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Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism
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Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 21188

Special Issue Editors

Dr. Huashan Shi

E-Mail Website
Guest Editor
1. State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, China
2. Collaborative Innovation Center for Biotherapy, Chengdu 610041, China
Interests: cancer vaccines; bioinformatics; clinical research; chemotherapy; tumor metastasis
Prof. Dr. Vishwanath Venketaraman

E-Mail Website
Guest Editor
College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA, USA
Interests: mycobacterial diseases; tuberculosis; host immune responses; pathogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Immunologists have long been puzzled by the self-destructive nature of the inflammatory response. Inflammation can be elicited by various harmful stimuli, such as microbial/viral infections, allergic reactions, chemical insults, lipotoxicity, tissue damage, or other types of traumas. Breaking down damaged cells and converting them into various nutrients which are useful for tissue regeneration is among the most important functions of the human immune system in maintaining health. A localized inflammatory response is protective if the human immune system can effectively eliminate the harmful stimuli and initiate the healing process. Cell self-destruction (programmed cell death) includes phenomena of apoptosis, pyroptosis, necroptosis, necrosis and so on. Phagocytosis is employed to remove various cell debris produced by cell self-destruction and for conversion into nutrients. The immune system thus represents a powerful nutrient generator. At these moments, digestion and immunity are interrelated and integrated, playing the essential role of disease prevention and immunonutrition acquisition. In the event of microbial/viral infections, the nutritional flux produced by infected host cell self-destruction (inflammation) may be much greater than those produced by normal apoptosis, and may even be much greater than the nutrition provided by daily food intake. Thus, infection-induced inflammation may induce illness-associated anorexia to avoid overnutrition. When the nutrition generated by the degradation of infection-damaged cells exceeds the nutritional requirements of tissue regeneration, most excess nutrients will be converted into lipid intermediates. Lipid intermediates will invade healthy non-adipose tissue, leading to lipotoxicity and further tissue damage. In such a case, the main product (lipid intermediates) of the inflammatory response is also a strong harming stimulus for tissue/cell damage. This is amplified during the inflammatory response, forming a vicious cycle, making inflammatory response extremely destructive. The state of overnutrition will be exacerbated by the loss of lean body mass, coupled with excess lipid intermediate spillover into healthy tissues and organs, exacerbating the inflammatory response, which is characteristic of critically ill or injured patients and of most autoimmune diseases. In this Special Issue, original research articles and reviews are welcomed. Research areas may include (but are not limited to) the following: microbial-/viral infection-induced host cell self-destruction as immunonutrition; programmed cell death and nutrients generation; cell self-destruction in illness, transient over-nutrition, lipotoxicity and involuntary weight loss.

Dr. Huashan Shi
Prof. Dr. Vishwanath Venketaraman
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • autoimmunity
  • cell self-destruction
  • infection
  • inflammation
  • immunonutrition
  • lipotoxicity
  • metabolism
  • programmed cell death

Published Papers (9 papers)

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Editorial

Jump to: Research, Review

3 pages, 217 KiB  
Editorial
Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism
by Ligen Yu
Biology 2023, 12(7), 949; https://doi.org/10.3390/biology12070949 - 03 Jul 2023
Cited by 1 | Viewed by 4176
Abstract
The main purpose of this Special Issue is to provide readers with current understandings of the interactions and causal relations among injury stimuli (including microorganism infections), immune response and overnutrition/lipotoxicity in disease pathogenesis [...] Full article
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)

