Progress in Inflammation Research – serie

Perinatal psychiatry is an emerging field that investigates the role of perinatal events – for example pregnancy complications and infections – in the development of neuropsychiatric conditions, such as schizophrenia and mood disorders. Among the implicated pathological mechanisms, perinatal-induced inflammation seems to play a major role and is being considered as a potential target for therapeutic intervention.  Bringing together various approaches in the field (preclinical and clinical, epidemiological, immunological and genetic methods), the book discusses the available evidence, the putative mechanisms and the challenges ahead.

Perinatal psychiatry is an emerging field that investigates the role of perinatal events – for example pregnancy complications and infections – in the development of neuropsychiatric conditions, such as schizophrenia and mood disorders.

Defects in Nrf2 and the relevant regulatory pathways are associated with a number of pathologies including inflammation, respiratory diseases, cardiovascular dysfunctions, metabolic syndrome and diabetes, neurodegeneration, and cancer.

M2 macrophages are not simply antagonists of M1 macrophages; M2 macrophages govern functions at the interfaces of immunity, tissue development and turnover, metabolism, and endocrine signaling.

M2 macrophages are not simply antagonists of M1 macrophages; M2 macrophages govern functions at the interfaces of immunity, tissue development and turnover, metabolism, and endocrine signaling.

TLR4 is one of the most important innate immunity receptors, its function mainly consisting in the activation of inflammatory pathways in response to stimulation by Pathogen-Associated Molecular Patterns (PAMPs) and Damage Associated Molecular Pattern molecules (DAMPs).This volume critically reviews the different types of TLR4 activators and inhibitors, discusses the role of molecular aggregates in agonism/antagonism as well as the pivotal role of the CD14 receptor in the modulation of TLR4 signal and the molecular details and actors of the intracellular cascade.The book presents the role of TLR4 in several pathologies, such as sepsis and septic shock caused by receptor activation by gram-negative bacterial lipopolysaccharide (LPS), in neurodegenerative and neurological diseases such as Parkinson and Alzheimer’s diseases,  and Amyotrophic Lateral Sclerosis (ALS). It reviews the role of TLR4 in neural stem cell-mediated neurogenesis andneuroinflammation and in Human Induced Pluripotent Stem Cells and Cerebral Organoids and discusses the emerging role of micro-RNA (miRNA) regulation by TLR4.

TLR4 is one of the most important innate immunity receptors, its function mainly consisting in the activation of inflammatory pathways in response to stimulation by Pathogen-Associated Molecular Patterns (PAMPs) and Damage Associated Molecular Pattern molecules (DAMPs).This volume critically reviews the different types of TLR4 activators and inhibitors, discusses the role of molecular aggregates in agonism/antagonism as well as the pivotal role of the CD14 receptor in the modulation of TLR4 signal and the molecular details and actors of the intracellular cascade.The book presents the role of TLR4 in several pathologies, such as sepsis and septic shock caused by receptor activation by gram-negative bacterial lipopolysaccharide (LPS), in neurodegenerative and neurological diseases such as Parkinson and Alzheimer’s diseases,  and Amyotrophic Lateral Sclerosis (ALS). It reviews the role of TLR4 in neural stem cell-mediated neurogenesis andneuroinflammation and in Human Induced Pluripotent Stem Cells and Cerebral Organoids and discusses the emerging role of micro-RNA (miRNA) regulation by TLR4.

This book provides comprehensive information, both for clinicians and scientists, on the basic mechanisms, clinical features, and therapeutic approaches to epilepsy as an inflammatory disease. Inflammation has been for many years considered as an etiologic player (and a therapeutic target) for a specific group of epilepsies.

This book provides comprehensive information, both for clinicians and scientists, on the basic mechanisms, clinical features, and therapeutic approaches to epilepsy as an inflammatory disease. Inflammation has been for many years considered as an etiologic player (and a therapeutic target) for a specific group of epilepsies.

Particular attention is given to the range of pathologies associated with inappropriate microbial exposures and inappropriate colonization, including immunoregulatory problems such as allergies and autoimmunity, metabolic problems such as obesity and diabetes, and problems of central nervous system function and neurodegeneration.

Particular attention is given to the range of pathologies associated with inappropriate microbial exposures and inappropriate colonization, including immunoregulatory problems such as allergies and autoimmunity, metabolic problems such as obesity and diabetes, and problems of central nervous system function and neurodegeneration.

