Modulation of Inflammatory Cell Apoptosis in Infection-associated Inflammation PDF Download
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Author: Christopher David Lucas
Publisher:
ISBN:
Category :
Languages : en
Pages : 0
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Author: Christopher David Lucas
Publisher:
ISBN:
Category :
Languages : en
Pages : 0
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Author: Supriya Shukla
Publisher: Frontiers Media SA
ISBN: 2889711897
Category : Science
Languages : en
Pages : 259
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Author: Heiko Mühl
Publisher: Frontiers E-books
ISBN: 2889190730
Category :
Languages : en
Pages : 139
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Book Description
Macrophages were initially identified as a key element in the innate host response to infection and injury due to their phagocytic clearance and elimination of pathogenic and non-pathogenic entities. However, as macrophage research advanced it became clear that not only are these cells amenable to the acquisition of multiple plastic phenotypes during inflammatory responses to different pathogens, they also play a paramount role in the termination of inflammation and acquired immune responses. In addition, macrophages profoundly affect host physiology when they migrate to distant sites and differentiate to specialized cells, like foam cells, osteoclasts, adipose tissue- and tumor -associated macrophages and other macrophage-derived cell types. These processes are affected by the inflammation-resolution axis and can result in health threats, such as atherosclerosis, bone loss, obesity, fibrosis and cancer. This Research Topic issue will cover a wide range of topics in macrophage biology: 1. Macrophages in immune responses to pathogens 2. Macrophages in the termination of acute and acquired immunity. 3. The role of macrophages and their descendents in inflammation-associated pathologies. 4. Macrophage polarization and differentiation. Particular focus will be given to the modulation of macrophage phenotype and function following their encounter with apoptotic cells and the signaling cascades that govern these changes.
Author: Han-Ming Shen
Publisher: Springer Science & Business Media
ISBN: 1461482208
Category : Science
Languages : en
Pages : 402
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Book Description
Starting with discussion of basic concepts and the molecular mechanisms of necrosis, this book looks first at several forms of necrotic cell death that have been identified, including necroptosis, autophagic cell death, and PARP-mediated cell death. As necrotic cell death is increasingly known to play a critical role in many physiological processes, the next chapters discuss its effect on metabolism, inflammation, immunity, and development. Necrotic cell death is closely implicated in human diseases like cancer, so the next chapters examine its relevance to human diseases, and final chapters cover methodologies for measuring necrosis. This book presents comprehensive coverage of necrosis from recognized experts from leading academic and medical institutions around the world. In contrast to apoptosis, well-defined as a form of programmed cell death, necrosis used to be considered as accidental (i.e., non-programmed) cell death, usually in response to a severe injury. Accumulating evidence now suggests, however, that necrosis is also programmed and controlled by distinctive "death machinery" in response to various stimuli like oxidative stress or DNA damage.
Author: Amal O. Amer
Publisher: Frontiers E-books
ISBN: 2889192806
Category : Apoptosis
Languages : en
Pages : 110
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Book Description
Infectious disease is the result of an interactive relationship between a microbial pathogen and its host. In this interaction both the host and the pathogen attempt to manipulate each other using a complex network to maximize their respective survival probabilities. Programmed host cell death is a direct outcome of host-pathogen interaction and may benefit host or pathogen depending on microbial pathogenesis. Apoptosis and pyroptosis are two common programmed cell death types induced by various microbial infections. Apoptosis is non-inflammatory programmed cell death and can be triggered through intrinsic or extrinsic pathways and with or without the contribution of mitochondria. Pyroptosis is an inflammatory cell death and is typically triggered by caspase-1 after its activation by various inflammasomes. Microbial pathogens are able to modulate host apoptosis and pyroptosis through different triggers and pathways. The promotion and inhibition of host apoptosis and pyroptosis vary and depend on the microbe types, virulence, and phenotypes. For example, virulent pathogens and attenuated vaccine strains may use different pathways to modulate host cell death. Specific microbial genes may be responsible for the modulation of host cell death. Different host cells, including macrophages, dendritic cells, and T cells, can undergo apoptosis and pyroptosis after microbial infections. The pathways of host apoptosis and pyroptosis induced by different microbes may also differ. Different methods can be used to study the interaction between microbes and host cell death system.
