European economist raises 'green growth' strategy as deficit solution

February 9, 2012

A solution to the global financial crisis may be in the hands of economists – notably those like Carlo Jaeger of the Potsdam Institute for Climate Impact Research (PIK) – who are embracing a bold economic model designed around green growth.

Jaeger, who has a joint appointment at the University of Potsdam and chairs the European Climate Forum, is at Arizona State University this winter as the Julie Wrigley Visiting Senior Scholar at the School of Sustainability. He has been interacting with ASU sustainability scientists, faculty members and students to discuss research on how a green growth strategy to address the global financial crisis can bring about transformational changes. Carlo Jaeger of the Potsdam Institute for Climate Impact Research (PIK) Download Full Image

“Green growth, in my view, is an economic dynamic by which you get higher growth than you would have otherwise and with fewer emissions,” explained Jaeger.

“The experience of the global financial crisis shows that the existing economic models were seriously limited. Against this background, a fundamental overhaul of European climate policy models is required,” wrote Jaeger and other co-authors of the 2011 study “A New Growth Path for Europe.” The study, commissioned by the German Federal Ministry for the Environment, Nature Conservation and Nuclear Safety, asserted that to identify and assess options for climate policy, models are needed “that meet the challenges exposed by the financial crisis.”

“For example, the models that were state-of-the-art before the crisis assumed that economic systems have a single stable equilibrium. Studies based on this kind of model imply that reducing greenhouse gas emissions creates extra costs in the coming years in order to avoid damages in the distant future – thereby win-win strategies are excluded by construction,” noted the report.

“A key problem of climate policy is, however, to balance the short-term view of businesses with the much longer-term view required by policy-makers aware of climate change. The financial crisis has exposed the fact that different expectations can lead to different investment behaviors, turning those expectations into sell-fulfilling prophecies,” wrote Jaeger and the co-authors. “Research has now started to take this into account in models used for policy advice.”

In a column published on the online Economists’ Forum of the Financial Times last fall, Jaeger focused on European financial instability. “Public debt is not the cause of financial turmoil in the eurozone,” he wrote

“What happened in Europe was that countries in its industrial core achieved massive export surpluses by combining high labour productivity with stagnant wages. The resulting revenues led to huge capital flows into peripheral countries that at the same time experienced matching export deficits. In the financial crisis, these capital flows came to a sudden stop,” he noted in the Oct. 24, 2011, column.

“Potential investors saw insufficient demand for the products of entrepreneurial investments and preferred to park their money at near-zero interest rates.”

A solution, according to Jaeger, is a green growth strategy. In his column he argued: “Potential investors must be faced with the prospect of sustainable growth and robust demand for their products. Retrofitting the built environment, building new power grids for renewable energy, renewing Mediterranean forests, developing new transport systems – these are examples of the initiatives that can turn the animal spirits of investors around.”

While he acknowledged that his work started in Europe, Jaeger is also looking at what transformational strategies would look like in America.

“The financial crisis has been handled to avoid disaster, but now we have serious unemployment and insufficient growth. The need for transformational changes is high in America and I hope ASU can play a leading role in a strategy to fix this current predicament,” Jaeger said.

During one of his lectures on ASU’s Tempe campus titled “Global Financial Crisis: is Green Growth the Answer?” Jaeger said it is possible in five years to turn the government deficit into a surplus, “if you have high growth.”

“But we do not have high growth. So, what needs to be done, is first to get the economy growing again. I’m arguing that with a green growth agenda you can focus investors’ minds on the line of investment where there are opportunities, where there is a need, and once you get growth going, then you reduce the deficit,” he said.

“But, trying to do this the other way around means we stay in a slump for a long time,” said Jaeger, who acknowledged there is much ongoing work in constructing new models in climate economics, which are built on existing models.

“It is crucial to take an existing model and modify it so we can study key aspects of desirable changes,” said Jaeger, who has a doctorate in economics from Goethe University in Frankfort, Germany, and a master’s degree in sociology from the University of Bern.

“Carlo Jaeger is a true visionary who has developed this very interesting model about how in this century we could change our environment and our society worldwide into a sustainable and more equitable one,” said Sander van der Leeuw, dean of ASU’s School of Sustainability

“His model is having considerable impact in Germany and in Europe more widely,” said van der Leeuw. “While at ASU, Professor Jaeger has met with faculty and students and presented a series of lectures on global system dynamics and policy. He is one of two senior fellows we have at ASU this year to engage with our sustainability scholars and students.” The other is Wallace “Wally” Broecker, the Newberry Professor of Earth and Environmental Sciences at Lamont-Doherty Earth Observatory at Columbia.

Secrets of immune response illuminated in new study

ASU researcher Roy Curtiss investigates the coordination of a particular type of immune response, involving the release of a cell-signaling protein molecule known as a cytokine.

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Secrets of immune response illuminated in new study

February 9, 2012

When disease-causing invaders like bacteria infect a human host, cells of various types swing into action, coordinating their activities to address the threat. Download Full Image

In new research appearing in this month’s issue of the journal Nature Immunology, Roy Curtiss, director of the Center for Infectious Diseases and Vaccinology at the Biodesign Institute at Arizona State University, along with international collaborators, investigates the coordination of a particular type of immune response, involving the release of of IFN-γ— a cell-signaling protein molecule known as a cytokine.