It explains how recent advances in our understanding of the mesenteric organ, have advanced the diagnosis and treatment abdominal and systemic conditions including cancer, inflammatory bowel disease and endocrine conditions such as diabetes, and circulatory disorders such as atherosclerosis.

It explains how recent advances in our understanding of the mesenteric organ, have advanced the diagnosis and treatment abdominal and systemic conditions including cancer, inflammatory bowel disease and endocrine conditions such as diabetes, and circulatory disorders such as atherosclerosis.

Imaging Inflammation provides updates on cutting-edge imaging methods being applied to problems in inflammation research.

Imaging Inflammation provides updates on cutting-edge imaging methods being applied to problems in inflammation research.

For over 50 years, clinicians have known that macrolide antibiotics have effects on inflammation and the immune system that are not related to their antimicrobial properties.

For over 50 years, clinicians have known that macrolide antibiotics have effects on inflammation and the immune system that are not related to their antimicrobial properties.

The circadian clock is a complex cellular mechanism that controls numerous key physiological processes and maintains cellular, tissue, and systemic homeostasis. There is increasing evidence that cellular inflammation affects sleep and circadian rhythms and vice-versa.

The inflammasome was first described in 2002 as a molecular complex activating proinflammatory caspases and therefore regulating the maturation and biological activities of cytokines such as IL-1 and IL-18. This finding was substantiated by the identification of several mutations in the cias1 gene, encoding the human NLRP3 protein, responsible for several autoinflammatory disorders such as the Muckle Wells syndrome. Since, the interest for this complex has constantly increased and several inflammasome complexes with different specificities have been described. These inflammasomes sense a wide variety of pathogens and danger signals and are key players in the inflammatory response. With the contributions of leading international experts in the field, this book provides an extensive overview of the current knowledge of inflammasome biology and their role in health and disease.

Proteases are everywhere from prokaryotes to eukaryotes, from virus to bacteria and in all human tissues, playing a role in many biological functions. Among these functions, the inflammatory reaction is of particular interest.  In inflamed tissues, proteases can have a microbial and/or host origin and are involved not only in tissue remodeling, but also in specific signaling to resident or inflammatory cells, thereby contributing to the innate immune response.This volume presents all advances in our knowledge of the role proteases and their inhibitors play in various diseases associated with inflammatory response. Mechanisms involved in protease signaling to cells are presented, and the different types of proteases that are present at inflammatory sites and their effects on the course of inflammation are discussed. Finally, the evidence for considering proteases and their receptors as potential molecular targets for therapeutic interventions in the treatment of inflammatory diseases is discussed in the context of specific organ inflammatory pathologies (the lung, gastrointestinal tract, skin, joints, etc.).

Proteases are everywhere from prokaryotes to eukaryotes, from virus to bacteria and in all human tissues, playing a role in many biological functions. Among these functions, the inflammatory reaction is of particular interest.  In inflamed tissues, proteases can have a microbial and/or host origin and are involved not only in tissue remodeling, but also in specific signaling to resident or inflammatory cells, thereby contributing to the innate immune response.This volume presents all advances in our knowledge of the role proteases and their inhibitors play in various diseases associated with inflammatory response. Mechanisms involved in protease signaling to cells are presented, and the different types of proteases that are present at inflammatory sites and their effects on the course of inflammation are discussed. Finally, the evidence for considering proteases and their receptors as potential molecular targets for therapeutic interventions in the treatment of inflammatory diseases is discussed in the context of specific organ inflammatory pathologies (the lung, gastrointestinal tract, skin, joints, etc.).

The inflammasome was first described in 2002 as a molecular complex activating proinflammatory caspases and therefore regulating the maturation and biological activities of cytokines such as IL-1 and IL-18. This finding was substantiated by the identification of several mutations in the cias1 gene, encoding the human NLRP3 protein, responsible for several autoinflammatory disorders such as the Muckle Wells syndrome. Since, the interest for this complex has constantly increased and several inflammasome complexes with different specificities have been described. These inflammasomes sense a wide variety of pathogens and danger signals and are key players in the inflammatory response. With the contributions of leading international experts in the field, this book provides an extensive overview of the current knowledge of inflammasome biology and their role in health and disease.

