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Immune Response to Viruses and Bacteria

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 25651

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Prof. Dr. Andrea Galli

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1. Department of Immunology and Microbiology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
2. Amager and Hvidovre Hospital, Copenhagen University Hospital, Hvidovre, Denmark
Interests: viral recombination; fluorescence microscopy applied to the study of viral life cycle; Hepatitis C Virus (HCV)

Special Issue Information

Dear Colleagues,

Immune therapies promise efficient, tolerable, and customizable interventions against human pathogens and diseases. The response to the current SARS-CoV-2 pandemic, for example, highlighted the tremendous impact that vaccine strategies can have in controlling pathogens.

Viral and bacterial infections are detected by several overlapping molecular mechanisms, resulting in the activation of innate and immune responses. Pathogens have evolved a wide range of strategies for avoiding or suppressing activities of the immune system, including camouflaging, hiding in plain sight, and killing immune cells. Although, based on different molecular effectors, these strategies are often shared between viruses and bacteria, whether the immune system can overcome such pathogens’ defense mechanisms determines whether an infection is cleared or not. Interventions that can tip the balance in favor of the immune system, such as vaccines, neutralizing antibodies, or countermeasures, to defense mechanisms would be beneficial to human health and disease control.

In order to properly design strategies and interventions, however, we require detailed understanding of how the immune system recognizes and interacts with pathogens and their countermeasures. The aim of this Special Issue is to present recent findings unraveling the responses of the immune system relative to bacterial and viral infections and their mechanisms of self-defense.

Prof. Dr. Andrea Galli
Guest Editor

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Keywords

viruses
bacteria
infection
immune response
immunology
innate immunity
adaptive immunity
infectious diseases

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Published Papers (9 papers)

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Research

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14 pages, 15759 KiB

Open AccessArticle

Interruption of Lymph Flow Worsens the Skin Inflammation Caused by Saprophytic Staphylococcus epidermidis

by Marta Cąkała-Jakimowicz, Anna Domaszewska-Szostek and Monika Puzianowska-Kuznicka

Biomedicines 2023, 11(12), 3234; https://doi.org/10.3390/biomedicines11123234 - 6 Dec 2023

Viewed by 1471

Abstract

Lymphedema is often complicated by chronic inflammation, leading to fibrosis, fat deposition, and inhibition of lymphangiogenesis. This study aimed to verify whether lymphedema itself or together with commensal bacterial flora infection contributes to the severity of local inflammation. Edema was induced by interruption of the lymph flow in the rat’s hind limb. Immune cell infiltrates were examined by flow cytometry and immunohistochemistry. Nine-day edema alone did not affect immune cell content in the skin but resulted in a decrease in CD4⁺ T helper lymphocytes and monocytes in the draining popliteal lymph nodes. In turn, local saprophytic Staphylococcus epidermidis infection of the edematous limb resulted in dense infiltrates of CD68⁺ macrophages and monocytes, MHC class II antigen-presenting cells, CD90⁺ stem cells, thymocytes, and immature B cells in the skin, accompanied by a simultaneous reduction in density of CD4⁺ T helper lymphocytes and monocytes, OX62⁺ dendritic cells, CD68⁺ macrophages and monocytes, HiS48⁺ granulocytes, CD90⁺ stem cells, thymocytes, and immature B cells in the draining popliteal lymph nodes. These results indicate that the combination of edema and saprophytic bacteria infection induces severe inflammation in the peripheral tissues and results in a delay of antibacterial protection processes in neighboring lymphatic organs. Full article

(This article belongs to the Special Issue Immune Response to Viruses and Bacteria)

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11 pages, 7056 KiB

Open AccessArticle

Choice of Polymer, but Not Mesh Structure Variation, Reduces the Risk of Bacterial Infection with Staphylococcus aureus In Vivo

by Sophia M. Schmitz, Marius J. Helmedag, Andreas Kroh, Daniel Heise, Uwe Klinge, Andreas Lambertz, Mathias W. Hornef, Ulf P. Neumann and Roman M. Eickhoff

