Here is the article that secured me a runner-up spot in the 2001 Daily Telegraph/BASF Young Science Writer competition. It doesn't have much to do with the other posts on this blog, but I thought it worth giving it an airing.(Note that this was written in 2001, so some of the science may haved moved on in the intervening years.)
“Go and wash your hands.”
“Don’t play with that – it’s filthy!”
As children, we’re left in no doubt that getting into the habit of keeping clean is a good thing. But there is growing evidence that being too clean can actually harm our health. When it comes to staying healthy, germs may be able to teach us a thing or two.
From birth our immune system calls on an army of specialist cells to destroy potentially dangerous intruders, such as bacteria and viruses, before they destroy us. But invasion by bacteria is not always a bad thing. As Professor Graham Rook, of the Royal Free and University College Medical School points out, we have 1.5 kilos of quite harmless bacteria in our gut alone. And bacterial infection may play a vital role in educating the immune system to grow in a balanced and more effective way.
Recent years have seen a huge rise in allergy-related illnesses such as asthma. Asthma can be triggered by allergens in the air, such as pollen and air pollution. But these allergens don’t cause the disease in the first place. Indeed, studies have shown that asthma is less common in Leipzig, East Germany, which is highly polluted, than in Munich in the West, which has cleaner air.
Instead it seems that a poorly educated immune system may be to blame.
Our immune system contains various types of white blood cell including T Helper 1 (Th1) and T Helper 2 (Th2) cells. The activity of these two types of cell needs to be balanced for the immune system to work efficiently. If there are too few Th1 cells in circulation then the balance swings towards Th2 cells. One ‘side effect’ of the overabundance of Th2 cells seems to be an increased susceptibility to inflammation. In the case of asthma it is the airways that become inflamed, making breathing difficult.
But how does the balance of Th1 and Th2 cells become upset?
A lack of Th1 cells may arise if they aren’t stimulated to proliferate at high enough levels. And one important stimulus is exposure to bacteria.
However in today’s clean society young children are being exposed to less bacteria than was the case just decades ago. Gone are the days of grubby faced children being called in to tea after spending an afternoon ‘mucking around’ the garden. Today, Playstations have replaced playing in the dirt.
“We need an input of certain bacteria to set up correctly the regulation of the immune system,” says Professor Rook.
But by living in a clean and hygienic environment it seems that we’re denying ourselves exposure to these important bacteria. And without this input from bacteria our immune system isn’t being ‘educated’ to operate as it should.
So how do we overcome this problem? According to Professor Rook, whose research looks at ways of countering the problems of clean living, we needn’t resort to living a life surrounded by dirt.
“We need to identify the necessary things that hygiene deprives us of, and put them back as vaccines or probiotics,” explains Professor Rook.
Essentially this means educating the immune system ourselves. If our Th1 cells aren’t being exposed to the necessary bacteria in the course of nature, we need to take controlled steps to ensure that this vital exposure occurs.
Initial clinical trials in humans are proving positive. Mycobacteria are a family of bacteria whose members include harmless species that are prevalent in the environment, in untreated water and soil. In the laboratory these bacteria can be shown to educate immune cells by changing the way they recognise allergen. In trials led by Dr Ratko Djukanovic at Southampton General Hospital, individuals suffering from allergic asthma have been injected with a vaccine containing dead, heat-killed Mycobacterium vaccae. After a single injection, the vaccine has been shown to partially inhibit allergic reactions that usually occur in the lungs of asthmatics.
“Further clinical trials are needed to investigate the potential of this vaccine as a treatment for asthma,” says Dr Djukanovic, “but our initial results are encouraging.”
So, although we’ve got some way to go until we fully understand precisely what bacterial input is needed to educate our immune system effectively, maybe parents need to be less hesitant about letting their children get ‘close’ to Nature.
Perhaps a bug a day can keep the doctor away...?
References:
Strachan, D.P. (2000). Family size, infection and atopy: the first decade of the “hygiene hypothesis”. Thorax 55(supplement): S2-S10
Hopkin, J.M. (2000). Atopy, asthma and the mycobacteria. Thorax 55: 443-445
Rook, G.A.W., and Stanford, J L. (1998). Give us this day our daily germs. Immunology Today 19: 113-116
Cookson, W.O.C.M., and Moffatt, M.F. (1997). Asthma – an epidemic in the absence of infection? Science 275: 41-42
Farooqi, I.S., and Hopkin, J.M. (1998). Early childhood infection and atopic disorder. Thorax 53: 927-932
Von Mutius, E., Martinez, F.D., Fritsch, C., et al. (1994). Prevalence of asthma and atopy in two areas of West and East Germany. Am J Respiar Crit Care Med 149: 358-364
von Mutius, E., Pearce, N., Beasley, R., Cheng, S., von Ehrenstein, O., Bjorksten, B., and Weiland, S. (2000). International patterns of tuberculosis and the prevalence of symptoms of asthma, rhinitis, and eczema. Thorax 55: 449-453
Camporota, L., Corkhill, A., Long, H., Lordan, J., Stancui, L., Tuckwell, N., Cross, A., Stanford, J.L., Rook, G.A.W., Holgate, S.T., Djukanovic, R. (2001). A randomised, controlled study of the effects of Mycobacterium vaccae (SRL172) on allergen-induced airway responses in atopic asthma. Personal communication from R. Djukanovic, March 2001.
