What causes Inflammatory Bowel Disease (IBD)?

Wondering what triggers inflammatory bowel disease (IBD)? Whether it’s Crohn’s or ulcerative colitis, this blog uncovers how your immune system, genetics, and gut bacteria all play a part in causing gut inflammation.

Five key takeaways

• IBD is driven by an immune system overreaction: Your immune system mistakenly attacks your gut lining, releasing chemicals called cytokines that fuel ongoing inflammation.
• Cytokines are the messengers of inflammation: Key cytokines like TNF-?, IFN-?, IL-12, and IL-17 play major roles in Crohn’s disease, while IL-13, IL-4, IL-5, and IL-9 are important in ulcerative colitis.
• Cytokine imbalance disrupts gut health: When cytokines are out of balance, they cause your immune system to keep attacking your gut, leading to symptoms like pain, diarrhoea, and tissue damage.
• Genes, gut bacteria, and environment all play a part: It’s not just bad luck—your genetics, the balance of bacteria in your gut, and outside factors like smoking or infections can all raise your risk of IBD. Sometimes, changes in key genes (like CARD-15/NOD2) or problems with gut bacteria tip the balance and trigger inflammation.
• The gut’s “security guards” can turn on you: Special immune cells (like macrophages and dendritic cells) usually protect you from germs, but in IBD, they mistake friendly gut cells for invaders. They call in T cells and release chemical messengers called cytokines, which ramp up inflammation and keep it going.
• Different immune cells drive Crohn’s and ulcerative colitis: Crohn’s disease is driven mostly by Th1 and Th17 immune cells, while ulcerative colitis is fuelled by Th2, Th9, and natural killer (NK) T cells. Each type releases its own set of cytokines—tiny messengers like TNF-?, IFN-?, and IL-13—that keep the gut inflamed.

Introduction

Inflammatory bowel disease (IBD) is a long-lasting condition that causes swelling and irritation in the digestive system. The two main kinds of IBD are Crohn’s disease (CD) and ulcerative colitis (UC). Both affect the body in similar ways and are treated using similar methods [1], [2].

How Inflammatory Bowel Disease (IBD) occurs

IBD basically occurs when the immune system is overzealous and starts attacking the gut lining. We will provide a quick snap shot of what is thought to occur and will go into more depth later.

Inflammatory bowel disease may start when the gut lining doesn’t properly handle things it comes into contact with, like bacteria or food particles. This could be caused by an overactive sensor called the Toll-like receptor and certain genetic factors (mutations in genes called DLG5 and OCTN).

Because of this, the immune system overreacts. Special immune cells called dendritic cells get activated and call in different types of T-cells (immune cells). These T-cells then set off a chain reaction of immune responses that cause inflammation in the gut lining.

Certain molecules, like ICAM1, help immune cells stick to and move through the blood vessels to reach the inflamed areas in the gut.

In Crohn’s disease, the immune response mainly involves T-cells called Th1 and Th17. In ulcerative colitis, the main players are Th2 cells and natural killer (NK) T-cells [3].

Ruling out other gut problems first

Before your doctor treats you for inflammatory bowel disease (IBD), they’ll want to make sure it’s not something else causing your symptoms. Common lookalikes include:

• irritable bowel syndrome (IBS),
• blockages in the gut,
• coeliac disease, or
• too many bacteria growing in the small intestine (called SIBO).

Making the right diagnosis means you’ll get the right treatment from the start.

Why your gut environment matters

Inside your gut, there’s a busy world of bacteria, genes, and outside influences all working together. This environment is vital for keeping your immune system balanced.

Normally, your gut lining has just the right amount of inflammation, controlled by different immune cells working in harmony[4][5][6][7][8][9].

What’s happens when the gut is out of balance?

If this balance is thrown off, your immune system can get confused and start attacking your own gut cells. That’s when the long-lasting inflammation of IBD can happen[10][11][12][13].

What actually causes IBD?

IBD starts when the balance of bacteria in your gut gets disrupted. Your gut is home to about ten times more bacteria than the number of human cells in your whole body! There are 300 to 500 different species of bacteria living peacefully together, helping to keep you healthy[14]. Your immune system’s job is to let the good bacteria do their thing, while fighting off any bad bugs.

