Tag Archives: IKM

A new mechanism explaining the anti-inflammatory effect of HDL is revealed



Bloggers: Nathalie Niyonzima and Eivind Samstad




Atherosclerosis is a progressive disease that was once believed to be a disease of cholesterol storage. Today, it is well acknowledged that atherosclerosis is an inflammatory disease, and that cells and signalling molecules from the innate immune system shape the course of the disease in various ways. The defence of the normal artery depends on innate immune responses provided by endothelial cells. When challenged by inflammation, macrophages and other cells of the immune responses are recruited to the artery wall. The macrophage is an integral component to the pathogenesis of atherosclerosis, functioning at the intersection of inflammation and cholesterol homeostasis. Atherosclerotic plaque formation is driven by the persistence of lipid-laden macrophages in the artery wall. The mechanisms by which these cells become trapped, and thereby establishing chronic inflammation, remain unknown (Peter Libby, Nature 2011).


Atherosclerosis. Illustration: iStock

There has long been a focus on finding therapeutic methods to reduce the levels of cholesterol in the arterial wall. Studies have shown that high HDL levels are associated with reduced cardiovascular risk. This is mainly due to HDL’s ability to transport excess cholesterol in arterial macrophages to the liver for excretion (i.e., reverse cholesterol transport). Despite considerable understanding of HDL and its metabolism, therapies that aim to increase HDL levels have not been successful. Because of the heterogeneity in HDL particles, just increasing HDL levels has not been beneficial, reflecting the qualitative changes in the particles. HDL has also been shown to have other functions beyond cholesterol transport – several studies have shown that HDL is anti-inflammatory, but the mechanisms behind this are not well understood (Xuewei Zhu, Ann.Rev.Nutr 2012).

In a recent study published in the prestigious journal Nature Immunology, our research partners have taken a closer look at the anti-inflammatory effects of HDL (De Nardo, et.al, Nature 2013). They identified that HDL’s anti-inflammatory effects are mediated through the induction of ATF3. ATF3 is a key transcriptional regulator of innate immune response genes, which is induced by TLR stimulation and other stimuli, and acts as negative regulator of proinflammatory cytokines (Elisabeth S.Gold, JEM 2012).

Using mouse model and human bone marrow dendritic cells (BMDMs) treated with native HDL or reconstituted HDL prior to TLR stimuli; they showed that HDL regulates inflammation in macrophages by inhibiting transcription of proinflammatory genes such as IL-1β, IL-6 and IL-12.

In order to confirm that the anti-inflammatory effects of HDL were mediated through an inflammatory repressor, they performed microarray analysis on resting BMDMs and HDL-pretreated BMDMs subsequently stimulated with TLR ligand. ATF3 was the most induced transcription factor in the presence of HDL, and it was shown to bind to the promoters of several proinflammatory genes, thereby regulating inflammation.

They demonstrated the relevance of these findings by using Apoe-deficient mice fed a high-fat diet and injected with HDL. They observed that mice treated with HDL had lesser inflammation than the untreated ones, and that the induction of ATF3 correlated with the downregulation of proinflammatory cytokines.

Besides promoting cholesterol efflux from macrophages, HDL has been shown to protect endothelial integrity by promoting endothelial repair mechanisms. Using a model of vascular repair, they showed that the protective effects of HDL on endothelial repair are for the most part driven by ATF3.

These results provide us a link between HDL and its anti-inflammatory properties that has been a puzzle over long time. The fact that ATF3 is required for the anti-inflammatory effects of HDL shows that ATF3 is a key point for endothelial damage and inflammation. The current study has laid the foundation for understanding the regulatory mechanisms that control inflammation in atherosclerosis and other chronic inflammatory diseases.

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CEMIR recruits more researchers

Kari HålandBlogger: Kari Håland





Centre of Molecular Inflammation Research (CEMIR) keeps growing and is entering its second year with plans for increased research activity and more positions.

CEMIR was established on 1. January 2013 as part of the Research Council of Norway’s third round of Centres of Excellence (SFFs). CEMIR’s vision is to find out how sensors in the immune system initiates and regulates inflammatory responses. This new knowledge will be used in disease models to identify new therapeutic targets and diagnostic tools for inflammatory diseases.

