Cachexia is seen in patients with chronic inflammatory diseases including aggressive cancers (pancreatic, gastric, colorectal, and lung cancers) and chronic infections (acquired immunodeficiency syndrome (AIDS) and Mycobacterium tuberculosis infection). Cachexia accounts for 20% of all cancer-related deaths and serves as a poor prognostic indicator. It is a complex metabolic syndrome that underlies illness characterized by muscle loss with or without fat loss. The international consensus (What is the name of the consensus group) most recently defined cancer-associated cachexia (CAC) as a multifactorial syndrome comprising the skeletal muscle mass loss. This weight loss cannot be fully reversed by conventional nutritional support due to the involvement of various factors, including reduced food intake, altered metabolism, and the immune status of the host/patient.
An intact immune system is crucial for host defense and homeostasis. The immune system is altered in patients with cancer and chronic infections. The immune and metabolic crosstalk is conserved between invertebrates and vertebrates, indicating that altering the host immune status can subsequently alter the metabolic stage/status or vice versa. The recent recognition of immunometabolism (regulation of immune cell function and homeostasis through different metabolic pathways) further supports that altering the metabolic energy status of the host changes the immune cell reprogramming and function. Because cachexia is seen in patients who have limited metabolic and immune function, it will be interesting to understand how the immunology of cachexia correlates with clinical outcomes in patients with cancer.
This special issue is designed to precisely understand how cachexia alters immune cell functions. For example, the immune system has emerged as a player in the obesity-associated systemic inflammation responsible for different diseases. Similarly, it is essential to delineate the immune mechanisms involved in cachexia pathogenesis and immune function deregulation, including their immunometabolic reprogramming. Thus, this special issue is designed for a variety of articles, including full-length research and review articles, mini-reviews, short reports, and method articles. The subtopics of interest are:
1. Innate immune cells in cachexia
2. Adaptive immunity in cachexia
3. Immunometabolic reprogramming during cachexia
4. immunopathogenesis of cachexia
5. Immune bio-markers of cachexia
6 Interaction between systemic metabolism and immune system in cachexia
7 Immunomodulatory and immunotherapeutic approaches for cachexia
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
Cachexia is seen in patients with chronic inflammatory diseases including aggressive cancers (pancreatic, gastric, colorectal, and lung cancers) and chronic infections (acquired immunodeficiency syndrome (AIDS) and Mycobacterium tuberculosis infection). Cachexia accounts for 20% of all cancer-related deaths and serves as a poor prognostic indicator. It is a complex metabolic syndrome that underlies illness characterized by muscle loss with or without fat loss. The international consensus (What is the name of the consensus group) most recently defined cancer-associated cachexia (CAC) as a multifactorial syndrome comprising the skeletal muscle mass loss. This weight loss cannot be fully reversed by conventional nutritional support due to the involvement of various factors, including reduced food intake, altered metabolism, and the immune status of the host/patient.
An intact immune system is crucial for host defense and homeostasis. The immune system is altered in patients with cancer and chronic infections. The immune and metabolic crosstalk is conserved between invertebrates and vertebrates, indicating that altering the host immune status can subsequently alter the metabolic stage/status or vice versa. The recent recognition of immunometabolism (regulation of immune cell function and homeostasis through different metabolic pathways) further supports that altering the metabolic energy status of the host changes the immune cell reprogramming and function. Because cachexia is seen in patients who have limited metabolic and immune function, it will be interesting to understand how the immunology of cachexia correlates with clinical outcomes in patients with cancer.
This special issue is designed to precisely understand how cachexia alters immune cell functions. For example, the immune system has emerged as a player in the obesity-associated systemic inflammation responsible for different diseases. Similarly, it is essential to delineate the immune mechanisms involved in cachexia pathogenesis and immune function deregulation, including their immunometabolic reprogramming. Thus, this special issue is designed for a variety of articles, including full-length research and review articles, mini-reviews, short reports, and method articles. The subtopics of interest are:
1. Innate immune cells in cachexia
2. Adaptive immunity in cachexia
3. Immunometabolic reprogramming during cachexia
4. immunopathogenesis of cachexia
5. Immune bio-markers of cachexia
6 Interaction between systemic metabolism and immune system in cachexia
7 Immunomodulatory and immunotherapeutic approaches for cachexia
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.