Biomedicines 2023, 11(7), 2083; https://doi.org/10.3390/biomedicines11072083 - 24 Jul 2023

Viewed by 1289

Abstract

Background: Synthetic mesh material is of great importance for surgical incisional hernia repair. The physical and biochemical characteristics of the mesh influence mechanical stability and the foreign body tissue reaction. The influence on bacterial infections, however, remains ill-defined. The aim of the present study was to evaluate the influence of a modified mesh structure with variation in filament linking on the occurrence of bacterial infection that is indicated by the occurrence of CD68⁺, CD4⁺, and CD8⁺ cells in two different materials. Methods: A total of 56 male Sprague Dawley rats received a surgical mesh implant in a subcutaneous abdominal position. The mesh of two different polymers (polypropylene (PP) and polyvinylidenfluoride (PVDF)) and two different structures (standard structure and bold structure with higher filament linking) were compared. During the implantation, the meshes were infected with Staphylococcus (S.) aureus. After 7 and 21 days, meshes were explanted, and the early and late tissue responses to infection were histologically evaluated. Results: Overall, the inflammatory tissue response was higher at 7 days when compared to 21 days. At 7 days, PP meshes of the standard structure (PP-S) showed the strongest inflammatory tissue response in comparison to all the other groups. At 21 days, no statistically significant difference between different meshes was detected. CD8⁺ cytotoxic T cells showed a significant difference at 21 days but not at 7 days. PP meshes of both structures showed a higher infiltration of CD8⁺ T cells than PVDF meshes. CD4⁺ T helper cells differed at 7 days but not at 21 days, and PVDF meshes in a bold structure showed the highest CD4⁺ T cell count. The number of CD68⁺ macrophages was also significantly higher in PP meshes in a standard structure when compared to PVDF meshes at 21 days. Conclusion: The inflammatory tissue response to S. aureus infection appears to be highest during the early period after mesh implantation. PP meshes showed a higher inflammatory response than PVDF meshes. The mesh material appears to be more important for the risk of infection than the variation in filament linking. Full article

(This article belongs to the Special Issue Immune Response to Viruses and Bacteria)

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12 pages, 8149 KiB

Open AccessArticle

Specific Cellular and Humoral Immune Responses to the Neoantigen RBD of SARS-CoV-2 in Patients with Primary and Secondary Immunodeficiency and Healthy Donors

by Kauzar Mohamed Mohamed, Kissy Guevara-Hoyer, Carlos Jiménez García, Laura García Bravo, Adolfo Jiménez-Huete, Antonia Rodríguez de la Peña, Beatriz Mediero Valeros, Cristina Cañizares Velázquez, Esther Culebras López, Noemí Cabello, Vicente Estrada, Ángel L. Corbí, Miguel Fernández-Arquero, Alberto Ocaña, Alberto Delgado-Iribarren, Mercedes Martínez-Novillo, Estefanía Bolaños, Eduardo Anguita, Ascensión Peña, Celina Benavente, Javier David Benítez Fuentes, Pedro Pérez Segura and Silvia Sánchez-Ramón Show full author list Hide full author list

Biomedicines 2023, 11(4), 1042; https://doi.org/10.3390/biomedicines11041042 - 28 Mar 2023