Author: Bharat B. Aggarwal
Publisher: Springer
ISBN: 3034808372
Category : Medical
Languages : en
Pages : 489
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Book Description
This volume examines in detail the role of chronic inflammatory processes in the development of several types of cancer. Leading experts describe the latest results of molecular and cellular research on infection, cancer-related inflammation and tumorigenesis. Further, the clinical significance of these findings in preventing cancer progression and approaches to treating the diseases are discussed. Individual chapters cover cancer of the lung, colon, breast, brain, head and neck, pancreas, prostate, bladder, kidney, liver, cervix and skin as well as gastric cancer, sarcoma, lymphoma, leukemia and multiple myeloma.
Author: Bidesh Mahata
Publisher: Frontiers Media SA
ISBN: 2889742903
Category : Medical
Languages : en
Pages : 133
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Author: Geanncarlo Lugo-Villarino
Publisher: Frontiers Media SA
ISBN: 2889630579
Category :
Languages : en
Pages : 790
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Book Description
The Mononuclear Phagocyte System (MPS) of vertebrates is composed of monocytes, macrophages and dendritic cells. Together, they form part of the first line of immune defense against a variety of pathogens (bacteria, fungi, parasites and viruses), and thus play an important role in maintaining organism homeostasis. The mode of transmission, type of replication and mechanism of disease-causing differ significantly for each pathogen, eliciting a unique immune response in the host. Within this context, the MPS acts as both the sentinel and tailor of the immune system. As sentinels, MPS cells are found in blood and within tissues throughout the body to patrol against pathogenic insult. The strategy to detect 'microbial non-self' relies on MPS to recognize conserved microbial products known as 'pathogen-associated molecular pattern' (PAMPs). PAMPs recognition represents a checkpoint in the response to pathogens and relies on conserved 'pattern recognition receptors' (PRRs). Upon PRR engagement, MPS mount a cell-autonomous attack that includes the internalization and compartmentalization of intracellular pathogens into toxic compartments that promote destruction. In parallel, MPS cells launch an inflammatory response composed of a cellular arm and soluble factors to control extracellular pathogens. In cases when innate immunity fails to eliminate the invading microbe, MPS serves as a tailor to generate adaptive immunity for pathogen eradication and generation of "memory" cells, thus ensuring enhanced protection against re-infection. Indeed, MPS cell functions comprise the capture, process, migration and delivery of antigenic information to lymphoid organs, where type-1 immunity is tailored against intracellular microbes and type-2 immunity against extracellular pathogens. However, this potent adaptive immunity is also a double-edge sword that can cause aberrant inflammatory disorders, like autoimmunity or chronic inflammation. For this reason, MPS also tailors tolerance immunity against unwanted inflammation. Successful clearance of the microbe results in its destruction and proper collection of debris, resolution of inflammation and tissue healing for which MPS is essential. Reciprocally, as part of the evolutionary process taking place in all organisms, microbes evolved strategies to circumvent the actions bestowed by MPS cells. Multiple pathogens modulate the differentiation, maturation and activation programs of the MPS, as an efficient strategy to avoid a dedicated immune response. Among the most common evasion strategies are the subversion of phagocytosis, inhibition of PRR-mediated immunity, resistance to intracellular killing by reactive oxygen and nitrogen species, restriction of phagosome maturation, modulation of cellular metabolism and nutrient acquisition, regulation of cell death and autophagy, and modulation of pro-inflammatory responses and hijacking of tolerance mechanisms, among others. The tenet of this eBook is that a better understanding of MPS in infection will yield insights for development of therapeutics to enhance antimicrobial processes or dampen detrimental inflammation for the host's benefit. We believe that contributions to this topic will serve as a platform for discussion and debate about relevant issues and themes in this field. Our aim is to bring expert junior and senior scientists to address recent progress, highlight critical knowledge gaps, foment scientific exchange, and establish conceptual frameworks for future MPS investigation in the context of infectious disease.
Author: Adriano Rossi
Publisher: Springer Science & Business Media
ISBN: 376437506X
Category : Medical
Languages : en
Pages : 246
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Book Description
This book provides readers with an up-to-date and comprehensive view on the resolution of inflammation and on new developments in this area, including pro-resolution mediators, apoptosis, macrophage clearance of apoptotic cells, possible novel drug developments.
Author: Ah-Ng Tony Kong
Publisher: CRC Press
ISBN: 1466503718
Category : Medical
Languages : en
Pages : 631
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Book Description
Increasing scientific evidence suggests that the majority of diseases including cancer are driven by oxidative stress and inflammation, attributed to environmental factors. These factors either drive genetic mutations or epigenetically modify expression of key regulatory genes. These changes can occur as early as gestational fetal development, and
