Harald Lesch

Martin Herrmann

Zwei streitbare Denker haben gemeinsam ein leidenschaftliches Plädoyer gegen Zukunftsangst und Fatalismus, einen Aufruf zu aktivem Eingreifen geschrieben. Die Erwärmung der Welt ist ein globaler Notfall. Wir haben die Welt in einem Ausmaß verändert, dass dies nicht nur uns und unsere Gesundheit, sondern die gesamte Erde gefährdet. Das Einzige, was helfen kann, ist eine umfassende Transformation unserer Lebens- und Wirtschaftsweise. Dennoch gehen die meisten besorgten Menschen davon aus, dass sie selbst im Angesicht der Größe der Bedrohung nichts verändern können. Das trifft auch auf Wissenschaftler*innen und Entscheider*innen in Wirtschaft und Politik zu. Zu Unrecht – wie dieses engagierte Buch uns vor Augen führt. Der Physiker Harald Lesch und der Mediziner Martin Herrmann richten in "Sprung über den Abgrund" einen gemeinsamen Appell an alle, ihre Lähmungen zu überwinden und sich für die "Große Transformation" einzusetzen.

Warum die Klimakrise uns zum Handeln zwingt

Sprung über den Abgrund

Christian Schulz

Claudia Traidl-Hoffmann

Babette Simon

Das Konzept Planetary Health befasst sich mit den Zusammenhängen zwischen der Gesundheit des Menschen und der Gesundheit unseres Planeten. Bereits jetzt hat die zunehmende Zerstörung der Ökosysteme durch die raumgreifende Lebensweise des Menschen negativen Einfluss auf unsere Gesundheit, zuvorderst durch Umweltverschmutzung, Artensterben und die voranschreitende Klimakrise. Diese zunehmende Überschreitung planetarer Grenzen ist für die Gesellschaften eine beispiellose Herausforderung. Es gilt nun, diese Entwicklung im Kontext von Gesundheit und Medizin zu berücksichtigen – und die Wissenschaften rund um die Medizin zu ertüchtigen, sich eingehend mit den Konsequenzen für die Gesundheit auseinanderzusetzen. Beispiele sind die tödlichen Auswirkungen von Hitzewellen, die Zunahme von Allergien oder auch das Auftreten neuartiger Krankheitserreger. Dieses Fachbuch bündelt das aktuelle, für viele der medizinischen Fachgebiete noch neue Wissen über die vielfältigen Folgen der Klimakrise. Es sind Folgen, die auch noch die Gesundheit kommender Generationen beeinflussen werden. Mit Geleitworten von Eckart von Hirschhausen, Detlev Ganten und Sabine Gabrysch

Klima, Umwelt und Gesundheit im Anthropozän

Planetary Health

Joachim R. Kalden

This is the first comprehensive book about the relationship between apoptosis and autoimmune diseases. It offers a unique up-to-date overview on research results on the defective execution of apoptosis and the incomplete clearance of apoptotic cel.

From Mechanisms to Treatments

Apoptosis and Autoimmunity

Hans-Joachim Anders

Shrikant R. Mulay

Rostyslav Bilyy

Alexander Gabibov

Nano- and microparticles including crystals, synthetic biomaterials, misfolded proteins or environmental particulates are involved in a wide range of biological processes and diseases. They may present as intrinsic or environmental toxins but may also be applied intentionally, e.g. as immune adjuvants, drug carriers or ion exchangers. The discovery that a wide range of nano- and microparticles share the capacity to induce IL-1β secretion via activation of the NLRP3 inflammasome in dendritic cells and macrophages has led to the hypothesis that nano- and microparticles may contribute in a uniform mechanistic manner to different disease entities. Other molecular mechanisms triggered by a range nano- and microparticles have also recently been identified including (i) the induction of regulated necrosis; (ii) neutrophil extracellular trap (NET) formation and (iii) foreign body granuloma formation as a mechanism of persistent tissue inflammation and scarring. Research on the biology of nano- and microparticle handling is currently under intense investigation. The cell type-specific responses of nano- and microparticle exposure deserves careful attention as well as the related secondary responses to these particles that lead to tissue remodeling. The immune system is at the center of these processes in terms of particle clearance, particle-induced cell death and inflammation, thereby limiting particle-related inflammation and orchestrating wound healing responses. In this Research Topic, we welcomed the submission of Original Research, Review and Mini-Review articles that addressed the significance of the immune system in particle-induced cell death, inflammation and immune responses. These findings will help facilitate new approaches to the prevention and management of particle-related diseases.

Nano- and Microparticle-Induced Cell Death, Inflammation and Immune Responses

Mariana J. Kaplan

Marko Radic

NETosis, a form of cell death that manifests by the release of decondensed chromatin to the extracellular space, provides valuable insights into mechanisms and consequences of cellular demise. Because extracellular chromatin can immobilize microbes, the extended nucleohistone network was called a neutrophil extracellular trap (NET), and the process of chromatin release was proposed to serve an innate immune defense function. Extracellular chromatin NETs were initially observed in studies of neutrophils and are most prominent in these types of granulocytes. Subsequent studies showed that other granulocytes and, in a limited way, other cells of the innate immune response may also release nuclear chromatin following certain kinds of stimulation. Variations of NETosis were noted with cells that remain temporarily motile after the release of chromatin. Numerous stimuli for NETosis were discovered, including bacterial breakdown products, inflammatory stimuli, particulate matter, certain crystals, immune complexes and activated thrombocytes. Fundamental explorations into the mechanisms of NETosis observed that neutrophil enzyme activity (PAD4, neutrophil elastase, proteinase 3 and myeloperoxidase) and signal transduction pathways contribute to the regulation of NETosis. Histones in NET chromatin become modified by peptidylarginine deiminase 4 (PAD4) and cleaved at specific sites by proteases, leading to extensive chromatin externalization. In addition, NETs serve for attachment of bactericidal enzymes including myeloperoxidase, leukocyte proteases, and the cathelicidin LL-37. NETs are decorated with proteases and may thus contribute to tissue destruction. However, the attachment of these enzymes to NET-associated supramolecular structures restricts systemic spread of the proteolytic activity. While the benefit of NETs in an infection appears obvious, NETs also participate as key protagonists in various pathologic states. Therefore, it is essential for NETs to be efficiently cleared; otherwise digestive enzymes may gain access to tissues where inflammation takes place. Persistent NET exposure at sites of inflammation may lead to a further complication: NET antigens may provoke acquired immune responses and, over time, could initiate autoimmune reactions, serve as antigen for nuclear autoantibodies and foster DNA immune complex-related inflammation. Neutrophil products and deiminated proteins comprise an important group of autoantigens in musculoskeletal disorders. Aberrant NET synthesis and/or clearance are often associated with inflammatory and autoimmune conditions. Recent evidence also implicates aberrant NET formation in the development of endothelial damage, atherosclerosis and thrombosis. Intravital microscopy provides evidence for conditions that induce NETosis in vivo. Furthermore, NETs can easily be detected in synovial fluid and tissue sections of patients with arthritis and gout. NETosis is thus of interest to researchers who investigate innate immune responses, host-pathogen interactions, chronic inflammatory disorders, cell and vascular biology, biochemistry, and autoimmunity. As we enter the second decade of research on NETosis, it is useful and timely to review the mechanisms and pathways of NET formation, their role in bacterial and fungal defense and their importance as inducers of autoimmune responses.

NETosis 2: The Excitement Continues

Martin Herrmann

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