Cigarette smoke changes the gut microbiome

When we talk about smoking cigarettes, we usually discuss the harmful effects that it has on our lungs, mouth, skin, and other parts of the body. However, we don't often talk about the gut even though cigarette smoke is the best-known environmental risk factor for Inflammatory bowel diseases (IBD), Crohn’s disease and ulcerative colitis.  While the exact mechanism for why people get these diseases is not yet known, it is recognized that a dysbiosis of the gut plays a contributing role to the onset of these conditions. A research team in Germany investigated the effects that cigarette smoke exposure had on the mucus layer and the microbes in the gut.

The scientists exposed mice to cigarette smoke or air for a period of 24 weeks. They found there was a shift in the microbial community in the caecum and distal colon after exposure to smoke. Specifically, there was an increase in Lachnospiraceae in the colon however it remained the same in the ileum, the last part of the small intestine.

They also found that smoke exposure led to changes in mucin exposure. Mucin is a type of protein that is known for producing gels that act to lubricate and protect parts of the body, both internal and external. The most common mucins are Muc2, Muc3, and Muc4. Muc2 for example is a protein that is secreted onto the mucosal surfaces of the large intestine and serves as a protective barrier for the epithelium. In this study, they found that Muc2, Muc3, and Muc4 gene expression was altered after cigarette smoke exposure.

The authors hypothesize that cigarette smoke affects the immune system in the ileum and may lead to the inflammation associated with Crohn’s disease. Overall, this study found that exposure to cigarette smoke had a profound effect on the gut bacteria and mucin composition in the mouse. While this was not done in humans, the same effects would likely be seen.

A possible new treatment for Lupus by modulating the microbiome

Sweet potatoes are a natural rich source of Vitamin A.

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Lupus is a well-known autoimmune disease that causes inflammation in several organs and can sometimes be fatal.  Its cause is still unknown, but it has recently been implicated with the microbiome, and we have written about it before on this blog.  New research out of Virginia Tech has provided further evidence of this link by showing specific microbiome differences between control and Lupus affected mice.  They also showed that Vitamin A may help improve the the Lupus mice’s conditions.

The researchers tested two groups of mice, one a healthy control group and the other that had a genetic mutation that causes Lupus-like symptoms.  When they studied the microbiomes of these mice they discovered that the Lupus mice had a significant reduction in Lactobacillaceae and increase in Lachnospiraceae.  The researchers then connected the severity of lupus symptoms directly with the levels of these two bacteria (worse symptoms with higher Lachnospiraceae abundance and lower Lactobacillaceae abundance).  Interestingly, Lupus affects almost 10 times more females than males.  These researchers showed that while there was little difference between genders in the control group microbiomes, there was a much higher diversity in the microbiomes of female Lupus mice as compared to male Lupus mice. 

Vitamin A has been shown in humans to relieve the symptoms of Lupus, so the researchers fed the Lupus mice both retinol (pure vitamin A), as well retinoic acid (a metabolite of vitamin A).  While the retinol did not seem to help the Lupus mice, the retinoic acid restored populations of Lactobacillaceae, and relieved symptoms in the Lupus mice.

We know that mice are not a perfect model for humans, but this research shows that the microbiome may be an important factor in Lupus.  As such, it also shows a potential prebiotic, retinoic acid, for the treatment of Lupus.  Lupus is a complex disease, and we do not expect it to be completely understood through the lens of the microbiome, but research like this is important in elucidating possible connections between the two.

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