Celleforskning. Foto: Geir Mogen

Trude Helen Flo with colleague Jane Awuh. (Photo: Geir Mogen)

This spring, CEMIR is recruiting for several research positions: 3 Post Docs, 2 PhD positions and 1 Staff Engineer. The Post Doc positions have now been announced.

“When CEMIR announced similar positions in 2013, we saw 220 applications,” says Director Terje Espevik. “This gives us a great opportunity to choose the best researchers and to find the most promising research talents.”

CEMIR moved into the new Kunnskapssenteret at Øya Campus in Trondheim in 2013. “We have excellent premises with plenty of room for our employees. The colocation of the centre gives us an excellent basis for establishing a unified milieu, and for cooperation and the exchange of ideas across the research groups,” Espevik says. “At the same time we remain close to the Department (the Department of Cancer Research and Molecular Medicine) in the neighbouring Gastrosenteret, which makes it easy to cooperate both organisationally and translationally.”

As part of becoming a centre, CEMIR has introduced several fixed meeting points bringing together the researchers at the centre. This includes weekly seminars and an article club where the aim is the share knowledge and to get feedback in terms of potential improvements or new research ideas from other colleagues at the centre. The SFF consist of research groups from various related subject fields, and there is no doubt that such close cooperation and exchange of ideas is beneficial.

“We look forward to having even more talented people that will contribute to the knowledge in our field. We constantly discover new research questions that we would like to explore further,” Espevik says.

A central question to CEMIR’s research is how inflammation can be so closely connected to many seemingly different chronic diseases. CEMIR’s research programme has a hypothesis that the key to new therapeutic targets for chronic inflammatory diseases can be found in the early stages of the inflammatory response where sensors in the innate immune system are activated.

The announced Post Docs are in the following areas:

  • Inflammation and Bone Disease. Project leader: Therese Standal, therese.standal@ntnu.no
  • Inflammation in Pregnancy. Project leader: Ann-Charlotte Iversen, ann-charlotte.iversen@ntnu.no
  • Host-pathogen Interactions in Mycobacterial Infection. Project leader: Trude Helen Flo, trude.flo@ntnu.no

Full job descriptions and more information can be found at the recruitment site Jobbnorge:

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Looking for the perfect immune response


Blogger:Trude Helen Flo, co-director CEMIRtrude_helen_flo_FotografGei

The Research Council of Norway has recently awarded grants under the funding scheme Independent Basic Research Projects – Medicine, Health Sciences and Biology (FRIMEDBIO). There is tough competition for this funding nationally, and only the best projects get through. The Faculty of Medicine, NTNU, has been awarded funding for three talented young researchers, three research projects and two post docs. You can read about all these projects on the blog over the coming weeks. Trude Helen Flo and her colleagues at CEMIR were awarded funding to their research project: New Principles of mycobacterial killing in host macrophages (MycoHosPath).

Mycobacterial infections are a global health problem. Tuberculosis (TB) is caused by a bacterium known as Mycobacterium tuberculosis (Mtb) and kills more than 1.4 million people worldwide each year. Environmental mycobacteria like Mycobacterium avium can cause disease in immunocompromised people like HIV/AIDS patients who are not on anti-retroviral treatment. Mycobacterial infections require long treatment with antibiotics and drug resistance is emerging. Thus we need new drugs and vaccines in order to reach the UN millennium goal of eradication of tuberculosis.

To discover new therapeutic targets we need to learn more about the mycobacterium and how it interacts with its human host.


Mycobacterium tuberculosis (Mtb) and kills more than 1.4 million people worldwide each year

To discover new therapeutic targets we need to learn more about the mycobacterium and how it interacts with its human host.

Some major scientific and technological advances during the last decade have contributed significantly to progress in the field: studying the genetic makeup of mycobacteria provides clues about how the bacteria may infect and survive in the host. On the other hand, studying genetic variations in humans also provides insights in to how humans may become susceptible to mycobacterial infections.

Major breakthroughs in how our first line of defense, the innate immune response, can discriminate between different pathogens and shape the following second line of defense, the adaptive immune response, was awarded the 2011 Nobel Prize in Medicine. The adaptive immune response is crucial for the development of immunological memory. Despite these major advances, we still lack a complete understanding of mycobacterial immunity.

TB incidence rates and multidrug-resistant TB cases (click to enlarge image)


The primary research goal of the MycoHosPath project is to identify new principles of mycobacterial killing during acute and chronic infection. We will approach this by studying the interplay between three cellular pathways that are central for killing and intracellular survival of mycobacteria: Phagocytosis, Inflammatory signaling and Autophagy.