Research

Jump to: Editorial, Review

12 pages, 3999 KiB  
Article
Modulation of Apoptosis by Bovine Gammaherpesvirus 4 Infection in Bovine Endometrial Cells and the Possible Role of LPS in This Process
by Florencia Romeo, Santiago Delgado, Marisol Yavorsky, Lucía Martinez Cuesta, Susana Pereyra, Erika González Altamiranda, Enrique Louge Uriarte, Sandra Pérez and Andrea Verna
Biology 2024, 13(4), 249; https://doi.org/10.3390/biology13040249 - 08 Apr 2024
Viewed by 490
Abstract
The prevalent pathogens associated with bovine uterine infections are bacteria that appear to increase the host’s susceptibility to secondary infections with other bacteria or viruses, among which BoGHV4 is the most frequently found. In this work, the study of the pathways of apoptosis [...] Read more.
The prevalent pathogens associated with bovine uterine infections are bacteria that appear to increase the host’s susceptibility to secondary infections with other bacteria or viruses, among which BoGHV4 is the most frequently found. In this work, the study of the pathways of apoptosis induction was carried out on an experimental model of primary culture of endometrial cells, in order to know the implication of BoGHV4 and the presence of bacterial LPS in the pathogenesis of the bovine reproductive tract. For this, different staining techniques and molecular analysis by RT-PCR were used. The results obtained allowed us to conclude that the level of cell death observed in the proposed primary culture is directly related to the time of viral infection and the presence of LPS in BoGHV4 infection. The apoptosis indices in cells infected with BoGHV4 and BoGHV4 + LPS revealed a maximum that correlated with the appearance of cytopathic effects and the maximum viral titers in the model studied. However, morphological, biochemical, and molecular changes were evident during both early and late stages of apoptosis. These findings provide information on the factors that may influence the pathogenesis of BoGHV4 and help to better understand the mechanisms involved in virus infection. Full article
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)
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Review