Cited by 1 | Viewed by 2264

Abstract

Patients with antibody deficiency disorders, such as primary immunodeficiency (PID) or secondary immunodeficiency (SID) to B-cell lymphoproliferative disorder (B-CLPD), are two groups vulnerable to developing the severe or chronic form of coronavirus disease caused by SARS-CoV-2 (COVID-19). The data on adaptive immune responses against SARS-CoV-2 are well described in healthy donors, but still limited in patients with antibody deficiency of a different cause. Herein, we analyzed spike-specific IFN-γ and anti-spike IgG antibody responses at 3 to 6 months after exposure to SARS-CoV-2 derived from vaccination and/or infection in two cohorts of immunodeficient patients (PID vs. SID) compared to healthy controls (HCs). Pre-vaccine anti-SARS-CoV-2 cellular responses before vaccine administration were measured in 10 PID patients. Baseline cellular responses were detectable in 4 out of 10 PID patients who had COVID-19 prior to vaccination, perceiving an increase in cellular responses after two-dose vaccination (p < 0.001). Adequate specific cellular responses were observed in 18 out of 20 (90%) PID patients, in 14 out of 20 (70%) SID patients and in 74 out of 81 (96%) HCs after vaccination (and natural infection in some cases). Specific IFN-γ response was significantly higher in HC with respect to PID (1908.5 mUI/mL vs. 1694.1 mUI/mL; p = 0.005). Whereas all SID and HC patients mounted a specific humoral immune response, only 80% of PID patients showed positive anti-SARS-CoV-2 IgG. The titer of anti-SARS-CoV-2 IgG was significantly lower in SID compared with HC patients (p = 0.040), without significant differences between PID and HC patients (p = 0.123) and between PID and SID patients (p =0.683). High proportions of PID and SID patients showed adequate specific cellular responses to receptor binding domain (RBD) neoantigen, with a divergence between the two arms of the adaptive immune response in PID and SID patients. We also focused on the correlation of protection of positive SARS-CoV-2 cellular response to omicron exposure: 27 out of 81 (33.3%) HCs referred COVID-19 detected by PCR or antigen test, 24 with a mild course, 1 with moderate symptoms and the remaining 2 with bilateral pneumonia that were treated in an outpatient basis. Our results might support the relevance of these immunological studies to determine the correlation of protection with severe disease and for deciding the need for additional boosters on a personalized basis. Follow-up studies are required to evaluate the duration and variability in the immune response to COVID-19 vaccination or infection. Full article

(This article belongs to the Special Issue Immune Response to Viruses and Bacteria)

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13 pages, 2579 KiB

Open AccessArticle

Porphyromonas gingivalis Outer Membrane Vesicles Stimulate Gingival Epithelial Cells to Induce Pro-Inflammatory Cytokines via the MAPK and STING Pathways

by Yuta Uemura, Yuka Hiroshima, Ayano Tada, Keiji Murakami, Kaya Yoshida, Yuji Inagaki, Tomomi Kuwahara, Akikazu Murakami, Hideki Fujii and Hiromichi Yumoto

Biomedicines 2022, 10(10), 2643; https://doi.org/10.3390/biomedicines10102643 - 20 Oct 2022

Cited by 19 | Viewed by 3394

Abstract

Porphyromonas gingivalis (Pg) is a keystone pathogen associated with chronic periodontitis and produces outer membrane vesicles (OMVs) that contain lipopolysaccharide (LPS), gingipains, and pathogen-derived DNA and RNA. Pg-OMVs are involved in the pathogenesis of periodontitis. Pg-OMV-activated pathways that induce the production of the pro-inflammatory cytokines, interleukin (IL)-6, and IL-8 in the human gingival epithelial cell line, OBA-9, were investigated. The role of mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB in levels of Pg-OMV-induced pro-inflammatory cytokines was investigated using Western blot analysis and specific pathway inhibitors. Pg-OMVs induced IL-6 and IL-8 production via the extracellular signal-regulated kinase (Erk) 1/2, c-Jun N-terminal kinase (JNK), p38 MAPK, and NF-κB signaling pathways in OBA-9 cells. In addition, the stimulator of interferon genes (STING), an essential innate immune signaling molecule, was triggered by a cytosolic pathogen DNA. Pg-OMV-induced IL-6 and IL-8 mRNA expression and production were significantly suppressed by STING-specific small interfering RNA. Taken together, these results demonstrated that Pg-OMV-activated Erk1/2, JNK, p38 MAPK, STING, and NF-κB signaling pathways resulting in increased IL-6 and IL-8 expression in human gingival epithelial cells. These results suggest that Pg-OMVs may play important roles in periodontitis exacerbation by stimulating various pathways. Full article

(This article belongs to the Special Issue Immune Response to Viruses and Bacteria)