Untitled-1Phagocytosis is the process by which bacteria are taken up by innate immune cells like macrophages and dendritic cells. Normally this leads to destruction, but pathogenic mycobacteria have found ways to avoid it.

Autophagy is a similar process used by cells to detect and degrade garbage in their interior, including intracellular pathogens. Understanding how mycobacteria avoid these killing mechanisms and survive within macrophages may aid in discovery of new drug targets.

Inflammatory signaling is the macrophage response to infection. Infected macrophages produce potent molecules to alarm and recruit other immune cells to help clear the infection. Some of these molecules also help the infected cell to directly kill the invading micobes. However, since pathogenic mycobacteria can live in our body for a lifetime, this does not work perfectly. If we can improve our understanding on how a perfect immune response to mycobacteria should look like we could contribute to new vaccine strategies.

The combined processes of phagocytosis, autophagy and inflammatory signaling in host macrophages, and strategies used by the mycobacterium to manipulate them to its own advantage, will influence activation of mycobacterium-specific immune cells that we need to clear the infection and create immunity to further infection.

Our research group studies several of these aspects in the bacterium, in cells isolated from healthy and HIV-infected individuals, and in mouse model systems. As part of SFF-CEMIR we have access to national and international expertise on inflammation research and advanced imaging, state-of-the-art methodologies and new labs in Kunnskapssenteret.

We have also engaged strong national and US collaborators on autophagy and mycobacterial research who will contribute in what we hope will be a successful project. We are looking forward to realizing MycoHosPath next year.

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The tumour’s microenvironment important in breast cancer development

Tonje SteigedalBlogger: Tonje Strømmen Steigedal





Our bodies constantly renew their cells. In healthy individuals this is tightly regulated so that old cells are removed at the same time as new ones are produced. Cancer arises when this regulation gets out of control due to, for example, mutations in the DNA. A tumour consisting of large numbers of cancer cells is formed.

Lungevev fra mus

Lung tissue from mice: Healthy lung cells in blue with metastasis (cancer cells) shown in brown. (Photo: TS Steigedal)

In the environment around the cancer cells there are also many other types of cells that affect how the tumour develops. These cells are called stromal cells and include fibroblasts (connective tissue cells), macrophages (inflammation cells) and endothelium cells (blood vessel cells). Cancer cells can programme the stromal cells to their advantage so that the cancer cells get even better growing conditions.

In addition to cancer cells and stromal cells, there are also many other molecular components in the tumour’s microenvironment. Examples of such proteins include growth factors that stimulate cell division and cytokines that regulate inflammation reactions. In addition there are also large scaffold proteins outside the cells ensuring structure and support to all cells. Without such framework proteins the body would just be a random heap of different types of cells. This type of scaffold is called an extracellular matrix.

Exploiting the environment

Cancer cells exploit the other cells and proteins in the tumour microenvironment to their advantage so that the tumour can grow, divide and eventually spread (metastasise) to other organs. More and more attention is now given to the mapping and understanding of the tumour microenvironment’s composition in connection with cancer development.

Much speaks for the makeup of the tumour microenvironment playing a decisive role in how tumours develop and whether they spread. And perhaps this information could say something about how the tumour will respond to treatment. We now work on characterising tumours’ microenvironment and the goal is to understand how the composition of the microenvironment affects cancer development.

We have used a mouse model of breast cancer which has been modified so that the mice develop breast cancer in a predictable manner. By analysing the tumour microenvironment’s composition in tumours from different stages of cancer, we can say something about how they change throughout the tumour development. We have used advanced methods to map the complete composition of proteins in the tumour microenvironment.


Tumour samples from modified mice models: 1) Low-grade tumour with few cancer cells (red) and very little visible ECM/collagen (blue). White areas are normal fat tissue. 2) Late-stage: invasive, aggressive tumour packed with cancer cells and lots of ECM/collagen. The tumour becomes fibrous and hard. (Photo: TS Steigedal).

New biomarkers for breast cancer?

We now see that some of these proteins also seem to appear in human breast cancer, and we wish to understand what function these proteins have. If we could understand what they mean to the cancer cells, we could perhaps use these proteins as new biomarkers for diagnosis and prognosis, and the goal is also to identify new targets for treatment and therapy of breast cancer.

