

Language: Английский

Citations

18
Inflammasome Activation by RNA Respiratory Viruses: Mechanisms, Viral Manipulation, and Therapeutic Insights DOI Open Access
Tamara Silva Rodrigues, Dario S. Zamboni

Immunological Reviews, Journal Year: 2025, Volume and Issue: 330(1)

Published: Jan. 31, 2025

Respiratory viruses, including SARS-CoV-2, influenza, parainfluenza, rhinovirus, and respiratory syncytial virus (RSV), are pathogens responsible for lower tract infections, particularly in vulnerable populations such as children the elderly. Upon infection, these viruses recognized by pattern recognition receptors, leading to activation of inflammasomes, which essential mediating inflammatory responses. This review discusses mechanisms RNA activate emphasizing roles various signaling pathways components involved this process. Additionally, we highlight specific interactions between viral proteins inflammasome sensors, elucidating how manipulate host immune response facilitate infection. Understanding dynamics provides critical insights developing immunomodulatory therapeutic strategies aimed at mitigating inflammation improving outcomes infections.

Language: Английский

Citations

1
SARS-CoV-2 S1 subunit produces a protracted priming of the neuroinflammatory, physiological, and behavioral responses to a remote immune challenge: A role for corticosteroids DOI
Matthew G. Frank, Jayson B. Ball, Shelby Hopkins

et al.

Brain Behavior and Immunity, Journal Year: 2024, Volume and Issue: 121, P. 87 - 103

Published: July 21, 2024

Language: Английский

Citations

5
Towards an understanding of physical activity-induced post-exertional malaise: Insights into microvascular alterations and immunometabolic interactions in post-COVID condition and myalgic encephalomyelitis/chronic fatigue syndrome DOI Creative Commons
Simon Haunhorst, Diana Dudziak, Carmen Scheibenbogen

et al.

Infection, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 6, 2024

Language: Английский

Citations

5
CD147-high classical monocytes: a cellular biomarker for COVID-19 disease severity and treatment response DOI Creative Commons

Teruaki Murakami,

Yuta Yamaguchi,

Saori Amiya

et al.

Inflammation and Regeneration, Journal Year: 2025, Volume and Issue: 45(1)

Published: April 7, 2025

Abstract Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to severe disease 2019 (COVID-19), which is characterized by cytokine storm and organ dysfunction. The spike S1 subunit induces inflammatory production, but the immune cell subsets that respond stimulation contribute severity remain unclear. Methods We analyzed serum samples peripheral blood mononuclear cells (PBMCs) from patients with COVID-19 (moderate: n = 7; severe: 25) healthy controls ( 38). Using mass cytometry (cytometry time-of-flight; CyTOF), we responses in PBMCs donors COVID-19. examined correlations among identified populations, levels, clinical parameters. Results Serum levels correlated concentrations. induced dose-dependent production PBMCs, predominantly myeloid cells. CyTOF analysis classical monocytes high CD147 expression (CD147hi cMono) as primary source of S1-induced cytokines. proportion CD147hi cMono increased significantly decreased improvement. frequency showed a stronger positive correlation markers younger compared older patients. Conclusions are cellular cytokines may serve potential biomarkers for monitoring treatment response.

Language: Английский

Citations

0
The effect of asparagine-13 in porcine epidemic diarrhea virus envelope protein on pathogenicity DOI Creative Commons
Zhiwei Li,

Zhiqian Ma,

Xiaojing Zhao

et al.

Veterinary Research, Journal Year: 2025, Volume and Issue: 56(1)

Published: April 19, 2025

Language: Английский

Citations

0
SARS-CoV-2 S Protein Reduces Cytoprotective Defenses and Promotes Human Endothelial Cell Senescence DOI Creative Commons
Alicia Villacampa, Licia Shamoon, Inés Valencia

et al.

Aging and Disease, Journal Year: 2024, Volume and Issue: unknown, P. 0 - 0

Published: Jan. 1, 2024

Premature vascular aging and endothelial cell senescence are major risk factors for cardiovascular diseases atherothrombotic disturbances, which main complications of both acute long COVID-19. The S protein SARS-CoV2, acts as the receptor binding viral infection, is able to induce cells inflammation it has been found an isolated element in circulation human tissues reservoirs months after infection. Here, we investigated whether directly deciphered some mechanisms involved. In primary cultures umbilical vein (HUVEC), SARS-CoV-2 enhanced a concentration-dependent manner cellular content DNA damage response markers (senescence-associated-β galactosidase, γH2AX), well growth-arrest effectors (p53, p21, p16). parallel, reduced availability cytoprotective proteins, such anti-aging klotho, Nrf2 or heme oxygenase-1, caused functional harm by impairing ex vivo endothelial-dependent vasorelaxation murine microvessels. These effects were prevented pharmacological inhibition NLRP3 inflammasome with MCC950. Furthermore, supplementation either recombinant klotho angiotensin-(1-7), equally protected against pro-senescence, pro-inflammatory pro-oxidant action protein. Globally, this study proposes novel disease context COVID-19 its sequelae provides clues order prevent complications.

Language: Английский

Citations

3
Multifaceted role of SARS-CoV-2 structural proteins in lung injury DOI Creative Commons
Guoping Zheng,

Guanguan Qiu,

Huifeng Qian

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Feb. 5, 2024

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the third human to cause distress (ARDS) and contains four structural proteins: spike, envelope, membrane, nucleocapsid. An increasing number of studies have demonstrated that all proteins SARS-CoV-2 are capable causing lung injury, even without presence intact virus. Therefore, topic protein-evoked injury warrants more attention. In current article, we first synopsize features proteins. Second, discuss mechanisms for protein-induced inflammatory responses in vitro . Finally, list findings indicate themselves toxic sufficient induce vivo Recognizing triggered by may facilitate development targeted modalities treating COVID-19.

Language: Английский

Citations

2
Thrombosis in Critically Ill Influenza Patients: Incidence and Risk Factors DOI Creative Commons
Xianming Qiu,

Mingjie Liu,

Quanzhen Wang

et al.

Clinical and Applied Thrombosis/Hemostasis, Journal Year: 2024, Volume and Issue: 30

Published: Jan. 1, 2024

Influenza infection is associated with a risk of thrombosis. Whether factors reduced thrombosis might also be in patients severe influenza unknown. To investigate influenza. We used cohort data set to identify adults diagnosed Univariable and multivariable logistic regression models explored potential for events Cox analysis was examine the mortality A total 854 were included analysis. The incidence VTE 9.37% (80/854). Multivariable showed that previous aspirin medication (OR: 0.37; 95%CI: 0.14-0.84; P = .029) could reduce factor Compared non-thrombosis group, group required more mechanical ventilation ( < .001), tracheostomy ECMO .046), high-frequency .004). co-infection higher compared .025). (HR 0.52, 0.33-0.82, .005) statin 0.54, 0.34-0.87, .011) 60-day Patients are at high effect on needs further investigation.

Language: Английский

Citations

1
Aggravating mechanisms from COVID-19 DOI Creative Commons
Jong‐Hoon Lee, Consolato Sergi, Richard E. Kast

et al.

Virology Journal, Journal Year: 2024, Volume and Issue: 21(1)

Published: Sept. 27, 2024

Language: Английский

Citations

1