Commission 10: Solar Activity

Commission 10 aims at the study of various forms of solar activity, including networks, plages, pores, spots, fibrils, surges, jets, filaments/prominences, coronal loops, flares, coronal mass ejections (CMEs), solar cycle, microflares, nanoflares, coronal heating etc., which are all manifestation of the interplay of magnetic fields and solar plasma. Increasingly important is the study of solar activities as sources of various disturbances in the interplanetary space and near-Earth “space weather”. Over the past three years a major component of research on the active Sun has involved data from the RHESSI spacecraft. This review starts with an update on current and planned solar observations from spacecraft. The discussion of solar flares gives emphasis to new results from RHESSI, along with updates on other aspects of flares. Recent progress on two theoretical concepts, magnetic reconnection and magnetic helicity is then summarized, followed by discussions of coronal loops and heating, the magnetic carpet and filaments. The final topic discussed is coronal mass ejections and space weather. The discussions on each topic is relatively brief, and intended as an outline to put the extensive list of references in context. The review was prepared jointly by the members of the Organizing Committee, and the names of the primary contributors to the various sections are indicated in parentheses

A Convenient Model of Severe, High Incidence Autoimmune Gastritis Caused by Polyclonal Effector T Cells and without Perturbation of Regulatory T Cells

Autoimmune gastritis results from the breakdown of T cell tolerance to the gastric H+/K+ ATPase. The gastric H+/K+ ATPase is responsible for the acidification of gastric juice and consists of an α subunit (H/Kα) and a β subunit (H/Kβ). Here we show that CD4+ T cells from H/Kα-deficient mice (H/Kα−/−) are highly pathogenic and autoimmune gastritis can be induced in sublethally irradiated wildtype mice by adoptive transfer of unfractionated CD4+ T cells from H/Kα−/− mice. All recipient mice consistently developed the most severe form of autoimmune gastritis 8 weeks after the transfer, featuring hypertrophy of the gastric mucosa, complete depletion of the parietal and zymogenic cells, and presence of autoantibodies to H+/K+ ATPase in the serum. Furthermore, we demonstrated that the disease significantly affected stomach weight and stomach pH of recipient mice. Depletion of parietal cells in this disease model required the presence of both H/Kα and H/Kβ since transfer of H/Kα−/− CD4+ T cells did not result in depletion of parietal cells in H/Kα−/− or H/Kβ−/− recipient mice. The consistency of disease severity, the use of polyclonal T cells and a specific T cell response to the gastric autoantigen make this an ideal disease model for the study of many aspects of organ-specific autoimmunity including prevention and treatment of the disease

Plasmacytoid Dendritic Cells Provide Protection Against Bacterial-Induced Colitis

We have examined the influence of depleting plasmacytoid dendritic cells (pDC) in mice on the immune response to the gut pathogen Citrobacter rodentium, an organism that is a model for human attaching effacing pathogens such as enterohaemorraghic E. coli. A significantly higher number of C. rodentium were found in mice depleted of pDC from 7 days after infection and pDC depleted mice showed increased gut pathology and higher levels of mRNA encoding inflammatory cytokines in the colon upon infection. pDC-depletion led to a compromising of the gut mucosal barrier that may have contributed to increased numbers of C. rodentium in systemic organs. pDC-depleted mice infected with C. rodentium suffered substantial weight loss necessitating euthanasia. A number of observations suggested that this was not simply the result of dysregulation of immunity in the colon as pDC-depleted mice infected intravenously with C. rodentium also exhibited exacerbated weight loss, arguing that pDC influence systemic immune responses. Overall, these data indicate that pDC contribute at multiple levels to immunity to C. rodentium including control of bacterial numbers in the colon, maintenance of colon barrier function and regulation of immune responses to disseminated bacteria

IFNs Modify the Proteome of <i>Legionella</i>-Containing Vacuoles and Restrict Infection Via IRG1-Derived Itaconic Acid

Macrophages can be niches for bacterial pathogens or antibacterial effector cells depending on the pathogen and signals from the immune system. Here we show that type I and II IFNs are master regulators of gene expression during Legionella pneumophila infection, and activators of an alveolar macrophage-intrinsic immune response that restricts bacterial growth during pneumonia. Quantitative mass spectrometry revealed that both IFNs substantially modify Legionella-containing vacuoles, and comparative analyses reveal distinct subsets of transcriptionally and spatially IFN-regulated proteins. Immune-responsive gene (IRG)1 is induced by IFNs in mitochondria that closely associate with Legionella-containing vacuoles, and mediates production of itaconic acid. This metabolite is bactericidal against intravacuolar L. pneumophila as well as extracellular multidrug-resistant Gram-positive and -negative bacteria. Our study explores the overall role IFNs play in inducing substantial remodeling of bacterial vacuoles and in stimulating production of IRG1-derived itaconic acid which targets intravacuolar pathogens. IRG1 or its product itaconic acid might be therapeutically targetable to fight intracellular and drug-resistant bacteria