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Pictures from the CEMIR opening

Today we open our new  Centre of Excellence, CEMIR, Centre of Molecular Inflammation Research. A central topic for the centre is how inflammation can play a part in so many apparently different chronic diseases. Here are some pictures from the opening and the opening seminar.

Mange ville få med seg det spennende seminaret ifm åpningen av CEMIR.

Many wished to participate at the seminar held in connection with the opening of CEMIR.

Fornøyde forskere, fra venstre: nestleder CEMIR, Trude Helene Flo, leder for CEMIR, Terje Espevik, Insituttleder Institutt for kreftforskning og molekylær medisin Magne Børset.

Happy researchers, from the left: Co-Director at CEMIR, Trude Helene Flo, Director of CEMIR, Terje Espevik, Head of the Department of cancer research and molecular medicine, Magne Børset.

Dekan Stig Slørdahl var overlykkelig da han fant ut at begge  søknadene fra Det medisinske fakultet for Senter for Fremragende Forskning gikk gjennom.

Dean Stig Slørdahl was extremely pleased when he found out that both applications for Centres of Excellence from the Faculty of medicine were granted.


Instituttleder Magne Børset sier vi har grunn til å være stolte, og spesielt lederne ved CEMIR, for det nye senteret.

Head of Department Magne Børset says we have reasons to be proud, and especially the leaders of CEMIR, for the new CoE status.



Liv Furuberg from the Research Council of Norway.


Noen av tilbakemeldingene fra ekspertpanelet ifm tildeling av Senter for Fremragende Forskning

Some of the feedback from the panel of experts in connection with the awarding of the CoE status.

Fra presentasjonen til Forskningsrådet.

From the Research Council of Norway’s presentation.


Leder for CEMIR viser at betennelser har betydning for flere sykdommer som fedme, diabetes, alzheimer, allergier og kreft.

The Director of CEMIR shows that inflammation plays a part in several diseases such as obesity, diabetes, Alzheimer’s, allergies and cancer.

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Proteins: The building blocks

In this video, Geir Slupphaug talks about proteins. Nearly all diseases are caused by dysfunctional proteins. At the proteomics and metabolomics core facility they are using advanced mass spectrometry to study proteins in many different diseases. This information can provide a deeper understanding of biological processes at the molecular level, and aid discovery of e.g. novel protein targets for diagnosis and treatment of diseases.


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Filed under Blood, Cancer, Inflammatory and Immune System, NTNUmedicine, Research

Understanding mycobacteria to fight tuberculosis

Tuberculosis kills about 1,5 million people each year and about 1/3 of the world’s population is infected. Trude Flo and the CEMIR research group at NTNU studies the interactions between the bacteria that cause tuberculosis and the immune system of the host. Understanding these interactions is crucial for the development of new vaccines and medicines to treat tuberculosis.

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Understanding myeloma cells to find a better treatment

Kristine Misund and her co-workers at K. G. Jebsen Center for Myeloma Research focus on multiple myeloma which is a special kind of cancer in the bone marrow. This disease is today incurable but the researchers are hoping that their work to understand how the myeloma cells survive in the bone marrow can identify new targets for treatments.


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Why study chronic intestinal inflammation?

Bloggers: Arne Kristian Sandvik og Jan Kristian Damås

For patients with these diseases, and for the health professionals who are involved in their treatment, this question seems misplaced. However, many others perceive these to be rare conditions, and a marginal medical problem.

Chronic intestinal inflammation consists of ulcerative colitis and Crohn’s disease. An international abbreviation for these diseases is IBD, which stands for Inflammatory Bowel Disease.

Stomach ache

This means that 5 out of 1,000 Norwegians at any time suffer from ulcerative colitis or Crohn’s disease. (Photo: istockphoto.com)

While it is true that there are not as many new cases of IBD each year compared to other diseases – perhaps 20 cases per 100,000 people – this number does not fully describe the clinical reality. These are chronic conditions, and although the health impact of the diseases varies from person to person, an individual will normally have a period of 10 to 20 years with active disease. This means that 5 out of 1,000 Norwegians at any time suffer from ulcerative colitis or Crohn’s disease.

We estimate that there are approximately 2.2 million patients in Europe with these diseases. They need medication, surgery and perhaps most often, regular contact with the national health service.