Molecules like IFN-γ have long been recognized as vital weapons in the immune system’s arsenal against viral, bacterial and parasitic pathogens, as well as tumors. They are known as interferons—named for their ability to interfere with the functioning or replication of infectious agents. Communication between cells enabled by interferons can trigger the protective defenses of the immune system, which will attempt by various means to eradicate the infectious pathogen.

“The inception of this study was based on studies conducted in collaboration with the Richard Strugnell group at the University of Melbourne when it was shown that flagella produced by S. Typhimurium—and especially by a mutant generated by Shifeng Wang in our group, that hyper produced the flagellin—were superior in inducing a cascade in host cells leading to the production of NFκB,” a protein complex that plays a key role in regulating the immune response to infection.

The cytokine IFN-γ is produced by a type of lymphocyte known as a memory CD8⁺ T cell. Memory T cells are a vital part of the adaptive immune system. Typically, they are activated and induced to proliferate when they come in contact with a specific antigen produced by the infectious agent and recognized by the T cell’s antigen receptor. After their initial encounter with the unfamiliar invader, memory T cells survive in the host in an inactive state, “remembering” the cognate antigen to which they are related. Should they re-encounter this antigen, they can speedily mount a response, liberating IFN-γ.

An understanding of how IFN-γ release is regulated and the complex pathways involved in the production of this key cytokine remains incomplete. The current study demonstrates that the release of IFN-γ by memory T cells can also occur without the activation of these cells by direct contact with the disease antigen. In this way, memory CD8⁺ T cells also contribute to the host’s innate immune response.

The mechanism for this antigen-independent immune response is the focus of the current study. The team’s results significantly advance the understanding of such pathways and their subtle regulation, and may stimulate new biomedical approaches to interfering with and disabling disease-causing intruders.

In the new study, the group found that the antigen-independent production of IFN-γ by memory T cells relies on another cell type, known as splenic dendritic cells. Such cells contain so-called NOD-like receptors (NLRs). The NLR’s are able to sniff out pathogen-associated molecular patterns. When they sense these distinctive patterns, the NLRs sound the alert.

While their more familiar cousins, the TOLL-like receptors, sense pathogen-associated molecular patterns in the extracellular space, NLRs sense pathogenic traces in the intracellular compartments. Further, once NLR’s have successfully detected their target, they assemble large protein complexes in the dendritic cell, known as inflammasomes.

In the case of bacterial invasion, the NLR inside the splenic dendritic cell is triggered when it senses flagellin—a protein associated with bacterial flagellum. The NLR then assembles the inflammasome complex, which produces two key pro-inflammatory interleukins—IL-1 and IL-18. It is the second of these that will migrate from the dendritic cell to the memory CD8⁺ T cell, triggering the release of IFN-γ. Figure 1 graphically describes this process.

In the current study, antigen-independent secretion of IFN-γ by memory CD8⁺ T cells was demonstrated in mice infected with the intracellular pathogen Salmonella Typhimurium. The response could be detected as soon as 2 hours post-infection—the NOD-like receptors representing the earliest response to pathogenic invasion. Further, by using strains of S. Typhimurium deficient in flaggelin, the group showed impaired IFN-γ secretion by CD8⁺ T cells.

Intriguingly, the group also found a robust IFN-γ response when dendritic cells were presented with heat-killed S. Typhimurium or even with the injection of purified flaggelin alone—powerful evidence that the dendritic cell inflammasome assembled by the NOD-like receptor’s sensing of flaggelin was sufficient to induce IFN-γ production in memory CD8⁺ T cells. This flaggelin-induced response was also demonstrated for two other pathogens: Yersinia and Pseudomonas.

The study also confirmed the hypothesis that production of IL-18 in dendritic cells, following inflammasome formation, generated the production of IFN-γ by attaching to a specific receptor-adaptor on the memory CD8⁺ T cells, which the group identified. The authors speculate that a particular inflammasome known as NAIP5 in splenic dendritic cells is responsible for sensing flaggelin and initiating the cascade of events leading to IFN-γ production in CD8⁺ T cells.

Previous research had suggested a mechanism for S. Typhimurium to transfer flagellin into the cell from the extracellular medium, through the pathogen’s specific secretion system. This is considered critical, as many bacteria are non-pathogenic and indeed, important to the host. An inflammasome response to these so-called commensal bacteria could therefore have disastrous consequences, triggering an inappropriate auto-immune response.

Experiments also demonstrated that not all bacterial flagellins are recognized by the inflammasomes—E. coli flagellins, for example, are not. The reasons for this have yet to be fully explored. The team further speculates that the inflammasome system and its NOD-like receptors may have evolved not only to deal with pathogenic invaders but to carefully regulate the balance of commensal bacteria, keeping populations of healthy microbes in check.

The study was the fruit of a multi-institute collaboration, co-authored by researchers from Department of Microbiology and Immunology, The University of Melbourne, Australia; Department of Biochemistry, University of Lausanne, Epalinges, Switzerland; Department of Infectious Diseases & Pulmonary Medicine, Charité University Hospital, Berlin, Germany and the Ludwig Institute of Cancer Research, Heidelberg, Australia.

As Curtiss explains, the group’s research findings lay the groundwork for future investigation: “We are now incorporating the findings from the current study to design a superior recombinant attenuated Salmonella vaccine strain with greatly enhanced ability to induce a CD8-dependent cellular immunity against viral, parasitic and bacterial pathogens in which a CD8 response is critical for successful control.”

In addition to his appointments at the Biodesign Institute, Roy Curtiss is a professor in the College of Liberal Arts and Sciences, School of Life Sciences.