The gut’s defence system

Your gut has its own mini-defence force, called the gut-associated lymphoid tissue (GALT). This includes special patches and nodes (like Peyer’s patches and mesenteric lymph nodes) that help the immune system keep watch[15]. But sometimes, things like your genes or things in your environment can upset this balance. One important process is called autophagy, which helps your cells clear out harmful germs and keeps your immune response in check. If autophagy doesn’t work properly—sometimes because of a change in a gene called ATG16L1—it can make you more likely to get Crohn’s disease[16].

How the immune system triggers IBD

When your immune system gets confused

Sometimes, your immune system stops recognising your gut’s own cells as friendly. This can happen because of an injury or because of genes you inherit from your family. When this mix-up happens, it can lead to conditions like Crohn’s disease or ulcerative colitis.

The gut’s security guards

Your gut has special immune cells, like macrophages and dendritic cells. Think of these as your gut’s security guards. They’re always on the lookout for troublemakers (harmful germs).

These cells use special tools called pattern recognition receptors (PRRs), which include toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD) receptors, to spot anything that shouldn’t be there.

Here are some of the key players:

• Macrophages: The “big eaters”—they patrol your gut, gobbling up germs and cleaning up any mess.
• Dendritic cells: The “lookouts”—they spot troublemakers (like harmful bacteria) and alert the rest of the immune system.
• T cells: The “special forces”—once they get the message from dendritic cells, they help attack anything that shouldn’t be there.

Two types of immunity

• Innate immunity: Your body’s first line of defence. It’s fast and acts the same way every time, using cells like macrophages and dendritic cells.
• Adaptive immunity: More like a memory bank. It learns from past infections to fight off the same germs faster next time. T cells are a big part of this team.

When things go wrong

Sometimes, the immune system gets confused and starts attacking the gut’s own cells. This can happen because of injuries or genes passed down in families.

The role of the CARD-15 gene

One important gene is called CARD-15. This gene makes a protein called NOD2, which helps your cells sense germs inside them. If there’s a change (mutation) in CARD-15, the NOD2 protein might not work properly. This can confuse your immune system and make it attack your gut lining, causing long-term inflammation—one of the main problems in Crohn’s disease[17][18].

How immune chemicals affect gut inflammation

What are cytokines?

Cytokines are tiny chemical messengers your immune system uses to send signals. In inflammatory bowel disease (IBD), these messengers help control how much and how long your gut gets inflamed. If these chemicals get out of balance, your gut inflammation can get worse[19].

Key players in gut inflammation

Some of the main cytokines involved in gut inflammation are:

• Tumour necrosis factor-alpha (TNF-?)[20][21]
• Transforming growth factor-beta (TGF-?) [19][22]
• Interferon-gamma (IFN-?)[23]

If your immune system starts attacking your own gut cells, it can make IBD symptoms worse and harder to control[24].

It’s more complicated than we thought

Doctors used to think that ulcerative colitis was mostly caused by one group of immune cells (Th2) and Crohn’s disease by another (Th1). But now, research shows it’s not that simple. These chemical messengers can have different, and sometimes even opposite, effects in the gut [25].

Other important immune chemicals

Another group of immune cells, called Th17 cells, release chemicals like IL-17 and IL-22. These can start and ramp up gut inflammation, but they also help put the brakes on when needed[26]. IL-23, made by immune cells in your gut, can increase inflammation even more[27]. In ulcerative colitis, IL-9 has been found to damage the gut lining[28].

What else can affect gut inflammation?

Things like smoking and other environmental factors may raise your risk of getting IBD, but scientists are still figuring out exactly how this works[29][30].

Crohn’s Disease

Crohn’s disease is a common type of inflammatory bowel disease (IBD) that can affect any part of your digestive system—from your mouth all the way to your bottom.

It causes swelling and irritation, which can lead to problems like narrow areas in the intestines (called strictures), tunnels between different parts of the gut (called fistulas), sores (ulcers), and small lumps called granulomas. The end part of the small intestine, called the terminal ileum, is often affected.

The symptoms of Crohn’s disease

Common symptoms include diarrhoea (sometimes with blood), tummy pain, weight loss, and trouble absorbing nutrients. Some people also experience problems outside the gut, like joint pain or skin issues, which can sometimes happen before gut symptoms appear [1].

The genetics of Crohn’s disease

Crohn’s disease tends to run in families, and if a close relative has it, your risk is about five times higher than average [31].

The cytokines of Crohn’s disease

The inflammation in Crohn’s disease happens because immune cells release chemicals called cytokines—such as IL-12, IL-17, TNF-?, and IFN-?—that cause and keep the swelling going [5].

