“Drinking several cups of coffee a day could halt the development of multiple sclerosis,” reads a story in The Daily Telegraph. The Head of Research and Information at the...
“Drinking several cups of coffee a day could halt the development of multiple sclerosis,” reads a story in The Daily Telegraph.
The Head of Research and Information at the MS Society, Dr Lee Dunster, was quoted by the newspaper as saying: "Over the years there have been numerous discoveries that have prevented EAE [an MS-like condition] in mice, but translating this into potentially beneficial therapies for humans remains a challenge. Based on the results of this study, we wouldn't advise people to change their caffeine intake.”
Where did the story come from?
Dr Jeffrey Mills and colleagues from Cornell University and the Oklahoma Medical research Foundation in the US and the University of Turku in Finland, carried out this research. The study was funded by the National Institutes of Health, the Finnish Academy and the Sigrid Juselius Foundation. It was published in the peer-reviewed scientific journal: Proceedings of the National Academy of Sciences of the USA.
What kind of scientific study was this?
This was a laboratory study, which looked at whether a particular protein called CD73 played a role in the worsening of a MS-like condition in mice called experimental autoimmune encephalomyelitis (EAE). EAE is induced in mice by injecting them with a fragment of protein (called MOG), which is normally found on the surface of cells in the brain. The MOG causes cells from the immune system to enter the brain and start attacking the mice’s own brain cells. EAE is used as a model for MS in humans.
CD73 is a protein found on the surface of some cells, including some immune system cells, and it breaks down a chemical called AMP into another chemical called adenosine, which can suppress the activity of the immune system. Because of this, the researchers were interested in whether the mice would develop EAE if the CD73 were removed from the cells.
The researchers genetically engineered mice that lacked the CD73 protein. They then tried to induce EAE in the mice by injecting them with the MOG fragment. They carried out more experiments to look at whether the immune system or brain of the mice lacking CD73 differed from those of normal mice.
The researchers obtained one type of immune system cell, called CD4 T cells, from normal mice or from mice lacking CD73 that had been injected with the MOG fragment. They then injected these T cells into mice that did not have T cells (this means that normally they would not develop EAE). The researchers looked to see whether any of these mice went on to develop EAE. The researchers also looked at the effect of transplanting normal T cells into mice lacking in CD73.
The researchers then looked at whether they could induce EAE in mice if they blocked the signalling pathway involving CD73 by giving the mice caffeine (4 milligrams per mouse per day) or a chemical called SCH58261, both of which are known to block the effects of adenosine. Normal mice were given caffeine or SCH58261 the day before injecting them with the MOG fragment and for the duration of the experiment (20 to 30 days).
What were the results of the study?
The researchers found that mice lacking CD73 did not develop EAE when injected with the MOG fragment, although normal mice did. Examination of the brains of these MOG-treated mice showed that mice lacking CD73 had much less infiltration of immune system cells into their brains than normal mice.
When CD4 T cells from MOG-exposed CD73-lacking mice were transplanted into mice that lacked their own T cells, these mice developed EAE that was more severe than if T cells from MOG-exposed normal mice were transplanted. If the mice lacking CD73 were transfused with T cells from normal mice then they could develop EAE on exposure to the MOG fragment.
These findings suggested that CD73 must be found in either the central nervous system or the T cells for EAE to occur. The researchers found that if they blocked the signalling pathway involving CD73 (by treating the mice with SCH58261 or caffeine before and after injecting them with the MOG fragment), the mice did not develop EAE.
What interpretations did the researchers draw from these results?
The researchers concluded that the presence of the CD73 protein is needed for EAE to develop. It does this by playing a role in allowing immune system cells to enter the central nervous system.
What does the NHS Knowledge Service make of this study?
This study investigated the role of the protein CD73 in the development of EAE in mice. Although this condition is similar to MS in humans, this protein may not play the same role in MS. Further research will be needed to determine if this is the case before scientists can begin to investigate whether they can use this knowledge to develop new kinds of treatment or prevention for MS.
Although the newspapers have focused on the possibility of caffeine or caffeine-containing drinks “preventing” or “halting” multiple sclerosis, this was not the focus of this study. The effects of caffeine on the development of EAE in mice were already known. The successfully induced MS-like condition in mice does not necessarily mean that caffeine would prevent MS in humans, the cause of which is not clearly understood. Clinical trials in humans would be needed to determine whether caffeine could have any beneficial effect, and whether it would be safe.
Sir Muir Gray adds...
If I had that dreadful disease MS I might give it a go, the likelihood of being helped to being harmed looks quite good. However, this is a few years away fron being shown to be an effective therapy.