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Biomedicines
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Neutrophils in Immunity and Diseases
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Neutrophils in Immunity and Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 11906

Special Issue Editor

Dr. Akrivi Chrysanthopoulou

E-Mail Website
Guest Editor
Department of Biological Applications & Technology, Faculty of Health Sciences, University of Ioannina, Ioannina, Greece
Interests: crosstalk between inflammation and coagulation; the impact of inflammation in fibrotic disorder or autoimmunity; neutrophils; endothelial cells; fibroblasts
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neutrophils have been historically linked to antimicrobial functions in acute infection. Recent evidence, however, has identified them as having hitherto unsuspecting functions, and thus, neutrophils are now valued as functionally versatile cells with important roles in chronic inflammation. In particular, shifts in the neutrophil phenotype enables them to adapt their function in different inflammatory contexts, in which they exert their regulatory role on both innate and adaptive immune leukocytes. The highly immunogenic products released by neutrophils and enhanced inflammatory pathogenic loops can cause chronic inflammation, as well as influence certain social, environmental and lifestyle factors. In turn, chronic inflammation can result in several diseases that collectively represent the leading causes of disability and mortality worldwide. Hence, the multifaceted involvement of neutrophils in several inflammatory conditions makes them exciting targets for therapeutic intervention. Of course, numerous challenges and controversies in the field remain. Overall, I would like to encourage the researchers involved in such research topics to provide their data, thoughts and concerns in order to establish a broader view of the current state of this specific research area. Thus, readers will enjoy reading innovative papers, while overall, we will help to determine the future directions of neutrophil biology.

Dr. Akrivi Chrysanthopoulou
Guest Editor

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Keywords

  • neutrophils
  • inflammation
  • neutrophil biology
  • Immunity

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Related Special Issue

Published Papers (6 papers)

