Thematic Focus Section
In addition to regular papers, every issue of the journal has a special section
with a thematic focus. Contributions to these special topic sections are highly welcome and
authors are asked to contact the Editors-in-Chief or the responsible section editors (see below) before
submitting a manuscript in order to avoid clashes with other pending papers. Planned Thematic Focus Topics Thematic Focus Sections in Production Published Thematic Focus Sections Planned Thematic Focus Topics Innate Immunity in Atherosclerosis
Editors: Harry Björkbacka (harry.bjorkbacka@med.lu.se) and Jan Nilsson (jan.nilsson@med.lu.se) Atherosclerosis is a chronic inflammatory disease of the arteries that is the underlying cause of most cardiovascular diseases, including coronary artery disease, myocardial infarction and stroke. Innate immunity plays important roles in the atherosclerotic disease process starting from the earliest events of endothelial cell expression of adhesion molecules, chemokine release and monocyte recruitment, to the complex cellular interactions in the mature lesion. Pattern recognition receptors, including Toll-like receptors and scavenger receptors, play pivotal roles in the development of the disease. Although the precise etiology of atherosclerosis remains to be fully elucidated, it is likely that endogenous molecules, formed during hyperlipidemia, lipid accumulation and oxidative modification of lipids retained in the vessel wall, can act as danger signals that activate innate immune responses. Importantly, exogenous microbes can amplify, accelerate and modulate the disease process by activation of innate immune receptors. Studies have shown that disruption of inflammatory mediators and deletion of key innate immune components can reduce atherosclerosis burden. This makes targeting the innate immune system a candidate for future therapies directed against atherosclerosis. Components of the innate immune system have also been proposed as potential biomarkers to follow the disease process.
This theme issue will focus on how innate immunity shapes the development of atherosclerosis. Apoptosis, Cell Death and Inflammation
Editor: Véronique Witko-Sarsat (veronique.witko@inserm.fr) In this issue, apoptosis of inflammatory cells and their subsequent clearance by professional phagocytes or by bystander cells, will be discussed. This is a key event in the resolution of inflammation. For instance, the life span of neutrophils must be strictly regulated. Delayed neutrophil apoptosis is beneficial for pathogen elimination while apoptosis on the other hand is necessary to prevent release of cytotoxic content from activated neutrophils at sites of inflammation. Interestingly, apoptosis of inflammatory cells can be triggered and in other ways modulated by pathogens, which add another level of complexity to the regulation of apoptosis.
Recognition of apoptotic cells by macrophages triggers an anti-inflammatory response. The ability of macrophages to recognize ligands on apoptotic cells, respond appropriately, and engulf these cells is an important event in host defence, which could predispose to development of autoimmunity if dysregulated. Engulfment of apoptotic cells by macrophages, also called "efferocytosis", is a process that confers an anti-inflammatory phenotype to macrophages conducing to resolution of inflammation. "SIRS" and "CARS" in sepsis
Editors: Tom van der Poll (t.vanderpoll@amc.uva.nl) and Joost C.M. Meijers (j.c.meijers@amc.uva.nl) Sepsis represents 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 have survived 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"). The timing of the first occurrence of immunosuppression in
sepsis is a matter of debate: whereas some investigators favour the subsequent initiation of an hyperinflammatory and anti-inflammatory response, others have suggested that immunosuppression is a primary rather than a compensatory response of sepsis. In this theme issue several aspect related to SIRS and CARS in sepsis will be discussed, including the inflammatory pathways that contribute to tissue damage and organ failure (including the cytokine network, the complement system and coagulation), and the anti-inflammatory mechanisms that have been implicated in sepsis pathogenesis (including immune cell apoptosis, inhibition of Toll-like receptor signalling and
reprogramming of gene expression). Pathogens versus Host Phagocyte Defenses
Editor: Victor Nizet (vnizet@ucsd.edu) A critical first-line element of mammalian innate immunity is the function of phagocytic cells, such as neutrophils and
macrophages. The effectiveness of these specialized leukocytes in host defense reflects their capacity for directed migration, microbial uptake, and direct intra- and extracellular microbial killing – the latter achieved through the concerted action of reactive oxygen species, enzymatic proteolysis, and cationic antimicrobial peptides. Stimulated phagocytes also amplify inflammatory and immune responses through the release of cytokines, nitric oxide and vasoactive peptides.
Their general importance is further exemplified by the increased susceptibility of patients to invasive bacterial infection when phagocyte numbers are markedly reduced. However, it is also apparent that several leading bacterial pathogens such as Staphylococcus aureus, Streptococcus pyogenes and others are capable of causing severe invasive infections, even in previously healthy individuals. Such intrinsic disease-producing capacity defines a superior ability of these pathogens to resist host phagocytic clearance, through the expression of virulence determinants that interfere with phagocyte trafficking or opsonophagocytosis, or instead neutralize the action of the molecular effectors of phagocyte killing. This special issue focuses on the elucidation of
new virulence factors or innate defense pathways that together determine the outcome of the pathogen-host encounter. Thematic Focus Sections in Production Innate Immunity and Airway Inflammation
to be published in Vol. 2, No. 2, 2010; February 2010
Editor: Marc A. Williams ·Summary Ficolins in Innate Immunity
to be published in Vol. 2, No. 1, 2010; December 2009
Editor: Niels Borregaard and Peter Garred ·Summary Published Thematic Focus Sections NADPH Oxidases in Innate Immunity
Vol. 1, No. 6, 2009; October 2009
Editor: Gary Bokoch ·Summary ·Articles (Table of Contents) Innate Immunity in Viral Infections
Vol. 1, No. 5, 2009; August 2009
Editor: Carol Shoshkes Reiss ·Summary ·Articles (Table of Contents) Invertebrate Immunity
Vol. 1, No. 4, 2009; June 2009
Editor: Ulrich Theopold and David Schneider ·Summary ·Articles (Table of Contents) Neutrophil Extracellular Traps
Vol. 1, No. 3, 2009; April 2009
Editor: Eva Medina ·Summary ·Articles (Table of Contents) Corruption of Innate Immunity by Bacterial Proteases
Vol. 1, No. 2, 2009; January 2009
Editor: Jan Potempa ·Summary ·Articles (Table of Contents)
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