Jump to: Editorial, Research

21 pages, 1440 KiB  
Review
Exercise-Mediated Protection against Air Pollution-Induced Immune Damage: Mechanisms, Challenges, and Future Directions
by Xingsheng Jin, Yang Chen, Bingxiang Xu and Haili Tian
Biology 2024, 13(4), 247; https://doi.org/10.3390/biology13040247 - 08 Apr 2024
Viewed by 643
Abstract
Air pollution, a serious risk factor for human health, can lead to immune damage and various diseases. Long-term exposure to air pollutants can trigger oxidative stress and inflammatory responses (the main sources of immune impairment) in the body. Exercise has been shown to [...] Read more.
Air pollution, a serious risk factor for human health, can lead to immune damage and various diseases. Long-term exposure to air pollutants can trigger oxidative stress and inflammatory responses (the main sources of immune impairment) in the body. Exercise has been shown to modulate anti-inflammatory and antioxidant statuses, enhance immune cell activity, as well as protect against immune damage caused by air pollution. However, the underlying mechanisms involved in the protective effects of exercise on pollutant-induced damage and the safe threshold for exercise in polluted environments remain elusive. In contrast to the extensive research on the pathogenesis of air pollution and the preventive role of exercise in enhancing fitness, investigations into exercise resistance to injury caused by air pollution are still in their infancy. In this review, we analyze evidence from humans, animals, and cell experiments on the combined effects of exercise and air pollution on immune health outcomes, with an emphasis on oxidative stress, inflammatory responses, and immune cells. We also propose possible mechanisms and directions for future research on exercise resistance to pollutant-induced damage in the body. Furthermore, we suggest strengthening epidemiological studies at different population levels and investigations on immune cells to guide how to determine the safety thresholds for exercise in polluted environments. Full article
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)
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25 pages, 2310 KiB  
Review
Overnutrition and Lipotoxicity: Impaired Efferocytosis and Chronic Inflammation as Precursors to Multifaceted Disease Pathogenesis
by Vivek Mann, Alamelu Sundaresan and Shishir Shishodia
Biology 2024, 13(4), 241; https://doi.org/10.3390/biology13040241 - 06 Apr 2024
Viewed by 594
Abstract
Overnutrition, driven by the consumption of high-fat, high-sugar diets, has reached epidemic proportions and poses a significant global health challenge. Prolonged overnutrition leads to the deposition of excessive lipids in adipose and non-adipose tissues, a condition known as lipotoxicity. The intricate interplay between [...] Read more.
Overnutrition, driven by the consumption of high-fat, high-sugar diets, has reached epidemic proportions and poses a significant global health challenge. Prolonged overnutrition leads to the deposition of excessive lipids in adipose and non-adipose tissues, a condition known as lipotoxicity. The intricate interplay between overnutrition-induced lipotoxicity and the immune system plays a pivotal role in the pathogenesis of various diseases. This review aims to elucidate the consequences of impaired efferocytosis, caused by lipotoxicity-poisoned macrophages, leading to chronic inflammation and the subsequent development of severe infectious diseases, autoimmunity, and cancer, as well as chronic pulmonary and cardiovascular diseases. Chronic overnutrition promotes adipose tissue expansion which induces cellular stress and inflammatory responses, contributing to insulin resistance, dyslipidemia, and metabolic syndrome. Moreover, sustained exposure to lipotoxicity impairs the efferocytic capacity of macrophages, compromising their ability to efficiently engulf and remove dead cells. The unresolved chronic inflammation perpetuates a pro-inflammatory microenvironment, exacerbating tissue damage and promoting the development of various diseases. The interaction between overnutrition, lipotoxicity, and impaired efferocytosis highlights a critical pathway through which chronic inflammation emerges, facilitating the development of severe infectious diseases, autoimmunity, cancer, and chronic pulmonary and cardiovascular diseases. Understanding these intricate connections sheds light on potential therapeutic avenues to mitigate the detrimental effects of overnutrition and lipotoxicity on immune function and tissue homeostasis, thereby paving the way for novel interventions aimed at reducing the burden of these multifaceted diseases on global health. Full article
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)
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50 pages, 2313 KiB  
Review
Exploring beyond Common Cell Death Pathways in Oral Cancer: A Systematic Review
by Leonardo de Oliveira Siquara da Rocha, Everton Freitas de Morais, Lilianny Querino Rocha de Oliveira, Andressa Vollono Barbosa, Daniel W. Lambert, Clarissa A. Gurgel Rocha and Ricardo D. Coletta
Biology 2024, 13(2), 103; https://doi.org/10.3390/biology13020103 - 06 Feb 2024
Viewed by 1488
Abstract
Oral squamous cell carcinoma (OSCC) is the most common and lethal type of head and neck cancer in the world. Variable response and acquisition of resistance to traditional therapies show that it is essential to develop novel strategies that can provide better outcomes [...] Read more.
