Chemokines play an important role in recruiting inflammatory cells into tissues in response to infection and inflammation. They also play an important role in coordinating the movement of T-cells, B-cells and dentritic cells, necessary to generate an immune response (response to injury, allergens, antigens, invading microorganisms). They selectively attract leukocytes to inflammatory foci, inducing both cell migration and activation. They are involved in various diseases, like atherosclerosis, lung and skin inflammation, multiple sclerosis, or HIV. Volume 2 of this two-volume set discusses the pathophysiology of chemokines. It is divided into two parts: a) chemokines in animal disease models, and b) chemokines as drug targets. Together with volume 1, which discusses the immunobiology of chemokines, both volumes give a comprehensive overview of chemokine biology.

Chemokines play an important role in recruiting inflammatory cells into tissues in response to infection and inflammation. They also play an important role in coordinating the movement of T-cells, B-cells and dentritic cells, necessary to generate an immune response (response to injury, allergens, antigens, invading microorganisms). They selectively attract leukocytes to inflammatory foci, inducing both cell migration and activation. They are involved in various diseases, like atherosclerosis, lung and skin inflammation, multiple sclerosis, or HIV. Volume 1 of this two-volume set discusses the immunobiology of chemokines. It is divided into two parts: a) cellular targets in innate and adaptive immunity, and b) effector cell traffic-unrelated functions. Together with volume 2, which discusses the pathophysiology of chemokines, both volumes give a comprehensive overview of chemokine biology.

This much-needed text develops current knowledge on the mechanisms of angiogenesis at the molecular and cellular levels as they relate to inflammation, including acute and chronic inflammation, neurogenic initiation, and the role of the multiple cellular components that comprise inflammation. The volume brings together experts in each of these fields to link the molecular and cellular processes in angiogenesis to those of inflammation and disease, culminating in a discourse on areas for future therapies.

This volume gives a comprehensive overview on the most relevant leukocyte and endothelial adhesion molecules. The chapters are written by leaders in the field and focus on the biology, structure, function, and regulation of adhesion molecules. Currently approved adhesion molecule-based therapies are reviewed and an outlook for future approaches is also provided. The book is of interest to clinicians and scientists from immunology, physiology, cancer research, rheumatology, allergology, infectious diseases, gastroenterology, pulmonology and cardiology.

Sodium channels confer excitability on neurons in nociceptive pathways and exhibit neuronal tissue specific and injury regulated expression. This volume provides recent insights into the control of expression, functioning and membrane trafficking of nervous system sodium channels and reviews why sodium channel sub-types are potentially important drug targets in the treatment of pain. The roles of sodium channels in dental and visceral pain are also addressed. The emerging role of sodium channel Nav1.3 in neuropathic states is another important theme. Authors from the pharmaceutical industry discuss pharmacological approaches to the drug targeting of sodium channels, and in particular Nav1.8, exclusively expressed in nociceptive neurons. The final chapter highlights the functional diversity of sodium channels in part provided by post-transcriptional processing and the insights into sodium channel function that are being provided by tissue specific and inducible gene knock-out technology.

The understanding how complement relates to glomerular diseases has evolved considerably during the last years. Substantial evidence has accumulated that explain how a defective or deregulated complement system results in kidney diseases. The combination and close interaction of basic research with clinical medicine has demonstrated an important role of complement effector and regulatory proteins in pathological settings of the kidney. A large panel of distinct human kidney diseases such as hemolytic uremic syndrome (HUS), membrano proliferative glomerulonephritis (MPGN), systemic lupus erythematosus (SLE) and in ischemic reperfusions injury and transplantation are caused by defective complement control. Genetic analyses have identified mutations in complement regulators that are associated with these diseases. Mutations have been identified in the fluid phase alternative pathway regulator Factor H and the membrane regulator Membrane Cofactor Protein MCP (CD46). The functional characterization of the mutant proteins allows to define the pathophysiological events on a molecular level. These new concepts and data on disease mechanisms already allowed to establish new diagnostic and novel promising therapeutic approaches for several human kidney diseases.

Despite tremendous advances in the understanding of the sensory nervous system which have accompanied the recent explosive growth of the neurosciences, rema- ably few innovative medicines directed towards pain and inflammation are ava- able. Indeed, many patients are still prescribed analgesic and anti-inflammatory medications that were identified long ago as components of herbal remedies. Si- larly, potential new medicines in clinical evaluation based on capsaicin and the c- saicin receptor are both grounded firmly on folk traditions and yet rely upon the most contemporary techniques of drug discovery and delivery. The first formal report of the pain-relieving properties of capsaicin appeared in 1850 [1]. However, for centuries before this, capsaicin-containing extracts had been used as folk medicines in cultures with access to pepper plants, much in the same way as poppy or willow-bark extracts were. Despite widespread use, it was not until 1878 that the selective action of capsaicin on the sensory nervous system was r- ognized [2]. In Chapter 1 of this volume, Janos Szolcsányi reviews this early research, which culminated with the seminal studies of Nicholas Jansco and his c- leagues in Hungary in the 1940s. Since then, capsaicin and related vanilloid c- pounds have played a prominent role in analgesia and inflammation investigations because of their ability to selectively activate a subpopulation of sensory neurons and produce sensations of pain and localized erythema.

"In this book, experts in the field analyze recent evidence supporting the role of NPY family peptides in regulation of the immune/inflammatory system with special reference to its medical and therapeutic implications. Of special interest are the NPY functions in angiogenesis that provide new insights into vascular and neural remodeling, inflammation, tissue regeneration and tumor biology as well as offer new strategies for treatment of atherosclerosis, cancer and vascular ischemic diseases."--BOOK JACKET.

The IL-17 cytokines represent a novel family of cytokines, which defines a new effector T cell, the Th17 cell, and extend the Th1-Th2 paradigm. Th17 cells in part co-express at least IL-17A and IL-17F, IL-21 and IL-22. IL-17 A/F are produced by T cells ( and ), iNKT cells, and possibly neutrophils, dendritic cells and Paneth cells. The regulation of IL-17 family member’s expression, and the identification of effector mechanisms are an area of intense current research. Recognized regulators of IL-17A expression include the nuclear receptor ROR t, proinflammatory cyt- ines such as IL-1, IL-6 with TGF- , IL-21, IL-23 IL-25 in the absence of IFN- and IL-4, which are discussed. Recent data suggest that IL-17A may have a dual fu- tion – pro-inflammatory and anti-inflammatory- suggesting that IL-17A may also contribute to terminate inflammation. Further, a reciprocal regulation of Th17 and regulatory T cells including the role of retinoic acid and TGF- is discussed. The discovery that patients with rheumatoid arthritis, allergic disorders, psor- sis and inflammatory bowel disease express IL-17A generated interest in the medical community and instigated a flurry of experimental research on the potential role of Th17 in inflammatory diseases. Experimental studies confirmed that IL-17A is induced and is critical for the development of allergic lung inflammation, arthritis, bacterial sepsis, experimental allergic encephalomyelitis and myocarditis, as well as other inflammatory con- tions including organ transplantation. The role of IL-17F and IL-22 is still poorly defined and is only slowly emerging.

This volume provides new advances regarding the involvement of MMPs in various diseases associated with inflammatory processes. Moreover, the recent development of selective and non selective inhibitors of MMPs give new insights in the relationship between activation of inflammatory cells and tissue remodelling and advise new therapeutics possibilities to the treatment of inflammatory disease. The volume has an international authorship and is written by leading experts in the field.