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Research

19 pages, 8759 KiB  
Article
IL-4R and CXCR2 Contribute to Downregulating Neutrophil-Mediated Response in the Early Stage of Fungal Extract-Induced Allergic Airway Inflammation
by Marina A. Shevchenko, Ekaterina A. Servuli, Dina E. Murova, Julia D. Vavilova, Elena L. Bolkhovitina, Ekaterina N. Chursanova and Alexander M. Sapozhnikov
Biomedicines 2024, 12(12), 2743; https://doi.org/10.3390/biomedicines12122743 - 30 Nov 2024
Viewed by 936
Abstract
Background/Objectives: Airborne exogenous antigen inhalation can induce neutrophil infiltration of the airways, while eosinophils migrate to the airways in allergic airway inflammation. During a bacterial infection, Th2-associated cytokine IL-4, by binding to the IL-4 receptor (IL-4R), can suppress neutrophil recruitment to the [...] Read more.
Background/Objectives: Airborne exogenous antigen inhalation can induce neutrophil infiltration of the airways, while eosinophils migrate to the airways in allergic airway inflammation. During a bacterial infection, Th2-associated cytokine IL-4, by binding to the IL-4 receptor (IL-4R), can suppress neutrophil recruitment to the site of inflammation. In the present study, we estimated whether the IL-4-dependent suppression of neutrophil recruitment contributed to the development of an immune response in asthma. Methods: Using a mouse model of Aspergillus fumigatus extract-induced allergic airway inflammation, we investigated the proportions of eosinophils and neutrophils in blood, lungs, and bone marrow over time. Bronchoalveolar lavage (BAL) fluid cytokine (including IL-4) levels and the proportions of bone marrow IL-4Rα (CD124)-expressing neutrophils were estimated. Results: We identified skewing from the neutrophil- to eosinophil-mediated immune response in the blood after five extract applications. At this point, the BAL fluid IL-4 level was not elevated, while IL-12p40 and CXCL1 levels were considerably increased. At the early stage of allergic airway inflammation, the proportions of neutrophils expressing CD124 and circulating neutrophils expressing CXCR2 (CD182) were significantly increased. Upon inflammation progression, the former remained elevated, but the latter significantly decreased. Conclusions: Thus, in allergic airway inflammation, bone marrow neutrophils become insensible to the attractive chemokine CXCL1 signals and susceptible to IL-4 effects. Full article
(This article belongs to the Special Issue Neutrophils in Immunity and Diseases)
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23 pages, 4536 KiB  
Article
Proteomic Profile Regulated by the Immunomodulatory Jusvinza Drug in Neutrophils Isolated from Rheumatoid Arthritis Patients
by Mabel Hernández-Cedeño, Arielis Rodríguez-Ulloa, Yassel Ramos, Luis J. González, Anabel Serrano-Díaz, Katharina Zettl, Jacek R. Wiśniewski, Gillian Martinez-Donato, Gerardo Guillen-Nieto, Vladimir Besada and María del Carmen Domínguez-Horta
Biomedicines 2024, 12(12), 2740; https://doi.org/10.3390/biomedicines12122740 - 29 Nov 2024
Viewed by 1599
Abstract
Jusvinza is an immunomodulatory drug composed of an altered peptide ligand (APL) designed from a novel CD4+ T cell epitope of human heat shock protein 60 (HSP60), an autoantigen involved in the pathogenesis of rheumatoid arthritis (RA). The peptide induces regulatory T cells [...] Read more.
Jusvinza is an immunomodulatory drug composed of an altered peptide ligand (APL) designed from a novel CD4+ T cell epitope of human heat shock protein 60 (HSP60), an autoantigen involved in the pathogenesis of rheumatoid arthritis (RA). The peptide induces regulatory T cells and decreases levels of TNF-α and IL-17; pre-clinical and phase I clinical studies support its use for the treatment of RA. This peptide was repositioned for the treatment of COVID-19 patients with signs of hyperinflammation. Neutrophils play a pathogenic role in both RA and severe forms of COVID-19. To add novel evidence about the mechanism of action of Jusvinza, the proteomic profile regulated by this peptide of neutrophils isolated from four RA patients was investigated using LC-MS/MS and bioinformatics analysis. A total of 149 proteins were found to be differentially modulated in neutrophils treated with Jusvinza. The proteomic profile regulated by Jusvinza is characterized by the presence of proteins related to RNA splicing, phagocytosis, endocytosis, and immune functions. In response to Jusvinza treatment, several proteins that regulate the NF-κB signaling pathway were differentially modulated, supporting the peptide’s anti-inflammatory effect. Proteins related to metabolic pathways that supply ATP for cellular functions or lipid metabolites with immunoregulatory properties were also identified. Additionally, several structural components of neutrophil extracellular traps (NETs) were decreased in Jusvinza-treated cells, supporting its impairment of this biological process. Of note, these findings were validated by in vitro experiments which confirmed that Jusvinza decreased NET formation. Such results provide evidence of the molecular mechanism of action and support the therapeutic potentialities of Jusvinza to treat other diseases characterized by hyperinflammation besides RA and COVID-19. Full article