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14 pages, 2604 KiB

Open AccessArticle

High Glucose Induces in HK2 Kidney Cells an IFN–Dependent ZIKV Antiviral Status Fueled by Viperin

by Alawiya Reslan, Juliano G. Haddad, Philippe Desprès, Jean-Loup Bascands and Gilles Gadea

Biomedicines 2022, 10(7), 1577; https://doi.org/10.3390/biomedicines10071577 - 1 Jul 2022

Cited by 4 | Viewed by 2046

Abstract

Zika virus (ZIKV) is an emerging mosquito-borne flavivirus that rapidly became a major medical concern worldwide. We have recently reported that a high glucose level decreases the rate of Zika virus (ZIKV) replication with an impact on human kidney HK-2 cell survival. However, the mechanisms by which cells cultured in a high glucose medium inhibit ZIKV growth remain unclear. Viperin belongs to interferon-stimulated genes (ISG) and its expression is highly up-regulated upon viral infection, leading to antiviral activity against a variety of viruses, including flaviviruses. As such, viperin has been shown to be a major actor involved in the innate immune response against Zika virus (ZIKV). Our present study aims to further characterize the involvement of viperin in ZIKV growth inhibition under high glucose concentration (HK-2^HGC). We show for the first time that endogenous viperin is over-expressed in HK-2 cells cultured under high glucose concentration (HK-2^HGC), which is associated with ZIKV growth inhibition. Viperin knockdown in HK-2^HGC rescues ZIKV growth. In addition, our results emphasize that up-regulated viperin in HK-2^HGC leads to ZIKV growth inhibition through the stimulation of IFN-β production. In summary, our work provides new insights into the ZIKV growth inhibition mechanism observed in HK-2 cells cultured in a high glucose environment. Full article

(This article belongs to the Special Issue Immune Response to Viruses and Bacteria)

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16 pages, 1395 KiB

Open AccessArticle

Towards Understanding the Lymph Node Response to Skin Infection with Saprophytic Staphylococcus epidermidis

by Marta Cąkała-Jakimowicz and Monika Puzianowska-Kuznicka

Biomedicines 2022, 10(5), 1021; https://doi.org/10.3390/biomedicines10051021 - 28 Apr 2022

Cited by 2 | Viewed by 2651

Abstract

In individuals with lymphedema, diabetic foot, or other diseases, infections with saprophytes are common. The response of major cell subpopulations in the draining lymph nodes to skin infection with Staphylococcus epidermidis was assessed using the rat model. After massive subepidermal infection, a cytometric evaluation showed an increase in cytotoxic and helper T lymphocytes and major subpopulations of the innate immune response. Three weeks later, signs of inflammation reduction with an increase in the content of memory T helper lymphocytes and effector memory T cytotoxic lymphocytes were observed. After skin re-infection, a rapid response of cytotoxic, helper, and memory T lymphocytes, memory B lymphocytes and plasmablasts, and macrophages was detected. In addition, a reduction in the number of naïve B lymphocytes, activated MHC class II+ cells, and some cells of the innate immune system was observed. T regulatory lymphocyte response after the initial and secondary S. epidermidis skin infection was not detected. The morphometric evaluation showed significant changes in the main cell subpopulations in each functional zone of the node and then confirmed the efficient elimination of the administered antigen, as evidenced by the observations on day 28. Notably, after re-infection, the cellular response did not exceed the level after the initial infection and was reduced in many cell subpopulations. Understanding how the lymph nodes eliminate S. epidermidis can provide valuable insights into creating immunological therapies against infections with saprophytes. Full article

(This article belongs to the Special Issue Immune Response to Viruses and Bacteria)

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19 pages, 2896 KiB

Open AccessReview

Immune Recognition versus Immune Evasion Systems in Zika Virus Infection

by Yee Teng Chan, Yi Ying Cheok, Heng Choon Cheong, Ting Fang Tang, Sofiah Sulaiman, Jamiyah Hassan, Chung Yeng Looi, Kim-Kee Tan, Sazaly AbuBakar and Won Fen Wong

Biomedicines 2023, 11(2), 642; https://doi.org/10.3390/biomedicines11020642 - 20 Feb 2023

