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Vaccine-Induced Reprogramming of Innate Immune Response

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A special issue of Vaccines (ISSN 2076-393X). This special issue belongs to the section "Innate and Adaptive Immunity in Vaccination".

Deadline for manuscript submissions: closed (30 July 2023) | Viewed by 8540

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Dr. Safder Ganaie

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Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, KS, USA
Interests: Vaccines;Innate immune response;RNA viruses;Infectious diseases;Virus infection;pathogenesis

Special Issue Information

Dear Colleagues,

The innate immune system is the first line of host defense against pathogens. The invading pathogens are rapidly detected by the host pattern-recognition receptors (PRRs) such as Toll-like receptors (TLRs), C-type lectin-like receptors, retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), and the nucleotide-binding oligomerization domain (NOD)-like receptor family proteins (NLRs). The activation of these receptors results in cytokine and chemokine production, phagocytosis, as well as antigen presentation to the adaptive immune system. However, over-activation of the innate immune response can cause systemic inflammation and tissue damage. Both RNA-based or Non-RNA vaccines influence the innate immune response through promoting the development of adaptive immunity or reprogramming of the innate immunity known as “trained immunity”, which imparts non-specific protection to the host against the pathogen.

It is still unclear how host innate immunity responds to pathogens post-vaccination and what the broad impact of vaccination on the innate immune response is. Therefore, this Special Issue seeks original contributions in the form of both research and review articles that advance our understanding of the vaccine-induced innate immune response. Articles related to host responses to different pathogens such as bacteria, viruses, and fungi post-SARS-CoV-2, flu, and other types of vaccination are also welcome.

Dr. Safder Ganaie
Guest Editor

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Dr. Safder Ganaie
Guest Editor

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Keywords

vaccine
innate immune response
virus infection
pathogenesis
RNA sensors
cytokine storm
inflammation

Published Papers (4 papers)

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Research

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10 pages, 481 KiB

Open AccessArticle

Tixagevimab and Cilgavimab (Evusheld™) Prophylaxis Prevents Breakthrough COVID-19 Infections in Immunosuppressed Population: 6-Month Prospective Study

by Dejan Jakimovski, Svetlana P. Eckert, Omid Mirmosayyeb, Sangharsha Thapa, Penny Pennington, David Hojnacki and Bianca Weinstock-Guttman

Vaccines 2023, 11(2), 350; https://doi.org/10.3390/vaccines11020350 - 03 Feb 2023

Cited by 6 | Viewed by 2126

Abstract

Background: Persons with neuroinflammatory diseases (pwNID) treated with potent immunosuppressives are at risk of severe COVID-19 outcomes and reduced vaccine seroconversion. We aimed at determining the real-world efficacy of tixagevimab and cilgavimab (Evusheld™) in immunosuppressed pwNID in preventing breakthrough COVID-19 infections. Methods: 31 immunosuppressed pwNID were followed for 6 months after administration of tixagevimab and cilgavimab as a prophylactic COVID-19 medication (January 2022–July 2022). Only pwNID treated with anti-CD20 monoclonal antibodies and sphingosine-1-phosphate modulators were considered eligible for the study. A control group of 126 immunosuppressed pwNID (38 seropositive and 88 seronegative after SARS-CoV-2 vaccination) were included. Breakthrough COVID-19 infections rate and their severity was determined over the follow-up. Results: The pwNID treated with tixagevimab and cilgavimab had more comorbidities when compared with the total and seronegative pwNID control group (54.8% vs. 30.2% vs. 27.3%, p = 0.02 and p = 0.005, respectively). After a 6-month follow-up, significantly lower numbers of pwNID treated with tixagevimab and cilgavimab had breakthrough COVID-19 when compared with the control pwNID group (6.5% vs. 34.1%, p = 0.002) and seronegative control pwNID group (6.5% vs. 38.6%, p < 0.001). All COVID-19 infections in Evusheld-treated pwNID were mild, whereas 9/43 COVID-19 infections in the control group were moderate/severe. No side effects to tixagevimab and cilgavimab were recorded. Conclusion: In pwNID treated with immunosuppressive therapies, tixagevimab and cilgavimab (Evusheld™) significantly reduced the numbers and severity of breakthrough COVID-19 infections during the Omicron (BA.2–BA.5 variants) wave. Full article

(This article belongs to the Special Issue Vaccine-Induced Reprogramming of Innate Immune Response)

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11 pages, 1805 KiB

Open AccessArticle

A Novel Approach to Vaccine Development: Concomitant Pathogen Inactivation and Host Immune Stimulation by Peroxynitrite

by Shahar Rotem, Erez Bar-Haim, Uri Elia, Hila Cohen, Shirley Lazar, Ofer Cohen, Theodor Chitlaru and Yoav Gal

Vaccines 2022, 10(10), 1593; https://doi.org/10.3390/vaccines10101593 - 22 Sep 2022

Cited by 2 | Viewed by 1453

Abstract

The design of efficient vaccines for long-term protective immunity against pathogens represents an objective of utmost public health priority. In general, live attenuated vaccines are considered to be more effective than inactivated pathogens, yet potentially more reactogenic. Accordingly, inactivation protocols which do not compromise the pathogen’s ability to elicit protective immunity are highly beneficial. One of the sentinel mechanisms of the host innate immune system relies on the production of reactive nitrogen intermediates (RNI), which efficiently inactivate pathogens. Peroxynitrite (PN) is a prevalent RNI, assembled spontaneously upon the interaction of nitric oxide (NO) with superoxide. PN exerts its bactericidal effect by via the efficient oxidation of a broad range of biological molecules. Furthermore, the interaction of PN with proteins results in structural/chemical modifications, such as the oxidation of tryptophan, tyrosine, and cysteine residues, as well as the formation of carbonyl, dityrosine, and nitrotyrosine (NT). In addition to their role in innate immunity, these PN-mediated modifications of pathogen components may also augment the antigenicity of pathogen peptides and proteins, hence contributing to specific humoral responses. In the study reported here, a novel approach for vaccine development, consisting of pathogen inactivation by PN, combined with increased immunity of NT-containing peptides, is implemented as a proof-of-concept for vaccination against the intracellular pathogen Francisella tularensis (F. tularensis). In vivo experiments in a murine model of tularemia confirm that PN-inactivated F. tularensis formulations may rapidly stimulate innate and adaptive immune cells, conferring efficient protection against a lethal challenge, superior to that elicited by bacteria inactivated by the widely used formalin treatment. Full article