(This article belongs to the Special Issue Neutrophils in Immunity and Diseases)
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17 pages, 1449 KiB  
Article
Impact of Nitric Oxide on Polymorphonuclear Neutrophils’ Function
by Richard Kraus, Elena Maier, Michael Gruber and Sigrid Wittmann
Biomedicines 2024, 12(10), 2353; https://doi.org/10.3390/biomedicines12102353 - 16 Oct 2024
Cited by 1 | Viewed by 1168
Abstract
Background: There is increasing evidence that nitric oxide (nitrogen monoxide, NO) significantly influences immune cellular responses, including those from polymorphonuclear leukocytes (PMNs). Objective: The aim of this study was to examine a possible effect of NO on PMNs’ function (chemotaxis, production of reactive [...] Read more.
Background: There is increasing evidence that nitric oxide (nitrogen monoxide, NO) significantly influences immune cellular responses, including those from polymorphonuclear leukocytes (PMNs). Objective: The aim of this study was to examine a possible effect of NO on PMNs’ function (chemotaxis, production of reactive oxygen species (ROS), and NETosis) using live cell imaging. Moreover, we investigated PMN surface epitope and neutrophil oxidative burst under the influence of NO by flow cytometric analysis. Methods: Whole blood samples were obtained from healthy volunteers, and PMNs were isolated by density centrifugation. Live cell imaging using type I collagen matrix in µSlide IBIDI chemotaxis chambers was conducted in order to observe N-formyl-L-methionyl-L-leucyl-phenylalanine (fMLP)-stimulated PMN chemotaxis, ROS production, and NETosis. In the test group, NO was continuously redirected into the climate chamber of the microscope, so the chemotaxis chambers were surrounded by NO. The same experimental setup without NO served as a control. In addition, isolated PMNs were incubated with nitrogen monoxide (NO) or without (the control). Subsequently, flow cytometry was used to analyze neutrophil antigen expression and oxidative burst. Results: Our live cell imaging results demonstrated a migration-promoting effect of NO on PMNs. We observed that in the case of prior stimulation by fMLP, NO has no effect on the time course of neutrophil ROS production and NET release. However, flow cytometric analyses demonstrated an increase in ROS production after pretreatment with NO. No NO-dependent differences for the expression of CD11b, CD62L, or CD66b could be observed. Conclusions: We were able to demonstrate a distinct effect of NO on PMNs’ function. The complex interaction between NO and PMNs remains a major research focus, as the exact mechanisms and additional influencing factors remain elusive. Future studies should explore how varying NO concentrations and the timing of NO exposure relative to PMN activation affect its influence. Full article
(This article belongs to the Special Issue Neutrophils in Immunity and Diseases)
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12 pages, 2738 KiB  
Article
The Cytological Energy Detection of Purulent Inflammation in Synovial Fluid Is Not All Black and White
by Petr Kelbich, Eliska Vanaskova, Karel Hrach, Jan Krejsek, Frantisek Smisko, Pavla Hruskova, Eva Hanuljakova and Tomas Novotny
Biomedicines 2024, 12(3), 667; https://doi.org/10.3390/biomedicines12030667 - 16 Mar 2024
Viewed by 2660
Abstract
Neutrophils are frequently found in the cytological picture of synovial fluid in several joint pathologies, and a higher proportion of them can even wrongly indicate these cases as purulent inflammation. For reliable differentiation between purulent and non-purulent cases, we use the cytological energy [...] Read more.
Neutrophils are frequently found in the cytological picture of synovial fluid in several joint pathologies, and a higher proportion of them can even wrongly indicate these cases as purulent inflammation. For reliable differentiation between purulent and non-purulent cases, we use the cytological energy analysis of the synovial fluid. Using this method, we examined 350 knee joint synovial fluid samples. Overall, we found that the percentage of neutrophils ranged between 20.0% and 50.0% in 44 (12.6%) cases and was above 50.0% in 231 (66.0%) cases. In the same group, only 85 (24.3%) highly anaerobic synovial fluid samples were evaluated as purulent inflammation, and another 17 (4.9%) cases were evaluated as very likely purulent inflammation. Further, we quantified the immediate risk of purulent inflammation using the “purulent score” (PS). Of the total of 350 samples, 103 (29.4%) cases were classified as having a very high risk of purulent inflammation (PS = 4), 53 (15.1%) cases were classified as having a significant risk of purulent inflammation (PS = 3), 17 (4.9%) cases were classified as having a moderate risk of purulent inflammation (PS = 2), and 75 (21.4%) cases were classified as having no immediate risk of purulent inflammation (PS = 1). Based on our results and analyses, the cytological energy analysis of synovial fluid is an effective method that can be used to detect and specify joint inflammation and the risk of septic arthritis development. Full article
