Macrophage-Mediated Inflammatory Disorders

Copyright © 2013 I-Ming Jou et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Mediators of inflammation induced by macrophages are critical for a variety of human inflammatory disorders, such as sepsis-related multiple organ dysfunction/multiple organ failure, microbial infection, acute brain/lung/hepatic/renal injuries, neurodegenerative disorders, tumorigenesis, osteo-porosis/osteonecrosis, cardiovascular and metabolic diseases , and autoimmune diseases. Most of these cases are proinflammatory and pathogenic for disease progression, once activated macrophages actively secrete and cause an imbalance of cytokines, chemokines, and mediators of inflammation. The primary focus of this special issue is on the current and updated knowledge of macrophage-mediated inflammatory disorders, particularly on the pathogenesis of the macrophage activation syndrome, mediators of inflammation and anti-inflammation, and strategies against such effects. Lots of papers were submitted and reviewed by Editors and Reviewers, and twenty-four papers are accepted for publication. The brief introductions of these papers are as follows. Due to the profile of released mediators (such as cy-tokines, chemokines, and growth factors), neoplastic cells modulate the activity of immune system, directly affecting its components both locally and peripherally. A. Eljaszewicz et al. reviewed, in the paper entitled " Collaborating with the enemy: function of macrophages in the development of neoplastic disease, " the specific functions of macrophages in the development of neoplastic disease. The study called " Regulatory role of GSK-3í µí»½ on NF-í µí¼…B, nitric oxide, and TNF-í µí»¼ in group A streptococcal infection, " investigates the interaction between GSK-3í µí»½, NF-í µí¼…B, and possible related inflammatory mediators in vitro and in a mouse model. The results revealed that GAS could activate NF-í µí¼…B, followed by an increased expression of inducible nitric oxide synthase (iNOS) and NO production in a murine macrophage cell line. Y.-T. Chang et al. demonstrated that the inhibition of GSK-3í µí»½ to moderate the inflammatory effect might be an alternative therapeutic strategy against GAS infection. During the early and short inflammatory phase, ma-crophages exert proinflammatory functions like antigen-presenting phagocytosis and the production of inflammatory cytokines and growth factors that facilitate the resolution of inflammation. However, persistence of proinflammatory activity and altered function of macrophages result in the development of chronic inflammatory diseases such as AD. In " Role of macrophages in the pathogenesis of atopic dermatitis, " S. Kasraie and T. Werfel highlight the new …