Oral squamous cell carcinoma (OSCC) is the most common and lethal type of head and neck cancer in the world. Variable response and acquisition of resistance to traditional therapies show that it is essential to develop novel strategies that can provide better outcomes for the patient. Understanding of cellular and molecular mechanisms of cell death control has increased rapidly in recent years. Activation of cell death pathways, such as the emerging forms of non-apoptotic programmed cell death, including ferroptosis, pyroptosis, necroptosis, NETosis, parthanatos, mitoptosis and paraptosis, may represent clinically relevant novel therapeutic opportunities. This systematic review summarizes the recently described forms of cell death in OSCC, highlighting their potential for informing diagnosis, prognosis and treatment. Original studies that explored any of the selected cell deaths in OSCC were included. Electronic search, study selection, data collection and risk of bias assessment tools were realized. The literature search was carried out in four databases, and the extracted data from 79 articles were categorized and grouped by type of cell death. Ferroptosis, pyroptosis, and necroptosis represented the main forms of cell death in the selected studies, with links to cancer immunity and inflammatory responses, progression and prognosis of OSCC. Harnessing the potential of these pathways may be useful in patient-specific prognosis and individualized therapy. We provide perspectives on how these different cell death types can be integrated to develop decision tools for diagnosis, prognosis, and treatment of OSCC. Full article
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)
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29 pages, 1744 KiB  
Review
Types of Cell Death from a Molecular Perspective
by Fatemeh Hajibabaie, Navid Abedpoor and Parisa Mohamadynejad
Biology 2023, 12(11), 1426; https://doi.org/10.3390/biology12111426 - 13 Nov 2023
Cited by 3 | Viewed by 2257
Abstract
The former conventional belief was that cell death resulted from either apoptosis or necrosis; however, in recent years, different pathways through which a cell can undergo cell death have been discovered. Various types of cell death are distinguished by specific morphological alterations in [...] Read more.
The former conventional belief was that cell death resulted from either apoptosis or necrosis; however, in recent years, different pathways through which a cell can undergo cell death have been discovered. Various types of cell death are distinguished by specific morphological alterations in the cell’s structure, coupled with numerous biological activation processes. Various diseases, such as cancers, can occur due to the accumulation of damaged cells in the body caused by the dysregulation and failure of cell death. Thus, comprehending these cell death pathways is crucial for formulating effective therapeutic strategies. We focused on providing a comprehensive overview of the existing literature pertaining to various forms of cell death, encompassing apoptosis, anoikis, pyroptosis, NETosis, ferroptosis, autophagy, entosis, methuosis, paraptosis, mitoptosis, parthanatos, necroptosis, and necrosis. Full article
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)
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23 pages, 2999 KiB  
Review
Cellular Stress: Modulator of Regulated Cell Death
by Prem Prasad Lamichhane and Parimal Samir
Biology 2023, 12(9), 1172; https://doi.org/10.3390/biology12091172 - 25 Aug 2023
Cited by 1 | Viewed by 2903
Abstract
Cellular stress response activates a complex program of an adaptive response called integrated stress response (ISR) that can allow a cell to survive in the presence of stressors. ISR reprograms gene expression to increase the transcription and translation of stress response genes while [...] Read more.
Cellular stress response activates a complex program of an adaptive response called integrated stress response (ISR) that can allow a cell to survive in the presence of stressors. ISR reprograms gene expression to increase the transcription and translation of stress response genes while repressing the translation of most proteins to reduce the metabolic burden. In some cases, ISR activation can lead to the assembly of a cytoplasmic membraneless compartment called stress granules (SGs). ISR and SGs can inhibit apoptosis, pyroptosis, and necroptosis, suggesting that they guard against uncontrolled regulated cell death (RCD) to promote organismal homeostasis. However, ISR and SGs also allow cancer cells to survive in stressful environments, including hypoxia and during chemotherapy. Therefore, there is a great need to understand the molecular mechanism of the crosstalk between ISR and RCD. This is an active area of research and is expected to be relevant to a range of human diseases. In this review, we provided an overview of the interplay between different cellular stress responses and RCD pathways and their modulation in health and disease. Full article
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)
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31 pages, 9155 KiB  
Review
The ACSL4 Network Regulates Cell Death and Autophagy in Diseases
by Fangquan Chen, Rui Kang, Jiao Liu and Daolin Tang
Biology 2023, 12(6), 864; https://doi.org/10.3390/biology12060864 - 15 Jun 2023