These diseases typically start at a young age, usually in individuals between 15 and 25 years old. One-quarter of all cases are diagnosed by paediatricians. IBD patients are thus affected during what is perhaps the most important part of their lives, when they should be studying, establishing their careers and raising a family.

There is no cure for ulcerative colitis or Crohn’s disease, but there are drugs and other treatments that aim to induce remission and to otherwise reduce the impact of IBD on daily life. Some of the drugs are easy to use and have minimal side effects, others require careful monitoring by experienced clinicians. The cost of drugs for an individual patient varies from about NOK 1000 to well over NOK 100,000 per year. Given all these factors, it is safe to conclude that chronic intestinal inflammation is a major problem for patients and costly for the national health service.

What causes ulcerative colitis and Crohn’s disease? The gut usually tolerates the presence of a wide variety of bacteria without any detrimental inflammation, but in patients with ulcerative colitis and Crohn’s disease, the gut has somehow lost this “tolerance”. This results in an inappropriate inflammatory response, and much of the research in the field is designed to understand why and how this takes place.

The IBD Research Group at NTNU and St. Olavs Hospital/the Central Norwegian Health Authority has been built up over the past few years. The principal investigators are clinical specialists in digestive diseases and also experienced laboratory scientists, and the group is now part of CEMIR and positioned to work in a close collaboration between clinical medicine and advanced molecular inflammation research.

The group has a large biobank of intestinal tissue samples, blood samples and relevant clinical information collected with consent from patients and healthy volunteers. This material has been used to form hypotheses about how the inflammation mechanism is activated in patients with established ulcerative colitis or Crohn’s disease.

Researchers in the project are primarily examining mucosal samples using advanced methods that allow them to detect the activation of all genes in a single tissue sample. The mucosa from patients with IBD contains several thousand activated genes that are potentially important in the inflammatory reaction. The most interesting findings are followed up by doing a microscopic examination of tissue samples, where we can determine the types of cells in which the genes are activated. We can then determine how to best proceed with specific, detailed laboratory studies.

We have already made several important findings from the analyses of these clinical tests, two of which are currently being intensively pursued. One is that we found a little-known group of proteins, the so-called REG proteins, to be strongly activated by intestinal inflammation.

The function of these proteins is almost unknown, but they likely play an important role, since they are upregulated as much as 80 times in the intestinal mucosa of IBD patients. It is conceivable that REG proteins are important in the inflammation and in the repair of damaged mucosa, and even that they have a direct effect on bacteria penetrating the mucus layer.

The second main finding from these studies is that a receptor which is part of the innate immune system, TLR3, appears to be important in the inflammatory process in IBD. TLR3 is found inside the mucosal cells and is stimulated by fragments of genetic material, particularly RNA. This discovery suggests that fragments of genetic material released by inflammation in the intestines can maintain the inflammation. It is also possible that RNA from viruses or other microorganisms in the gut may act via TLR3 to induce an inflammatory process.

All we can learn about the biological mechanisms of IBD, and especially results generated directly from the survey of patient material, is potentially important in working towards an effective treatment of ulcerative colitis and Crohn’s disease.

What do these findings mean for patients with IBD? Right now – nothing. But – the reason we don’t have a cure, or a treatment that controls inflammation in all patients, is that we still do not fully understand the disease process. All we can learn about the biological mechanisms of IBD, and especially results generated directly from the survey of patient material, is potentially important in working towards an effective treatment of ulcerative colitis and Crohn’s disease.


CEMIR_logoThe official opening of the Norwegian University of Science and Technology’s four new centres of excellence (CoE) will take place on Monday 10 June. CEMIR, the Centre of Molecular Inflammation Research, is one of these new centres. CEMIR researchers will study new mechanisms that set off inflammatory responses. We hope this will provide us with information that could help in the development of new treatment methods and the diagnosis of diseases in which inflammation plays a crucial role. You can read more about CEMIR at http://www.ntnu.edu/cemir

In June there will be more blogs from CEMIR researchers.


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Sugar + inflammation = true?

Blogger: Eivind Samstadespevik_fotografGeirMogen-(




The immune system has sensors that recognize invaders such as bacteria and viruses, but also damage to the cells in the body. When the immune system is activated, the result is inflammation, which is designed to remove invaders and repair cell damage. Inflammation is characterized by redness, heat, pain and swelling.