Certain immune cells, like antigen-presenting cells and macrophages, produce more of these chemicals, which encourages other immune cells (called Th1 cells) to join in, creating a cycle of ongoing inflammation [32].

Ulcerative Colitis

Ulcerative colitis is another main type of inflammatory bowel disease (IBD), but it only affects the inner lining of the colon (large intestine). It causes shallow sores (ulcers), makes the surface look a bit rough or grainy, and can change the look of blood vessels in the gut wall [2].

Unlike Crohn’s disease, ulcerative colitis does not go through the whole thickness of the gut wall and never affects areas outside the colon.

Doctors use something called the Montreal classification system to describe the different types of ulcerative colitis, but because the disease can show up in different ways, it’s not always easy to fit everyone into neat categories [33].

The symptom of ulcerative colitis

Common symptoms include blood and mucus in your poo, tiny bleeding spots in the gut (called petechiae), and changes in the gut tissue. When the disease is quiet (remission), the gut lining may look normal, but if the disease is severe, you can get swelling, deeper ulcers, and even a risk of the colon tearing  [2].

The cytokines of ulcerative colitis

A chemical called IL-13 is very important in ulcerative colitis, as it keeps the inflammation going [34].

Other chemicals, like IL-4, IL-5, and IL-9, are also raised and are linked to certain immune cells called Th2 and Th9 cells [5], [35]. There’s also a protein called PU.1 that helps cells talk to each other, and IL-9 from Th9 cells can slow down gut lining repair and make the barrier between cells weaker, which lets bacteria get in and cause more inflammation [36]. Like Crohn’s disease, ulcerative colitis also has higher levels of inflammation-related chemicals from Th17 cells  [26].

Conclusion: Hope for IBD – and what’s next

Living with IBD can feel overwhelming, but you’re not alone. Understanding how your immune system, gut bacteria, and genetics all play a part is the first step in taking back control. Treatments are improving all the time, and new options are giving hope to people with Crohn’s disease and ulcerative colitis.

Exciting prospects: Low Dose Naltrexone (LDN)

One newer treatment that’s getting a lot of attention is Low Dose Naltrexone (LDN). LDN works by gently adjusting your immune system, helping to calm inflammation in the gut without the harsh side effects of some older medicines. Early studies and real-life experiences suggest that LDN may help some people with IBD manage their symptoms better and enjoy a better quality of life [37]. While more research is ongoing, many patients are already benefiting from this exciting option.

How to order LDN from Courier Pharmacy

Getting started with LDN or any IBD treatment through Courier Pharmacy is simple and discreet. Here’s how it works:

1.      Complete a quick online consultation: 

Just answer a few questions about your health on our secure website. This helps our pharmacy team understand your needs and make sure LDN or another treatment is right for you.

2.      Prescriber review: 

A registered prescriber will review your answers. If approved, they’ll issue a prescription for the most suitable treatment.

3.      FREE LDN consultations

All LDN consultations are FREE when you order online from Courier Pharmacy. There are no hidden costs. Simply, contact us for your FREE LDN consultation.

4.      Fast, discreet delivery: 

Your medication will be delivered straight to your door in plain packaging, so you can focus on feeling better.

How the Nutrigen genetic test can help you on your IBD journey

Understanding and managing Inflammatory Bowel Disease (IBD) can be challenging, but the Nutrgen Genetic Test Kit offers a powerful tool to help you take control of your gut health. This advanced test analyses your unique genetic makeup to identify specific variations that may influence how your body responds to diet, inflammation, and gut microbiome balance—key factors involved in IBD.

By uncovering genetic markers linked to IBD risk and inflammation pathways, the Nutrgen test provides personalised insights into how your genes may affect your immune system and gut environment. With this information, you can work with healthcare professionals to tailor dietary choices, lifestyle changes, and treatment plans that suit your genetic profile, potentially reducing flare-ups and improving symptom management.

At courierpharmacy.co.uk, we believe that personalised medicine is the future of IBD care. The Nutrgen Genetic Test Kit empowers you with knowledge about your body’s unique needs, helping you make informed decisions to support a healthier, more balanced gut and a better quality of life.

Frequently Asked Questions (FAQs)

1. What is inflammatory bowel disease (IBD)?

IBD is a long-term condition that causes swelling and irritation in your digestive system. The two main types are Crohn’s disease and ulcerative colitis. Both can cause tummy pain, diarrhoea, and other gut symptoms.