The knowledge of Th17 cells and other cell populations which secrete IL-17A, and/or IL-22 has expanded tremendously since the publication of the first edition “Th17 Cells: Role in Inflammation and Autoimmune Disease” in 2008. The present volume has been completely revised with the addition of new chapters on the IL-17 receptor family and signaling, and an in-depth review of IL-22 and innate lymphoid cells. The differentiation of naïve T cells into regulatory T cells and Th17 cells as well as the plasticity of Th17 cells is discussed. The role of IL-22 in cutaneous inflammation including psoriasis has been reviewed. In addition, the volume contains critical updates on autoimmunity, organ transplantation, tumor immunology and genetic mouse models for mechanistic studies. Lastly, the latest clinical progress in neutralizing antibodies to IL-17A, IL-17RA not only confirms the therapeutic promise foreseen in 2008, but also improves our knowledge of the pathogenesis of autoimmune diseases. In summary, this is a timely update and important review of the clinical and experimental aspects of IL-17, IL-22 and their producing cells.

Antimicrobial peptides have been the subject of intense research in the past decades, and are now considered as an essential part of the defense system in bacteria, plants, animals and humans. his book provides an update on these effector molecules of the innate immune system both for researchers who are already actively involved in the area, and for those with a general interest in the topic. The book starts with an overview of the evolution of cysteine-containing antimicrobial peptides (including defensins), and the role of these peptides in host defense in plants and micro-organisms. The realization that antimicrobial peptides also display functions distinct from their direct antimicrobial action is the focus of the next chapters, and puts these peptides center stage in immunity and wound repair.  Further chapters discuss the role of antimicrobial peptides in disease, by providing an overview of mechanisms in bacterial resistance to antimicrobial peptides and a discussion of their role in inflammatory bowel disease, cystic fibrosis lung disease and chronic obstructive pulmonary disease. Finally, the book shows how knowledge of the function of antimicrobial peptides and their regulation can be used to design new therapies for inflammatory and infectious disorders. This is a very important area of research because of the increase in resistance of micro-organisms to conventional antibiotics. Therefore the use of synthetic or recombinant peptides, or agents that stimulate the endogenous production of antimicrobial peptides, provides an attractive alternative for conventional antibiotics.

Further chapters discuss the role of antimicrobial peptides in disease, by providing an overview of mechanisms in bacterial resistance to antimicrobial peptides and a discussion of their role in inflammatory bowel disease, cystic fibrosis lung disease and chronic obstructive pulmonary disease.

The knowledge of Th17 cells and other cell populations which secrete IL-17A, and/or IL-22 has expanded tremendously since the publication of the first edition “Th17 Cells: Role in Inflammation and Autoimmune Disease” in 2008. The present volume has been completely revised with the addition of new chapters on the IL-17 receptor family and signaling, and an in-depth review of IL-22 and innate lymphoid cells. The differentiation of naïve T cells into regulatory T cells and Th17 cells as well as the plasticity of Th17 cells is discussed. The role of IL-22 in cutaneous inflammation including psoriasis has been reviewed. In addition, the volume contains critical updates on autoimmunity, organ transplantation, tumor immunology and genetic mouse models for mechanistic studies. Lastly, the latest clinical progress in neutralizing antibodies to IL-17A, IL-17RA not only confirms the therapeutic promise foreseen in 2008, but also improves our knowledge of the pathogenesis of autoimmune diseases. In summary, this is a timely update and important review of the clinical and experimental aspects of IL-17, IL-22 and their producing cells.

Heat shock proteins (HSP) have received ample interest by immunologists over recent years. Initially they were found to be dominantly immunogenic microbial antigens. The connection with inflammation was established when it was uncovered that T cells specific for these antigens have a crucial role in the induction and regulation of experimental arthritis. Since then, the raised presence of immunity to HSPs in virtually all conditions of inflammation, including autoimmune diseases, transplant rejection and atherosclerosis, has emphasised the critical significance of immunity to HSPs in inflammatory diseases.

Several new developments in the field of neuroimmunology with focus on the brain-to-immune system communication have been the incentive for this PIR volume. It covers topics such as brain-immune interactions, the impact of stress on the immune response, pain and immunosuppression, the modulation of inflammation and pain by the sympathetic nervous system, consequences of nerve injury for the immune system, neuronal mechanisms of immune cell recruitment, and the modulation of the immune response by corticotropin-releasing hormone or adenosine. The authors are a unique group of scientists who are all interested in brain-to-immune interactions; however, each from a different perspective. The volume will serve both neurobiologists and immunologists to understand the influence of the central nervous system on peripheral inflammation. Many aspects of this book will also be stimulating for researchers in the pain field.

Heart failure research is a most active area of research in academic, industrial and government-sponsored research and receives intense clinical attention. The recent recognition that inflammation is a risk factor and prognostic factor for heart disease has laid ground for preventive medicine and even anti-infective strategies in prevention and treatment of heart failure.