The body has to regulate inflammation carefully, because if the immune system overreacts, the response itself may cause more damage than the actual reason for the reaction. Chronic inflammation is linked to diseases such as atherosclerosis (hardening of the arteries), obesity, cancer, diabetes and dementia, among others.



Sugar + inflammation = true? Foto: istockphoto

Chronic inflammation is linked to diseases such as atherosclerosis (hardening of the arteries), obesity, cancer, diabetes and dementia, among others.

A key issue for us at the Centre of Molecular Inflammation Research (CEMIR) is how inflammation can be so closely associated with so many seemingly different chronic diseases.

The American Dr. Robert Lustig’s book “Fat Chance – The bitter truth about sugar,” is quite relevant here. Lustig blames high sugar consumption as the major culprit behind our generation’s greatest health challenge, metabolic syndrome1. Dr. Lustig, who is a pediatric endocrinologist and works every day with overweight children, is perhaps best known for his lecture “Sugar: The bitter truth” on YouTube. This video is now been seen by more than 3.5 million people.

Lustig and others raise issues with the prevailing view that obesity is due solely to too much energy in, and too little energy out2.

The World Health Organization’s definition of metabolic syndrome is insulin resistance, along with two or more of the following: hypertension (140/90), obesity (BMI> 30), high cholesterol (TG> 1.7), or increased excretion of protein into the urine (microalbuminuria). Metabolic syndrome results in enormous health care costs, and is more of a major public health problem worldwide than malnutrition.

Patients with metabolic syndrome are at higher risk of a number of different health problems, including heart attack and stroke. We have not been spared from this problem in Norway, and “Samhandlingsreformen” – the Coordination Reform – is an attempt by the Norwegian government to bring the issue to light through an increased focus on preventive health care.

When you consume sugar, your body must decide whether the energy should be used or stored. Sugar is an important source of energy – and it is therefore essential that we always have enough. Any surplus will mostly be stored, in a process that is managed by the liver and that results in a variety of wastes, including uric acid. Under normal conditions, the body can get rid of uric acid, but if it accumulates, it can form crystals.

In the first part of my doctoral research, we found a mechanism that explains how these crystals activate the immune system. The immune system tries to get rid of the crystals, but cannot (see video). The cells then send out a powerful cry for help, which activates the immune system further. This emergency signal is tightly regulated, because if the body overshoots its target, the result is chronic inflammation. If this inflammation manifests itself in a joint, we get redness, heat, pain, and swelling – all symptoms of a disease better known as gout.

The liver also converts sugar into fat for long-term storage. The fat is transported as LDL (better known as “bad cholesterol”) in the bloodstream and out to our fat cells. On the way, the cholesterol can stick to the walls of blood vessels and form the foundation for what we call atherosclerosis. Too much cholesterol in one place can also lead to the formation of crystals, cholesterol crystals.

We are currently completing a project where we have looked at whether cholesterol crystals activate the immune system in the same way. In this situation, the immune system overreacts, but the consequence may be that the vessel wall, and not the crystals, breaks down. This can cause a wound, which in turn can cause a blood clot. And depending on where the clot is located, it can cause a heart attack or a stroke.

The goal of our research is to improve our understanding of how the disease occurs. There are ongoing trials of immunosuppressive drugs to prevent heart attack and stroke. But it is also important from the patients’ perspective that we understand the mechanisms of disease as best we can.

But immunosuppressive drugs attack metabolic syndrome at the wrong end. If it really is correct that sugar + inflammation = true, then we can all approach this from the other end – namely by cutting our daily sugar intake.

1.     Lustig, R. Fat Chance: The bitter truth about sugar. (Fourth Estate, 2012).

2.     Taubes, G. The science of obesity: what do we really know about what makes us fat? An essay by Gary Taubes. BMJ 346, f1050 (2013).


CEMIR_logoThe official opening of the Norwegian University of Science and Technology’s four new centres of excellence (CoE) will take place on Monday 10 June. CEMIR, the Centre of Molecular Inflammation Research, is one of these new centres. CEMIR researchers will study new mechanisms that set off inflammatory responses. We hope this will provide us with information that could help in the development of new treatment methods and the diagnosis of diseases in which inflammation plays a crucial role. You can read more about CEMIR at http://www.ntnu.edu/cemir

In June there will be more blogs from CEMIR researchers.



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Filed under Cardiovascular, Generic Health Relevance, Inflammatory and Immune System, Metabolic and Endocrine, NTNUmedicine, Research, Stroke