2. What’s the difference between Crohn’s disease and ulcerative colitis?

Crohn’s disease can affect any part of your digestive tract, from your mouth to your bottom, and often causes deeper inflammation. Ulcerative colitis only affects the lining of your colon (large intestine) and rectum.

3. What causes IBD?

IBD happens when your immune system gets confused and starts attacking your gut lining. It’s thought to be a mix of genes, gut bacteria, and things in your environment that trigger the immune system.

4. Is IBD the same as IBS?

No, they’re different. IBS (irritable bowel syndrome) doesn’t cause inflammation or damage to your gut like IBD does. IBS is usually less serious and doesn’t increase your risk of bowel damage.

5. What are the symptoms of IBD?

Common symptoms include tummy pain, diarrhoea (sometimes with blood), weight loss, tiredness, and sometimes joint pain or skin problems.

6. How is IBD diagnosed?

Doctors use a mix of blood tests, stool tests, endoscopy, and scans to check for inflammation and rule out other gut problems like IBS, coeliac disease, or infections.

7. Can IBD be cured?

There’s no cure yet, but treatments can help control symptoms, reduce flare-ups, and improve your quality of life.

8. What treatments are available for IBD?

Treatments include medicines to reduce inflammation (like steroids and immune suppressants), newer options like Low Dose Naltrexone (LDN), and sometimes surgery. The right treatment depends on your symptoms and type of IBD.

9. What is Low Dose Naltrexone (LDN) and can it help with IBD?

LDN is a medicine that helps calm your immune system and reduce gut inflammation. Some people with IBD find it helps manage their symptoms, especially if other treatments haven’t worked well.

10. How can I order LDN or other IBD treatments from Courier Pharmacy?

It’s easy—just complete a quick online consultation at Courier Pharmacy. A registered pharmacist prescriber will check your answers, and if suitable, your treatment will be delivered straight to your door. All LDN consultations are FREE, to book yours today please contact us.

11. Is IBD genetic?

Yes, genes can play a role. If you have a close family member with IBD, your risk is higher, but lifestyle and environmental factors matter too.

12. Can diet or stress make IBD worse?

Certain foods or stress can trigger symptoms or flare-ups, but they don’t cause IBD. It’s important to find what works for you and speak to your healthcare team for personalised advice.

13. What is the gut microbiome, and why does it matter in IBD?

Your gut microbiome is the community of bacteria living in your digestive tract. A healthy balance helps protect your gut, but an imbalance may play a part in IBD.

14. Can smoking affect my IBD?

Yes—smoking can make Crohn’s disease worse and increase the risk of complications. If you smoke, quitting is one of the best things you can do for your gut health.

15. Will I need surgery for IBD?

Most people manage IBD with medicines, but some may need surgery if medicines don’t help or if there are complications.

16. Are there support groups for people with IBD?

Absolutely! Many charities and online communities offer support, advice, and a place to share experiences with others who understand what you’re going through.

Crohn’s & Colitis UK is a helpful charity for people with ulcerative colitis and their families. Their website is www.crohnsandcolitis.org.uk, and their helpline is 0300 222 5700.

Disclaimer: This article is for informational purposes only and does not replace professional medical advice.

References:

Introduction

• 1. NHS (2024) Crohn’s disease. Available at: https://www.nhs.uk/conditions/crohns-disease/ (Accessed: 16 October 2025)
• 2. NHS (2024) Ulcerative colitis. Available at: https://www.nhs.uk/conditions/ulcerative-colitis/ (Accessed: 16 October 2025)

How Inflammatory Bowel Disease (IBD) happens

• 3. D. Q. Shih and S. R. Targan, “Immunopathogenesis of Inflammatory Bowel Disease,” World Journal of Gastroenterology 14, no. 3 (January 2008): 390–400.

Why your gut environment matters

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What’s happens when the gut is out of balance?

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What actually causes IBD?

• 14. Quigley E. M. M. and Quera R., Small intestinal bacterial overgrowth: roles of antibiotics, prebiotics, and probiotics, Gastroenterology. (2006) 130, S78–S90

The gut’s defence system

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How the immune system triggers IBD

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What are cytokines?