(This article belongs to the Special Issue Vaccine-Induced Reprogramming of Innate Immune Response)

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14 pages, 657 KiB

Open AccessArticle

COVID-19 Vaccination in Multiple Sclerosis and Inflammatory Diseases: Effects from Disease-Modifying Therapy, Long-Term Seroprevalence and Breakthrough Infections

by Dejan Jakimovski, Karen Zakalik, Samreen Awan, Katelyn S. Kavak, Penny Pennington, David Hojnacki, Channa Kolb, Alexis A. Lizarraga, Svetlana P. Eckert, Rosila Sarrosa, Kamath Vineetha, Keith Edwards and Bianca Weinstock-Guttman

Vaccines 2022, 10(5), 695; https://doi.org/10.3390/vaccines10050695 - 28 Apr 2022

Cited by 15 | Viewed by 3195

Abstract

Background: To determine the effect of disease-modifying therapies (DMT) on humoral postvaccine seroconversion, long-term humoral response, and breakthrough COVID-19 infections in persons with multiple sclerosis (PwMS) and other neuroinflammatory disorders. Methods: A total of 757 PwMS and other neuroinflammatory disorders were recruited in two MS centers and vaccinated with one of the FDA-approved vaccines (BNT162b2, mRNA-1273, Ad26.COV2.S). The primary outcomes are the rate of humoral postvaccine seroconversion and anti-severe acute respiratory syndrome coronavirus 2 (anti-SARS-CoV-2) immunoglobulin G (IgG) differences between patients on different DMTs. Secondary measures include breakthrough infections and humoral response after six months. Other outcomes include differences in vaccine response between SARS-CoV-2 vaccines and the effects of age and comorbidities on the vaccine response. Results: A total of 465 (68.4%) PwMS and 55 (74.3%) patients with neuroinflammatory diseases were seropositive at 4–12 weeks after vaccination. A significant difference in seroconversion based on the DMT used at the time of vaccination (p < 0.001) was observed, with the lowest rates seen in patients treated with anti-CD20 antibodies (23.2%) and sphingosine-1-phosphate modulators (S1P) (30.8%). In seropositive patients, there was a significant decrease in anti-SARS IgG from mean 20.0 to 4.7 at six months (p = 0.004). Thirty-nine patients had breakthrough infection, but only two seronegative patients required hospitalization. mRNA vaccines resulted in significantly greater seroconversion compared to Ad26.COV2.S (p < 0.001). Older age and presence of cardiovascular comorbidities were associated with lower anti-SARS IgG (p = 0.021 and p = 0.003, respectively) Conclusions: PwMS and neuroinflammatory disorders treated with anti-CD20 and S1P medications have lower humoral response after anti-SARS-CoV-2 vaccination, even after booster dose. Waning of the humoral response puts vaccinated PwMS at a greater risk of COVID-19 breakthrough. Full article

(This article belongs to the Special Issue Vaccine-Induced Reprogramming of Innate Immune Response)

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Review

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22 pages, 865 KiB

Open AccessReview

Vaccine Responses in Patients with Liver Cirrhosis: From the Immune System to the Gut Microbiota

by Carlo Airola, Silvia Andaloro, Antonio Gasbarrini and Francesca Romana Ponziani

Vaccines 2024, 12(4), 349; https://doi.org/10.3390/vaccines12040349 - 23 Mar 2024

Viewed by 994

Abstract

Vaccines prevent a significant number of deaths annually. However, certain populations do not respond adequately to vaccination due to impaired immune systems. Cirrhosis, a condition marked by a profound disruption of immunity, impairs the normal immunization process. Critical vaccines for cirrhotic patients, such as the hepatitis A virus (HAV), hepatitis B virus (HBV), influenza, pneumococcal, and coronavirus disease 19 (COVID-19), often elicit suboptimal responses in these individuals. The humoral response, essential for immunization, is less effective in cirrhosis due to a decline in B memory cells and an increase in plasma blasts, which interfere with the creation of a long-lasting response to antigen vaccination. Additionally, some T cell subtypes exhibit reduced activation in cirrhosis. Nonetheless, the persistence of memory T cell activity, while not preventing infections, may help to attenuate the severity of diseases in these patients. Alongside that, the impairment of innate immunity, particularly in dendritic cells (DCs), prevents the normal priming of adaptive immunity, interrupting the immunization process at its onset. Furthermore, cirrhosis disrupts the gut–liver axis balance, causing dysbiosis, reduced production of short-chain fatty acids (SCFAs), increased intestinal permeability, and bacterial translocation. Undermining the physiological activity of the immune system, these alterations could impact the vaccine response. Enhancing the understanding of the molecular and cellular factors contributing to impaired vaccination responses in cirrhotic patients is crucial for improving vaccine efficacy in this population and developing better prevention strategies. Full article

(This article belongs to the Special Issue Vaccine-Induced Reprogramming of Innate Immune Response)

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