Cited by 3 | Viewed by 4879

Abstract

The reemergence of the Zika virus (ZIKV) infection in recent years has posed a serious threat to global health. Despite being asymptomatic or mildly symptomatic in a majority of infected individuals, ZIKV infection can result in severe manifestations including neurological complications in adults and congenital abnormalities in newborns. In a human host, ZIKV is primarily recognized by RIG-like receptors and Toll-like receptors that elicit anti-viral immunity through the secretion of type I interferon (IFN) to limit viral survival, replication, and pathogenesis. Intriguingly, ZIKV evades its host immune system through various immune evasion strategies, including suppressing the innate immune receptors and signaling pathways, mutation of viral structural and non-structural proteins, RNA modulation, or alteration of cellular pathways. Here, we present an overview of ZIKV recognition by the host immune system and the evasion strategies employed by ZIKV. Characterization of the host–viral interaction and viral disease mechanism provide a platform for the rational design of novel prophylactic and therapeutic strategies against ZIKV infection. Full article

(This article belongs to the Special Issue Immune Response to Viruses and Bacteria)

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28 pages, 1575 KiB

Open AccessReview

Antiviral Innate Immune Responses in Autoimmunity: Receptors, Pathways, and Therapeutic Targeting

by Eirini Maria Stergioti, Theodora Manolakou, Dimitrios T. Boumpas and Aggelos Banos

Biomedicines 2022, 10(11), 2820; https://doi.org/10.3390/biomedicines10112820 - 4 Nov 2022

Cited by 5 | Viewed by 3302

Abstract

Innate immune receptors sense nucleic acids derived from viral pathogens or self-constituents and initiate an immune response, which involves, among other things, the secretion of cytokines including interferon (IFN) and the activation of IFN-stimulated genes (ISGs). This robust and well-coordinated immune response is mediated by the innate immune cells and is critical to preserving and restoring homeostasis. Like an antiviral response, during an autoimmune disease, aberrations of immune tolerance promote inflammatory responses to self-components, such as nucleic acids and immune complexes (ICs), leading to the secretion of cytokines, inflammation, and tissue damage. The aberrant immune response within the inflammatory milieu of the autoimmune diseases may lead to defective viral responses, predispose to autoimmunity, or precipitate a flare of an existing autoimmune disease. Herein, we review the literature on the crosstalk between innate antiviral immune responses and autoimmune responses and discuss the pitfalls and challenges regarding the therapeutic targeting of the mechanisms involved. Full article

(This article belongs to the Special Issue Immune Response to Viruses and Bacteria)

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14 pages, 1377 KiB

Open AccessReview

Immune Response to Biofilm Growing Pulmonary Pseudomonas aeruginosa Infection

by Kim Thomsen, Niels Høiby, Peter Østrup Jensen, Oana Ciofu and Claus Moser

Biomedicines 2022, 10(9), 2064; https://doi.org/10.3390/biomedicines10092064 - 24 Aug 2022

Cited by 9 | Viewed by 2374

Abstract

Biofilm infections are tolerant to the host responses and recalcitrance to antibiotic drugs and disinfectants. The induced host-specific innate and adaptive immune responses by established biofilms are significantly implicated and contributes to the course of the infections. Essentially, the host response may be the single one factor impacting the outcome most, especially in cases where the biofilm is caused by low virulent opportunistic bacterial species. Due to the chronicity of biofilm infections, activation of the adaptive immune response mechanisms is frequently experienced, and instead of clearing the infection, the adaptive response adds to the pathogenesis. To a high degree, this has been reported for chronic Pseudomonas aeruginosa lung infections, where both a pronounced antibody response and a skewed Th1/Th2 balance has been related to a poorer outcome. In addition, detection of an adaptive immune response can be used as a significant indicator of a chronic P. aeruginosa lung infection and is included in the clinical definitions as such. Those issues are presented in the present review, along with a characterization of the airway structure in relation to immune responses towards P. aeruginosa pulmonary infections. Full article

(This article belongs to the Special Issue Immune Response to Viruses and Bacteria)

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