Professor G. A. Rook – personal e-mail correspondence (February 2001)
Professor J. M. Hopkin – personal e-mail correspondence (February 2001)
Saturday 29 January 2011
Tuesday 25 January 2011
Got a conundrum?
Has a particular chemical or biological concept left you mystified? Drop me an
e-mail with a note of the source of your confusion, and I'll endeavour to post a response (and hopefully a useful explanation) on this blog as soon as I can.
e-mail with a note of the source of your confusion, and I'll endeavour to post a response (and hopefully a useful explanation) on this blog as soon as I can.
Monday 10 January 2011
Honeybees and epigenetics
What links a queen honeybee to a particular group of four atoms (one carbon and three hydrogen atoms, to be precise)? The answer lies in the burgeoning field of epigenetics, which has revolutionized our understanding of how biological information is transmitted from one generation to the next.
The genetic information stored in our genome – the set of chromosomes that we inherit from our parents – directs the way in which we develop and behave. (We call the attributes and behaviours exhibited by an organism its ‘phenotype’.) Traditionally, the genetic information was thought to be encoded solely in the sequence of the four different chemical building blocks from which our DNA is constructed (that is, our genome sequence). If a DNA sequence changes, so the resulting phenotype changes too. (This is why identical twins, with genomes whose DNA sequences are identical, look the same, but other individuals, whose genomes comprise different DNA sequences, do not.) However, the field of epigenetics opens up a strong challenge to this traditional view of our DNA sequence being the sole dictator of phenotype.
So what actually is epigenetics? In broad terms, epigenetics refers to the way that the information carried in our genome – and the phenotype that results when this information is ‘deciphered’– can be modified not by changes in DNA sequence, but by chemical modifications either to the DNA itself, or to the special group of proteins called histones that associate with DNA in the cell. (It’s a bit like taking a book, with a story told in the author’s words, and adding notes on the page that alter how the story is interpreted by the next person to read it.)
But what has epigenetics to do with the group of four atoms, the one carbon and three hydrogen atoms mentioned at the start of this article? These four atoms can combine to form a methyl group – a central carbon atom, with three hydrogen atoms attached; the addition of methyl groups to both DNA and histone proteins in a process called methylation is a primary way in which epigenetic modification occurs. For example, the addition of a methyl group to one of the four chemical building blocks of DNA (called cytosine, C) either when it appears in the sequence CG (where G is the building block called guanine) or the sequence CNG (where N represents any of the four chemical building blocks of DNA) appears to result in that stretch of DNA being ‘switched off’. Consequently, the information stored in that stretch of DNA is not actively used by the cell; that stretch of DNA falls silent.
But what of our queen honeybee? Where does she fit into our story? A queen honeybee has an identical DNA sequence to her workers. Yet she bears some striking differences to them in terms of physical appearance and behavior (amongst other attributes). These differences are more than just skin-deep, however: the pattern of methylation between queen and worker larvae differs. Their genomes may be the same at the level of DNA sequence, but their different patterns of methylation direct different fates: the queen honeybee and her workers develop into quite distinct organisms.
Things take an interesting turn when we consider the cause of these different methylation patterns: the diets that the queen and workers experience during their development. The queen is fed on large quantities of royal jelly into adulthood, while worker larvae face a more meager feast, being switched to a diet of pollen and nectar early on. It is these diets that influence the way in which the queen and worker bees’ genes are switched on and off. (You can read more about the ‘epigenetics of royalty’ here.)
It is not just the queen honeybee whose genome is affected by the environment (in her case, diet). Mice exposed to certain chemicals during pregnancy have been found to produce offspring who became obese more often than would be expected (as explained here). In these offspring, the methylation of a particular gene associated with the onset of obesity (and other conditions) was seen to decrease, causing the gene to be switched on when it would normally be switched off.