(This article belongs to the Special Issue Neutrophils in Immunity and Diseases)
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19 pages, 3412 KiB  
Article
The Effect of Local Anesthetics on Neutrophils in the Context of Different Isolation Techniques
by Sara Sixt, Michael Gruber, Gesche Kolle, Thies Galla and Diane Bitzinger
Biomedicines 2023, 11(8), 2170; https://doi.org/10.3390/biomedicines11082170 - 2 Aug 2023
Cited by 2 | Viewed by 2317
Abstract
Various functions of polymorphonuclear neutrophils (PMNs) are related to diseases and postoperative plasma changes. The influence of some local anesthetics (LAs) on PMNs obtained by conventional isolation methods and their functions has already been demonstrated. This study investigates the effect of selected LAs [...] Read more.
Various functions of polymorphonuclear neutrophils (PMNs) are related to diseases and postoperative plasma changes. The influence of some local anesthetics (LAs) on PMNs obtained by conventional isolation methods and their functions has already been demonstrated. This study investigates the effect of selected LAs on PMNs, comparing a new isolation method with conventional ones. To obtain the PMNs, we performed either gelafundin sedimentation, hypotonic lysis or density gradient centrifugation. Subsequently, PMNs were mixed with different concentrations of bupivacaine, levobupivacaine, lidocaine or ropivacaine. Live cell imaging and flow cytometry were performed to quantify the migration, ROS production, NETosis and antigen expression of PMNs. We found the inhibition of chemotaxis and ROS production by LAs. PMNs showed a strong reduction in time to half maximal NETosis in response to bupivacaine and lidocaine, but not to levobupivacaine and ropivacaine. We also found distinct differences in survival time and migration duration between the isolation methods. This suggests that the careful selection of LAs has a short-term impact on in vitro PMNs. Full article
(This article belongs to the Special Issue Neutrophils in Immunity and Diseases)
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15 pages, 1661 KiB  
Article
Ιnterleukin-17A-Enriched Neutrophil Extracellular Traps Promote Immunofibrotic Aspects of Childhood Asthma Exacerbation
by Maria Ntinopoulou, Dimitrios Cassimos, Eugenia Roupakia, Evangelos Kolettas, Maria Panopoulou, Elpis Mantadakis, Theocharis Konstantinidis and Akrivi Chrysanthopoulou
Biomedicines 2023, 11(8), 2104; https://doi.org/10.3390/biomedicines11082104 - 26 Jul 2023
Cited by 5 | Viewed by 1988
Abstract
Childhood asthma is a chronic inflammatory airway disorder that can drive tissue remodeling. Neutrophils are amongst the most prominent inflammatory cells contributing to disease manifestations and may exert a potent role in the progression of inflammation to fibrosis. However, their role in asthma [...] Read more.
Childhood asthma is a chronic inflammatory airway disorder that can drive tissue remodeling. Neutrophils are amongst the most prominent inflammatory cells contributing to disease manifestations and may exert a potent role in the progression of inflammation to fibrosis. However, their role in asthma exacerbation is still understudied. Here, we investigate the association between neutrophil extracellular traps (NETs) and lung fibroblasts in childhood asthma pathophysiology using serum samples from pediatric patients during asthma exacerbation. Cell-based assays and NETs/human fetal lung fibroblast co-cultures were deployed. Increased levels of NETs and interleukin (IL)-17A were detected in the sera of children during asthma exacerbation. The in vitro stimulation of control neutrophils using the sera from pediatric patients during asthma exacerbation resulted in IL-17A-enriched NET formation. The subsequent co-incubation of lung fibroblasts with in vitro-generated IL-17A-enriched NETs led fibroblasts to acquire a pre-fibrotic phenotype, as assessed via enhanced CCN2 expression, migratory/healing capacity, and collagen release. These data uncover the important pathogenic role of the NET/IL-17A axis in asthma exacerbation, linking lung inflammation to fibroblast dysfunction and fibrosis. Full article
(This article belongs to the Special Issue Neutrophils in Immunity and Diseases)
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