Smoking Tied to Inflammatory Bowel Disease

Immunologists at RIKEN have discovered how inhaling tobacco smoke might, in some cases, alleviate the symptoms of one of the two main forms of inflammatory bowel disease (IBD).¹ Understanding the mechanism-linked to oral bacteria-could point to new treatments that don't involve inhaling noxious smoke.

It is well established that smoking tobacco can cause a litany of diseases. It is a risk factor for many cancers-famously lung cancer, but also cancers of the throat, stomach and liver among others. It can also give rise to cardiovascular conditions such as heart disease and stroke, metabolic disorders such as type 2 diabetes, and respiratory diseases such as bronchitis and emphysema.

But surprisingly, smoking has previously been linked to a lessening of symptoms in at least one condition: ulcerative colitis, a common IBD characterized by chronic inflammation and the formation of ulcers in the lining of the large intestine.²

Perversely, if you have the other most common type, Crohn's disease-which causes inflammation in the linings across the entire digestive tract-smoking will almost certainly make it worse.²

Both ulcerative colitis and Crohn's disease are complex conditions that are caused by a combination of genetic, immune and environmental factors, and both diseases involve immune cells mistakenly attacking the body's own gut lining.

Since they both involve inflammation in the gut, they produce very similar symptoms that include diarrhea, abdominal pain and cramping, fatigue and weight loss. But the two conditions vary in terms of the depth and location of the inflammation.

Currently, they both often require lifelong management, although some cases of ulcerative colitis can be cured with antibody treatments or surgical removal of the colon and rectum.

Collegial communication

Gastroenterologists have known for decades that people who smoke cigarettes are less likely to have ulcerative colitis than those who have never smoked. They are also aware that quitting smoking can cause ulcerative colitis to flare up. But many immunologists were ignorant of this link, according to Hiroshi Ohno of the RIKEN Center for Integrative Medical Sciences in Yokohama, Japan.

"The connection between smoking and the amelioration of ulcerative colitis is well known among gastroenterologists," he says. "But even now, many working in immunology and basic science are surprised to learn about it."

Ohno himself first found out about this curious effect of smoking through conversations with gastroenterologists. He and his team are exploring how gut microbes affect the health of their hosts and he immediately suspected that gut microbes could be the link between smoking and ulcerative colitis.

Obviously, prescribing smoking to patients with ulcerative colitis is never an option because of the serious potential health risks. But if scientists could discover how smoking exerts this beneficial effect, it may open the way to find alternative, safer ways for treating the condition.

Not smoke and mirrors

Now, in a study involving both mice and people, Ohno and his team have uncovered the mechanism behind the effect for the first time.

They found that smokers with ulcerative colitis had higher concentrations of so-called aromatic chemical compounds in their feces compared with people who had quit smoking. The team also showed that smokers had more bacteria that usually live in the oral cavity, such as Streptococcus mitis, in their colonic mucosal tissue than non-smokers.

These two findings suggest that aromatic compounds in smoke somehow help oral bacteria settle and grow in the colon, rather than passing through the digestive system entirely.

"The mechanism appears to involve aromatic compounds in tobacco smoke, such as hydroquinone, which can promote the colonization of oral bacteria on the gut lining," explains Ohno.

He says that his mouse studies show the bacteria may then play a key role in dampening the inflammation seen in ulcerative colitis, as S. mitis promotes a specific immune response in the colon.

In particular, S. mitis colonization results in the increase of T helper 1 cells-specialist immune cells that play an important role in attacking pathogenic viruses and bacteria in the gut.

These T helper 1 cells help to dampen the normal initial immune response of T helper 2 cells during an ulcerative colitis flare-up. T helper 2 cells specialize in helping B cells produce antibodies against pathogens such as parasites, bacteria, toxins and so on. Overactivation of these cells leads to attacks on healthy colon and rectal tissue and the resultant inflammation seen in ulcerative colitis patients.

Conversely, the presence of S. mitis increases the severity of Crohn's disease, which is caused by overactive T helper 1 cells mistakenly attacking the gut's tissues.

New treatment possibilities

Ohno and his team demonstrated this effect in mice models of ulcerative colitis and Crohn's disease. They found that administering S. mitis to the mice orally for five days produced a similar effect as smoking: it eased inflammation in mice with ulcerative colitis but exacerbated it in mice with Crohn's. Feeding the mice another Streptococcus strain, S. rubneri, found in the saliva of smokers had no such effect.

Having uncovered the links between smoking, hydroquinone, S. mitis and T helper 1 cells in the colon, Ohno believes it may be possible to alleviate ulcerative colitis using strategies that are safer than smoking. For example, patients with ulcerative colitis might be treated with hydroquinone, which could induce S. mitis to migrate to the colon. Alternatively, it could be possible to supply S. mitis directly to the gut by consuming it as a probiotic pill.

"By using one of these approaches, it could well be possible to mimic the beneficial effects of smoking while bypassing all its negative effects," says Ohno.

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References

• 1. Miyauchi, E., Taida, T., Uchiyama, K., Nakanishi, Y., Kato, T. et al. Smoking affects gut immune system of patients with inflammatory bowel diseases by modulating metabolomic profiles and mucosal microbiota. Gut advanced online publication August 2025. doi: 10.1136/gutjnl-2025-334922
• 2. Mahid, S. S., Minor, K. S., Sotoa, R. E., Hornung, C. A. & Galandiuk, S. Smoking and inflammatory bowel disease: a meta-analysis. Mayo Clinic Proceedings 81, 1462-1471 (2006). doi: 10.4065/81.11.1462

About the researcher

Hiroshi Ohno