Put that burger on hold – fast food makes the immune system more aggressive over time

Unhealthy food provokes our immune systems to react similarly to its response to a bacterial infection, apparently making the body’s defences more aggressive over the long term. These are the findings of a recent study, which also reveals an impact on genes.

The impact that a diet based on foods high in sugar and fat and low in fiber has on our bodies has long been a subject of interest to scientists. Studies supported by funding to three EU projects has revealed that not only is there a short-term, profound influence on immune systems, a large number of genes in progenitor cells were also activated. While the acute inflammation disappeared over time, the genetic reprogramming of the immune cells and their precursors was still active.

The study published in the journal ‘Cell’ shows that the impact unhealthy food has on the system, even after switching to a healthy diet, seems to involve long-term changes which may be involved in the development of arteriosclerosis and diabetes, diseases linked to a Western diet.

The team, in part supported by the EU-funded projects REPROGRAM, SYSCID and SYBIOFUN, placed mice on a diet associated with a Western diet. The animals consequently developed a strong inflammatory response throughout their bodies, similar to an infection with dangerous bacteria. There was also an unexpected increase in the number of certain immune cells in the blood of the mice, especially granulocytes and monocytes. This was an indication for an involvement of immune cell progenitors in the bone marrow.

To understand this better, bone marrow progenitors for major immune cell types were isolated from mice fed a Western diet or healthy control diet, and their function and activation state were systematically analysed. Genomic studies revealed the genes affected included those responsible for proliferation and maturation. When the researchers gave the mice their typical cereal diet for another four weeks, the acute inflammation disappeared. But the genetic reprogramming of the immune cells and their precursors remained. Even after these four weeks, many of the genes that had been switched on during the fast food phase were still active.

Innate immune systems remember

An infection causes a body to go into high alert, enabling it to initiate a response to a new attack. This referred to as innate immune training. But what is interesting in the study the team has just published is that it was ‘fast’ food, not bacteria that provoked the response. The scientists managed to establish the sensors in the immune cells responsible for the reaction in 120 subjects. In those which had a particularly strong training effect they found genetic evidence of what is known as inflammasone, key intracellular signaling complexes that recognise infectious agents and other harmful substances and subsequently release highly inflammatory messengers. Although how the inflammasones recognise the exposure to the diet remains unknown.

Long-term genetic impact

The Western diet caused epigenetic changes — changes the way genetic information is packaged, causing DNA to unwind which also makes it easier to ‘read’. Consequently the immune system reacts event to small stimuli with a stronger inflammatory response. These responses can accelerate the development of vascular diseases or type 2 diabetes.

These findings have societal relevance. Educating children in the need, and pleasure, of making healthy food choices will ‘immunise’ them early against the temptations of the food industry.

EU support helps to examine the hidden consequences of an unhealthy diet

The projects REPROGRAM (Targeting epigenetic REPROGRamming of innate immune cells in Atherosclerosis Management and other chronic inflammatory diseases), SYSCID (A Systems medicine approach to chronic inflammatory disease) and SYSBIOFUN (The interaction landscape between microbial colonisation and functional genome of the host: a systems biology approach in fungal infections) all helped to further the findings set out in this research.

For more information, please see:
REPROGRAM CORDIS project web page
SYSCID CORDIS project web page
SYSBIOFUN CORDIS project web page

published: 2018-02-09
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