Title: A Summing-Up of 2010 in the <i>Journal of Innate Immunity</i>
Abstract: During 2010, the second year of the Journal of Innate Immunity, the journal has continued to reflect a broad spectrum of research in this dynamic and rapidly expanding field. To achieve some focus, special topic sections have been assigned to each issue. We are happy that several prominent scientists agreed to engage themselves, compiling these theme issues. We would like to take this opportunity to highlight some of the articles.
In the first issue appearing in 2010, the special topic was ficolins (Editors: Niels Borregaard and Peter Garred). Ficolins belong to the collectin family of proteins, constituting an ancient and important part of innate immunity. Ficolins can bind conserved pathogen-associated molecular patterns on the surface of microbes. This binding may result in the activation of collectin receptor-bearing immune cells or the activation of complement via the lectin pathway described in a review by Matsushita [1]. In the same issue, Endo et al. [2] presented a research article where they showed that the lectin pathway, not least mannose-binding lectin, collaborates with coagulation. Airway inflammation (Editor: Marc A. Williams) was covered in the second issue. In a review, Eisen [3] discussed aspects of how MBL deficiency affects our ability to stay healthy and combat respiratory tract infections. In the same issue, Williams et al. [4] demonstrated a critical role for Muc1 during dendritic cell recognition of pathogen-associated molecular patterns by Toll-like receptors.
In addition to necrosis, recent years have advanced our understanding of how inflammation is regulated by other forms of cell death in immune cells, such as apoptosis and pyroptosis. In the third issue, apoptosis, cell death, and inflammation (Editor: Veronique Witko-Sarsat) were discussed in a series of articles. In a review, Fox et al. [5] discussed the physiological regulation of neutrophil apoptosis with respect to the innate immune system and highlighted recent advances in the mechanistic understanding of apoptotic pathways and their therapeutic manipulation in both appropriate and dysregulated innate immune responses. Cystic fibrosis is a disease where increasing attention is paid to key pathophysiological roles of neutrophils. A mechanism explaining the abundance of neutrophils in cystic fibrosis patients by delayed apoptosis was presented in a research article by Moriceau et al. [6].
The view on pathophysiologic mechanisms in atherosclerosis has since long focused on metabolic and physiological factors. However, in recent years major attention has been focused on innate immunity playing important roles in the atherosclerotic disease process from the earliest events of the endothelial cell expression of adhesion molecules, chemokine release, and monocyte recruitment, to the complex cellular interactions in the mature lesion. In the theme issue discussing atherosclerosis (Editors: Harry Bjorkbacka and Jan Nilsson) an emerging role for the Th17 concept was reviewed by Chen et al. [7]. In a research article, Hayashi et al. [8] showed that TLR2 is a key player in the inflammatory response, induced by the oral pathogen Porphyromonas gingivalis, leading to atherosclerosis.
Sepsis is a major health problem. Until very recently the prevailing concept of the pathogenesis of sepsis has been that mortality is the consequence of an uncontrolled, hyperinflammatory, predominantly cytokine-mediated response of the host, a reaction referred to as systemic inflammatory response syndrome (SIRS). However, evidence has accumulated that patients who survive the initial phase of sepsis have features consistent with immunosuppression characterized by a systemic anti-inflammatory phenotype referred to as compensatory anti-inflammatory response syndrome (CARS). In the special topic section SIRS and CARS in sepsis (Editors: Tom van der Poll and Joost C.M. Meijers), McCall et al. [9] discussed epigenetic processes of innate immune cells during serious infections with systemic inflammation in 4 stages: homeostasis, incitement, evolution, and resolution. In the same issue, Hoogerwerf et al. [10], having investigated the regulation of pro- and antiapoptotic genes in septic patents, concluded that the alterations in the apoptosis of circulating leukocytes occur in a cell-specific manner.
Recently, hitherto uncharacterized virulence factors have been shown to affect innate defense pathways. These interactions determine the outcome of the pathogen-host encounter, not least in neutrophils and macrophages. This topic was covered in the special topic sectionbacterial pathogens versus host phagocyte defenses (Editor: Victor Nizet). Neutrophils can, upon appropriate stimulation, release DNA that immobilizes antibacterial polypeptides, so-called NETs. In a research article, Berends et al. [11] showed that Staphylococcus aureus can escape the antibacterial activity of NETs by releaseing a DNA-degrading nuclease. In a very interesting study, Kobayashi et al. [12] showed that S. aureus can induce programmed necrosis in neutrophils following phagocytosis, a mechanism that may contribute to the enhanced virulence of this bacterium.
Needless to mention, many additional high-quality reviews and original research articles have been published but were not included in the special topic sections. We are eager to watch the continued development of the Journal of Innate Immunity, starting with an exciting 2011. We would also like to thank all contributing authors and reviewers for maintaining a high quality of published articles.