Cited by 6 | Viewed by 3900
Abstract
Lipid metabolism, cell death, and autophagy are interconnected processes in cells. Dysregulation of lipid metabolism can lead to cell death, such as via ferroptosis and apoptosis, while lipids also play a crucial role in the regulation of autophagosome formation. An increased autophagic response [...] Read more.
Lipid metabolism, cell death, and autophagy are interconnected processes in cells. Dysregulation of lipid metabolism can lead to cell death, such as via ferroptosis and apoptosis, while lipids also play a crucial role in the regulation of autophagosome formation. An increased autophagic response not only promotes cell survival but also causes cell death depending on the context, especially when selectively degrading antioxidant proteins or organelles that promote ferroptosis. ACSL4 is an enzyme that catalyzes the formation of long-chain acyl-CoA molecules, which are important intermediates in the biosynthesis of various types of lipids. ACSL4 is found in many tissues and is particularly abundant in the brain, liver, and adipose tissue. Dysregulation of ACSL4 is linked to a variety of diseases, including cancer, neurodegenerative disorders, cardiovascular disease, acute kidney injury, and metabolic disorders (such as obesity and non-alcoholic fatty liver disease). In this review, we introduce the structure, function, and regulation of ACSL4; discuss its role in apoptosis, ferroptosis, and autophagy; summarize its pathological function; and explore the potential implications of targeting ACSL4 in the treatment of various diseases. Full article
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)
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15 pages, 1228 KiB  
Review
New Perspectives on the Role of Nuclear Proteases in Cell Death Pathways
by Anastasia S. Frolova, Olga E. Chepikova, Anna S. Deviataikina, Alena D. Solonkina and Andrey A. Zamyatnin, Jr.
Biology 2023, 12(6), 797; https://doi.org/10.3390/biology12060797 - 31 May 2023
Cited by 1 | Viewed by 1753
Abstract
Multiple factors can trigger cell death via various pathways, and nuclear proteases have emerged as essential regulators of these processes. While certain nuclear proteases have been extensively studied and their mechanisms of action are well understood, others remain poorly characterized. Regulation of nuclear [...] Read more.
Multiple factors can trigger cell death via various pathways, and nuclear proteases have emerged as essential regulators of these processes. While certain nuclear proteases have been extensively studied and their mechanisms of action are well understood, others remain poorly characterized. Regulation of nuclear protease activity is a promising therapeutic strategy that could selectively induce favorable cell death pathways in specific tissues or organs. Thus, by understanding the roles of newly discovered or predicted nuclear proteases in cell death processes, we can identify new pharmacological targets for improving therapeutic outcomes. In this article, we delved into the role of nuclear proteases in several types of cell death and explore potential avenues for future research and therapeutic development. Full article
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Overnutrition and Lipotoxicity: Impaired Efferocytosis and Chronic Inflammation as Precursors to Multifaceted Disease Pathogenesis
Authors: Vivek Mann; Alamelu Sundaresan; Shishir Shishodia; Rehan Memon; Sarah F Banday
Affiliation: Texas Southern University
Abstract: Overnutrition, driven by the consumption of high-fat, high-sugar diets, has reached epidemic proportions and poses a significant global health challenge. Prolonged overnutrition leads to the deposition of excessive lipids in adipose and non-adipose tissues, a condition known as lipotoxicity. The intricate interplay between overnutrition-induced lipotoxicity and the immune system plays a pivotal role in the pathogenesis of various diseases. This review aims to elucidate the consequences of impaired efferocytosis, caused by lipotoxicity-poisoned macrophages, leading to chronic inflammation and the subsequent development of severe infectious diseases, autoimmunity, cancer, as well as chronic pulmonary and cardiovascular diseases. Chronic overnutrition promotes adipose tissue expansion which induces cellular stress and inflammatory responses, contributing to insulin resistance, dyslipidemia, and metabolic syndrome. Moreover, sustained exposure to lipotoxicity impairs the efferocytic capacity of macrophages, compromising their ability to efficiently engulf and remove dead cells. The unresolved chronic inflammation perpetuates a pro-inflammatory microenvironment, exacerbating tissue damage and promoting the development of various diseases. The interaction between overnutrition, lipotoxicity, and impaired efferocytosis highlights a critical pathway through which chronic inflammation emerges, facilitating the development of severe infectious diseases, autoimmunity, cancer, and chronic pulmonary and cardiovascular diseases. Understanding these intricate connections sheds light on potential therapeutic avenues to mitigate the detrimental effects of overnutrition and lipotoxicity on immune function and tissue homeostasis, thereby paving the way for novel interventions aimed at reducing the burden of these multifaceted diseases on global health.

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