These findings bring a new twist to the classic nature/nurture debate: while it still holds that our phenotype – the physical attributes and behaviours we display – is dictated by our DNA sequence, it happens in a way that can be modified by factors in the world around us, operating through epigenetic mechanisms. This should give us food for thought when we recognize that our own genome is susceptible to epigenetic modification too. How could the environment we experience in early life – in the womb, even – be determining our phenotype in later life – our health and wellbeing? Food for thought indeed.
This blog post previously appeared on the OUP Blog
The genetic information stored in our genome – the set of chromosomes that we inherit from our parents – directs the way in which we develop and behave. (We call the attributes and behaviours exhibited by an organism its ‘phenotype’.) Traditionally, the genetic information was thought to be encoded solely in the sequence of the four different chemical building blocks from which our DNA is constructed (that is, our genome sequence). If a DNA sequence changes, so the resulting phenotype changes too. (This is why identical twins, with genomes whose DNA sequences are identical, look the same, but other individuals, whose genomes comprise different DNA sequences, do not.) However, the field of epigenetics opens up a strong challenge to this traditional view of our DNA sequence being the sole dictator of phenotype.
So what actually is epigenetics? In broad terms, epigenetics refers to the way that the information carried in our genome – and the phenotype that results when this information is ‘deciphered’– can be modified not by changes in DNA sequence, but by chemical modifications either to the DNA itself, or to the special group of proteins called histones that associate with DNA in the cell. (It’s a bit like taking a book, with a story told in the author’s words, and adding notes on the page that alter how the story is interpreted by the next person to read it.)
But what has epigenetics to do with the group of four atoms, the one carbon and three hydrogen atoms mentioned at the start of this article? These four atoms can combine to form a methyl group – a central carbon atom, with three hydrogen atoms attached; the addition of methyl groups to both DNA and histone proteins in a process called methylation is a primary way in which epigenetic modification occurs. For example, the addition of a methyl group to one of the four chemical building blocks of DNA (called cytosine, C) either when it appears in the sequence CG (where G is the building block called guanine) or the sequence CNG (where N represents any of the four chemical building blocks of DNA) appears to result in that stretch of DNA being ‘switched off’. Consequently, the information stored in that stretch of DNA is not actively used by the cell; that stretch of DNA falls silent.
But what of our queen honeybee? Where does she fit into our story? A queen honeybee has an identical DNA sequence to her workers. Yet she bears some striking differences to them in terms of physical appearance and behavior (amongst other attributes). These differences are more than just skin-deep, however: the pattern of methylation between queen and worker larvae differs. Their genomes may be the same at the level of DNA sequence, but their different patterns of methylation direct different fates: the queen honeybee and her workers develop into quite distinct organisms.
Things take an interesting turn when we consider the cause of these different methylation patterns: the diets that the queen and workers experience during their development. The queen is fed on large quantities of royal jelly into adulthood, while worker larvae face a more meager feast, being switched to a diet of pollen and nectar early on. It is these diets that influence the way in which the queen and worker bees’ genes are switched on and off. (You can read more about the ‘epigenetics of royalty’ here.)
It is not just the queen honeybee whose genome is affected by the environment (in her case, diet). Mice exposed to certain chemicals during pregnancy have been found to produce offspring who became obese more often than would be expected (as explained here). In these offspring, the methylation of a particular gene associated with the onset of obesity (and other conditions) was seen to decrease, causing the gene to be switched on when it would normally be switched off.
These findings bring a new twist to the classic nature/nurture debate: while it still holds that our phenotype – the physical attributes and behaviours we display – is dictated by our DNA sequence, it happens in a way that can be modified by factors in the world around us, operating through epigenetic mechanisms. This should give us food for thought when we recognize that our own genome is susceptible to epigenetic modification too. How could the environment we experience in early life – in the womb, even – be determining our phenotype in later life – our health and wellbeing? Food for thought indeed.
This blog post previously appeared on the OUP Blog
Sunday 9 January 2011
How geckos defy gravity
The background to this blog shows a Day gecko (Phelsuma sp.). As the image suggests, geckos have the amazing ability to defy gravity and walk up walls (and along ceilings).
How do they do this? The answer lies in the anatomy of their toes. Gecko toe pads comprise rows of thousands of tiny hairs called setae (singular: seta). The gecko’s gravity-defying antics are made possible by forces of attraction, which exist between the surface the gecko is climbing on and the setae on the surface of the gecko’s toes. The forces of attraction are what we call dispersion forces.
Dispersion forces are relatively weak. However, while the dispersion force operating between a singe seta and the surface of the wall (or ceiling) is tiny, there are so many setae on the surface of each toe pad that the overall force of attraction (adding up the contributions from thousands of setae) is very strong indeed – strong enough to hold the gecko firmly in place, against the forces of gravity.
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