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Chapter 1: What is the main topic discussed in this episode?
Show Me The Science with Professor Luke O'Neill.
Hello, Luke O'Neill here and welcome to Show Me The Science, my weekly podcast here with Newstalk. Now, I do get loads of requests and keep them coming in. Now, I'm trying to do them as much as possible. And if stuff comes in that I know stuff about or I feel I can help with, I will certainly cover it. And this week, Emma Foley has sent in a request to do psoriasis.
And I jumped at this one because I know all about psoriasis and I've done some work. on psoriasis myself over the years. And in fact, I have mild psoriasis myself and it's very, very common. In Ireland, at least 5% of us have some kind of psoriasis. Now I'm lucky, it's very mild. It's on my elbows, knees, it comes and goes, you know. But some people have very severe psoriasis.
That's the severe end of it, I guess. But it's very common as a condition, so I'm very happy to cover it. I've been following this as a research area since the mid-80s, remarkably. It's a classic immune disease. In this case, the skin gets affected, of course, and my main specialty is immune diseases. especially what I call autoimmune diseases, where your own immune system attacks your own body.
Chapter 2: What is psoriasis and how common is it?
Auto means self, and your own self gets attacked by the immune system. And psoriasis is an autoimmune disease. And we can start off by saying we don't know what causes it. We know it's in the skin. The key feature, as anybody would be familiar with this disease, but now you get red scaly patches on your skin. And in severe cases, they can cover 80, 90% of your body.
So it's a very serious disease down that end of the spectrum. What's happening is the cells in your skin are dividing too much. Now in your skin, you've got things called keratinocytes. That's the cell type in your skin. And they're the ones that make the skin actually. And they turn over. All cells in our body turn over and they die and are replaced. In psoriasis, it's very simple.
They're dividing too much and they reckon overall they're dividing about three times the rate in normal skin. And they pile up and they pile up and they pile up in the skin and they die and then debris is formed and the immune system doesn't like this and it goes in and tries to handle this situation. And the trouble is that immune reaction then causes all the features of an immune type response.
You get redness, you get itchiness, you get pain, just as if you've scratched yourself, I suppose, in a way. And in this case, the scratch is being caused by your own cells in your skin dividing too much. In some ways, we see most autoimmune diseases, they're sometimes called wounds that won't heal properly.
Because you can imagine if you scratch yourself in the skin, it will go red, it will be sore. The immune system will go in and try to clear sort of any infection that's in the broken skin. That's what's happening in psoriasis, but there's no infection. That's the mystery. Why would the immune response be kicked off in that situation and mimic as if there's been an injury and infection?
And that's the thing we don't know.
There's some evidence that might be something wrong with the barrier. Their skin is a barrier. It's maybe slightly different in someone who has psoriasis and the barrier is a bit broken. Maybe some bacteria get in.
and begin to irritate further. But it's very hard to find a bacteria in the skin of psoriatic people. And so it's been caused by that. If it was caused by a bacteria, of course, it would respond to antibiotics. And it doesn't really, mostly speaking. So it can't really be bacterial in origins. It's a mystery as to what's causing this. And lots of research is trying to pin that down.
But we do know it's immune. We know cells called T-cells go in. That'll be very important later. And these T-cells are involved in fighting infection and they go in in droves into the psoriatic skin and they release all these sort of chemicals that will cause the inflammation that's happening in the skin. And inflammation, of course, is the hallmark of psoriasis redness.
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Chapter 3: How does the immune system contribute to psoriasis?
And it's quite true. All the immune components are there, but the T cell seems to dominate. Now, there are different types.
Chapter 4: What are the characteristics and symptoms of psoriasis?
There's plaque psoriasis. That's the most common one, really, where you get these big patches. They're called plaques that spread out from the lesion. That's plaque psoriasis. Gut eight, that's spots, little pimples, I suppose. And then you have pustular, and they are big spots full of pus. Pus is an interesting substance, actually, in itself.
You'll all be familiar with pus that you see in a spot for instance. What pus is actually is dead neutrophils. Now neutrophils are a very important cell in the immune system and they fight infection and when they die they form pus. So whenever you see a bacterial infection you often get pus because the neutrophils have fought the good fight. They've killed the bacteria and then they form pus.
And lo and behold, it's subtype of psoriasis. You see loads of neutrophils. You might call it neutrophilic psoriasis. And that ends up in pus in these lesions. And as I'll come back to, there's a slight difference with pustular psoriasis versus plaque psoriasis. So there's these different types that have been spotted.
They were mainly described, oh, decades ago, I suppose, because you could see the skin was slightly different between people with these different types of psoriasis. Now, there's one other type as well to mention, and it's called psoriatic arthritis.
Now, that is a really sort of a challenging condition for people because not only do you have psoriasis in your skin, you've also got arthritis, and that means your joints are sore. Because, of course, arthritis is an immune disease of the joints. So psoriatic arthritis, you get both. And that can be very debilitating.
Not only are you getting scaly red patches, but your joints are in agony as well. And it's slightly different to normal arthritis. The psoriasis is slightly different as well. So it's a subtype again. So in some ways, then, you have four subtypes. And often in medicine that happens, by the way. Now, let's say 150 years ago, something like a disease is described, like, say, whatever it might be.
It could be a skin disease. And then we realize over time there's actually subtypes. And the subtyping of disease could be very important because there could be different sort of factors in each subtype. And then you might design a medicine then to go after a specific subtype. And that's what's been happening here, as I will explain when I come on to that approach to how we treat these things.
So it's complicated enough in a way, but overall, to summarise that bit, it's in the skin, it's red, it's scaly, it's sore. And then remember, you get this flaking happening because eventually the dead skin falls off the skin. And that is the flakes you get, these opaque coloured flakes. That's happening all the time in normal skin, remember. You know, dust in your house is mainly dead skin.
Did you know that? I bet there's a fact for you. When you're dusting your house, you're dusting away dead skin. In this case, the dead skin has been made very fast. Because remember, the keratinocytes are dividing very fast and dying and forming these sheets of cells. And that's what's coming off your skin when you have psoriasis.
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Chapter 5: What are the different types of psoriasis?
And that tells us something. Stress can sort of provoke it. There's a bit of evidence for that. It's not fully clear, though, if stress is a reason why people flare up. Bit of evidence, but it's not for definite. But she said certainly before fashion shows that stress was a factor for her. And lastly, golf is in the air at the moment. What were the masters? Phil Mickelson. He again had psoriasis.
And Winston Churchill had psoriasis. Didn't affect him, now, did it? So it's a serious disease, certainly at the extreme end. But now we have these new therapies available. There will be a subset of people who won't respond, though, even though there's been a big breakthrough. We've got to keep working on this and make sure that eventually everybody will respond to treatments for psoriasis.
But certainly... It's night and day compared to what it was like when I began all those years ago, thanks to great immunology as ever. That's the science of psoriasis for Emma Foley. Thanks for that request, Emma. And as I say, send me your requests, laoneal, with two L's, at tcd.ie, and I'll do my best to cover it in the future.
And my podcast is a news talk production, available every Thursday, wherever you get your podcasts.