• 19. Neurath M. F., Fuss I., Kelsall B. L., Presky D. H., Waegell W., and Strober W., Experimental granulomatous colitis in mice is abrogated by induction of TGF-beta-mediated oral tolerance, Journal of Experimental Medicine. (1996) 183, no. 6, 2605–2616

Key players in gut inflammation

• 20. Kam L. Y. and Targan S. R., TNF-alpha antagonists for the treatment of Crohn?s disease, Expert Opinion on Pharmacotherapy. (2000) 1, no. 4, 615–622
• 21. Sandborn W. J. and Hanauer S. B., Antitumor necrosis factor therapy for inflammatory bowel disease: a review of agents, pharmacology, clinical results, and safety, Inflammatory Bowel Diseases. (1999) 5, no. 2, 119–1133.
• 22. Feagins L. A., Role of transforming growth factor-? in inflammatory bowel disease and colitis-associated colon cancer, Inflammatory Bowel Diseases. (2010) 16, no. 11, 1963–1968
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• 24. Lundgren B. A., Rorsman F., Portela-Gomes G. M., Grimelius L., Ekdahl K. N., Nilsson B., and Ekwall O., Identification of complement C3 as an autoantigen in inflammatory bowel disease, European Journal of Gastroenterology and Hepatology. (2010) 22, no. 4, 429–436

It’s more complicated than we thought

• 25. Muzes G., Molnár B., Tulassay Z., and Sipos F., Changes of the cytokine profile in inflammatory bowel diseases, World Journal of Gastroenterology. (2012) 18, no. 41, 5848–5861

Other important immune chemicals

• 26. Monteleone I., Sarra M., Pallone F., and Monteleone G., Th17-related cytokines in inflammatory bowel diseases: friends or foes?, Current Molecular Medicine. (2012) 12, no. 5, 592–597
• 27. Geremia A. and Jewell D. P., The IL-23/IL-17 pathway in inflammatory bowel disease, Expert Review of Gastroenterology and Hepatology. (2012) 6, 223–237
• 28. Gerlach K., Hwang Y., Nikolaev A., Atreya R., Dornhoff H., Steiner S., Lehr H.-A., Wirtz S., Vieth M., Waisman A., Rosenbauer F., McKenzie A. N. J., Weigmann B., and Neurath M. F., TH9 cells that express the transcription factor PU.1 drive T cell-mediated colitis via IL-9 receptor signaling in intestinal epithelial cells, Nature Immunology. (2014) 15, 676–686

What else can affect gut inflammation?

• 29. Lashner B. A., Shaheen N. J., Hanauer S. B., and Kirschner B. S., Passive smoking is associated with an increased risk of developing inflammatory bowel disease in children, The American Journal of Gastroenterology. (1993) 88, no. 3, 356–359, 2-s2.0-0027457039
• 30. Aujnarain A., Mack D. R., and Benchimol E. I., The role of the environment in the development of pediatric inflammatory bowel disease, Current Gastroenterology Reports. (2013) 15, article 326,

Crohn’s Disease

• 31. Tsianos, E.V., Katsanos, K.H. and Tsianos, V.E., 2012. Role of genetics in the diagnosis and prognosis of Crohn’s disease. World journal of gastroenterology: WJG, 18(2), p.105
• 32. Plevy S., The immunology of inflammatory bowel disease, Gastroenterology Clinics of North America. (2002) 31, no. 1, 77–92

Ulcerative Colitis

• 33. Spekhorst L. M., Visschedijk M. C., Alberts R. et al., Performance of the Montreal classification for inflammatory bowel diseases, World Journal of Gastroenterology. (2014) 20, 15374–15381
• 34. Hoving, J.C., 2018. Targeting IL-13 as a host-directed therapy against ulcerative colitis. Frontiers in cellular and infection microbiology, 8, p.395
• 35. Liu Z.-J., Yadav P.-K., Su J.-L., Wang J.-S.,and Fei K., Potential role of Th17 cells in the pathogenesis of inflammatory bowel disease, World Journal of Gastroenterology. (2009) 15, no. 46, 5784–5788,
• 36. Gerlach, K., Hwang, Y., Nikolaev, A., Atreya, R., Dornhoff, H., Steiner, S., Lehr, H.A., Wirtz, S., Vieth, M., Waisman, A. and Rosenbauer, F., 2014. TH9 cells that express the transcription factor PU. 1 drive T cell–mediated colitis via IL-9 receptor signaling in intestinal epithelial cells. Nature immunology, 15(7), pp.676-686.

Conclusion: Hope for IBD – and what’s next

• 37. Parker, C.E.; Nguyen, T.M.; Segal, D.; MacDonald, J.K.; Chande, N. Low dose naltrexone for induction of remission in Crohn’s disease. Cochrane Database Syst. Rev. 2018, 4, CD01041054.