United We Stand, Divided We Fall: Historical Trajectory of Strategic Renewal Activities at Scandinavian Airlines System, 1946-2012

Although the second half of the twentieth century saw the rise and fall of ‘multi-flag companies’ in the civil aviation industry, our understanding of how some managed to buck the trend and achieve longevity remains limited. This paper advances business history and strategic management research by examining the strategic renewal activities of Scandinavian Airlines (formerly Scandinavian Airlines System) during the period 1946-2012. The study sheds light on the key roles of private and state owners, rivals as well as banks, in critical financial phases are discussed in terms of longevity in the company. The longevity of the business stems from the leaders’ ability to develop as anticipated and respond to change in their competitive arena in close interaction with the owners. Thus, incumbent firms that strategically renew themselves prior to or during market reform, such as deregulation, enhance their chances of developing the size of their networks and revenue streams. Our main contribution to business history and strategic management literatures is the development of context-specific stages, which shed light on the evolution of strategic renewal activities and shifts from older processes and routines towards customer service and efficiency

Immune control of Legionella infection: an in vivo perspective

Legionella pneumophila is an intracellular pathogen that replicates within alveolar macrophages. Through its ability to activate multiple host innate immune components, L. pneumophila has emerged as a useful tool to dissect inflammatory signalling pathways in macrophages. However the resolution of L. pneumophila infection requires multiple cell types and abundant cross talk between immune cells. Few studies have examined the coordination of events that lead to effective immune control of the pathogen. Here we discuss what is known about L. pneumophila interactions with macrophages and dendritic cell subsets and highlight the paucity of knowledge around how these interactions recruit and activate other immune effector cells in the lung

A method for quantifying pulmonary <it>Legionella pneumophila</it> infection in mouse lungs by flow cytometry

Abstract Background Pulmonary load of Legionella pneumophila in mice is normally determined by counting serial dilutions of bacterial colony forming units (CFU) on agar plates. This process is often tedious and time consuming. We describe a novel, rapid and versatile flow cytometric method that detects bacteria phagocytosed by neutrophils. Findings Mice were infected with L. pneumophila via intratracheal or intranasal administration. At various times after bacteria inoculation, mouse lungs were harvested and analysed concurrently for bacterial load by colony counting and flow cytometry analysis. The number of L. pneumophila-containing neutrophils correlated strongly with CFU obtained by bacteriological culture. Conclusions This technique can be utilised to determine pulmonary bacterial load and may be used in conjunction with other flow cytometric based analyses of the resulting immune response.</p

A major linkage region on distal chromosome 4 confers susceptibility to mouse autoimmune gastritis.

Although much is known about the pathology of human chronic atrophic (type A, autoimmune) gastritis, its cause is poorly\ud understood. Mouse experimental autoimmune gastritis (EAG) is a CD41 T cell-mediated organ-specific autoimmune disease of the\ud stomach that is induced by neonatal thymectomy of BALB/c mice. It has many features similar to human autoimmune gastritis.\ud To obtain a greater understanding of the genetic components predisposing to autoimmune gastritis, a linkage analysis study was\ud performed on (BALB/cCrSlc 3 C57BL/6)F2 intercross mice using 126 microsatellite markers covering 95% of the autosomal\ud genome. Two regions with linkage to EAG were identified on distal chromosome 4 and were designated Gasa1 and Gasa2. The\ud Gasa1 gene maps within the same chromosomal segment as the type 1 diabetes and systemic lupus erythematosus susceptibility\ud genes Idd11 and Nba1, respectively. Gasa2 is the more telomeric of the two genes and was mapped within the same chromosomal\ud segment as the type 1 diabetes susceptibility gene Idd9. In addition, there was evidence of quantitative trait locus controlling\ud autoantibody titer within the telomeric segment of chromosome 4. The clustering of genes conferring susceptibility to EAG with\ud those conferring susceptibility to type 1 diabetes is consistent with the coinheritance of gastritis and diabetes within human\ud families. This is the first linkage analysis study of autoimmune gastritis in any organism and as such makes an important and novel\ud contribution to our understanding of the etiology of this disease