Exploring the Paradoxical Effects of Smoking on Inflammatory Bowel Diseases

Inflammatory bowel diseases (IBD) are a significant concern for doctors and researchers due to their chronic impacts, such as persistent abdominal pain, diarrhea, fatigue, and weight loss. Among these diseases are Crohn’s disease and ulcerative colitis, where smoking has contrasting effects. While smoking increases the risk of Crohn’s disease, it appears to protect against ulcerative colitis. This article aims to explore the role gut bacteria play in explaining this strange phenomenon.

Smoking and Its Contradictory Effects

Scientists and doctors have long been puzzled by the contradictory effects of smoking on IBD. While smoking is a risk factor for Crohn’s disease, it seems to offer some protection against ulcerative colitis. This contradiction prompted a research team at RIKEN IMS, led by Ohno, to investigate the role gut bacteria might play in this context.

The researchers based their study on human clinical data and mouse experiments to reach their conclusions. They found that in smokers with ulcerative colitis, certain bacteria typically found in the mouth, such as Streptococcus, appear in the gut, specifically in the colonic mucosa.

The Role of Gut Metabolites

When the researchers examined gut metabolites, the small molecules produced in the gut during food breakdown by the body and bacteria, they found that levels of several metabolites were higher in smokers with ulcerative colitis compared to former smokers. Among these metabolites, they discovered that “hydroquinone” promotes the growth of Streptococcus bacteria in the gut mucosa.

This discovery indicates that smoking-related metabolites, like hydroquinone, contribute to the proliferation of oral bacteria in the gut. However, the question remains: how do these bacteria help reduce inflammation? And why don’t they alleviate Crohn’s disease inflammation?

The Role of Oral Bacteria in the Immune System

The researchers revisited the oral bacteria they found growing in the guts of smokers with ulcerative colitis. They isolated 10 strains from the saliva of smokers and treated mouse models of Crohn’s disease and ulcerative colitis with each of these strains for five days.

The results showed that administering S. mitis bacteria to the mice had almost the same effect as smoking. It reduced inflammation in mice with ulcerative colitis and worsened it in those with Crohn’s disease. Analyses revealed that S. mitis stimulated the emergence of Th1 helper cells, an important part of the gut’s immune response against invaders.

Conclusion

The findings suggest that the transfer of bacteria from the mouth to the gut, particularly Streptococcus bacteria, and the subsequent immune response in the gut, is the mechanism by which smoking helps protect against ulcerative colitis. However, due to the significant health risks of smoking, relying on it as a treatment is unsustainable. The research offers hope that direct treatment with these types of bacteria or indirect treatment using hydroquinone might mimic the beneficial effects of smoking while avoiding its negative impacts.