Weekly Eczema News Report 01/25/2023: Cancer Microbiome and Salon Visits, Covid Immunity, TB Vaccine Boost and A Brief History of Lactose Intolerance

Greetings, everyone! Welcome back! Grab a fuzzy blanket and a cup of your favorite warm beverage, and get ready to cuddle up with the latest in immunology, biological anthropology, and microbiology.

Could a common self-care routine increase your risk of cancer? How do bacteria figure into cancer, obesity, and asthma? How does your first Covid 19 infection affect your immune response to future exposures to the virus? Could exposure to harmless bacteria increase the efficacy of a vaccine against a deadly disease? What does milk have to do with differences in the average height and weight of ancient Europeans? These are all questions science has made an effort to answer in this week’s news. 

Could Salon Visits Increase Your Risk of Cancer?

For years now, doctors and researchers have warned us about the hazards of exposure to UV rays. We know the value of SPF and avoiding tanning beds. You might be surprised that your manicure might be exposing you to the same risks. as sunbathing and tanning beds. 

Researchers at the University of California San Diego found that a single 20-minute session with UV-emitting gel nail polish dryers caused between 20 and 30 percent cell death in human skin cells. Three 20-minute exposures caused 65 to 70 percent cell death. The living cells were left with damage to the mitochondria, as well as several DNA mutations that are observed in skin cancers. 

The study was inspired by an article about a beauty pageant contestant who had been diagnosed with a rare form of skin cancer on her finger, which Ludmil Alexandrov, Professor of Bioengineering and Cellular and Molecular Medicine at UC San Diego, read in his dentist’s waiting room

He and Maria Zhivagui, a postdoctoral scholar and study co-author, began to investigate a possible cause for such a rare cancer in such an unusual place on the body. They found several reports of very rare skin cancers on the hands of estheticians and others who frequently use UV-emitting nail polish dryers. They found little corresponding data on the safety of the devices.

Alexandrov said that there has been “zero molecular understanding” of how the nail-dryers affect skin cells up until now.  Despite this lack of knowledge, Alexandrov says that “they are marketed as safe, with nothing to be concerned about.”

Both Alexandrov and Zhivagui acknowledge that epidemiological studies need to be done before a definitive statement about the association can be made.  Zhivagui, a former fan of the gel manicures, says that she is taking no chances, though: 

“Once I saw the effect of radiation emitted by the gel polish drying device on cell death and that it actually mutates cells even after just one 20-minute session, I was surprised,” she says. “I found this to be very alarming, and decided to stop using it."

The Microbiome of Cancer Cells

Continuing with cancer-related news, scientists have learned that some tumors have different “micro-niches,” with distinct bacteria colonizing these niches. As reported in a recent article in Immunity, these bacteria could be instrumental in the growth and spread of cancer cells. In fact, the researchers say that there are strong indications that bacteria  play several different roles at each stage of tumor formation and growth. 

Studying colorectal and oral cancer tissue samples, the study’s scientists found that a specific bacterium populating some microbiome niches in tumors suppress T-cell activity and recruit myeloid cells. The suppression of T-cell function inhibits the body’s immune response to abnormal cells, while the recruited myeloid cells supply the tumor with growth factors that enable it to generate new blood vessels, expand and send cancer cells through the bloodstream to other sites.

The scientists conducting the study say that they do not yet know on a molecular level how the bacteria influence these processes. However, they note that future cancer treatments might be able to target the niche microbiomes responsible for myeloid recruitment. 

These results in and of themselves are remarkable, but the study is significant for another reason. A novel technique developed by the study authors marks a giant leap in the study of cancers and their progression. Called INVADEseq (invasion-adhesion-directed expression sequencing), it allows researchers to simultaneously sequence human RNA and the 16S rRNA of bacteria within individual cancer cells, and in so doing, to map the molecular and cellular interactions between host and bacterial cells within different micro-niches of a tumor. 

Could Lung Microbiome Influence the Relationship Between Obesity and Asthma? 

There is a well-documented link between obesity and asthma. Obesity and asthma are both characterized by inflammation, and obesity correlates with a specific kind of adult-onset asthma. It is known to cause more severe asthmatic symptoms, with shorter intervals between attacks. Obesity-related asthma is also more likely to resist treatment. Maternal obesity during pregnancy even predisposes children to asthma. 

Over the past few years, disruption of the gut biome has been documented in obese patients, including those with obesity-related asthma. Until now, however, there has not been an examination of the lung microbiome and its relationship to obesity and asthma. 

A study recently published in Immunology Letters acknowledges that the presence of certain bacteria in the lungs–for example Haemophilus influenza and Streptococcus pneumoniae–correlates strongly with obesity-related asthma. The study asserts that maternal obesity influences the development of asthma in children because of epigenetic changes specific to obesity, as well as the obese mother’s influence upon the microbiome of the child. The study advises continued examination of the lung microbiome and its relationship to the gut biome in the development of obesity-related asthma.  

First Covid 19 Infection Influences Immunity to Future Strains of the Virus

Covid 19 has now been with us for just over three years. During this time, multiple waves with rapidly-mutating variants have challenged efforts at developing an effective vaccine against the virus. 

As it turns out, your immune system appears to permanently adapt itself to the strain of the virus that causes your first infection–a process called “imprinting.” With your first infection, memory B cells are generated within your lymph nodes. They circulate throughout the bloodstream and produce antibodies against the virus. However, with Covid 19, new or “naive” B cells are not made for each new strain of the virus you encounter. The memory B cells are “programmed” by the first strain. 

In the case of Covid 19, people who were initially infected with the first strain of the virus or with the Alpha or Beta strains that followed all had different immune responses to the Omicron infection, depending upon which strain they contracted first. In addition, infection with Omicron did not influence the imprinted response, allowing subsequent reinfection. 

Imprinting was observed by the developers of the first influenza vaccine in 1947 (one of those developers–Jonas Salk–went on to develop one of the first successful polio vaccines). They noticed that people who were vaccinated against the current strain of the flu produced antibodies against the first strain with which they’d been infected. 

Imprinting complicates efforts at establishing widespread immunity; even the efficacy of mRNA multiplex vaccines is lessened by these effects. However, even limited immunity is preferable to none, and the mRNA multiplexes remain a promising development.

Scientists Find Potential Environmental Boost for TB Vaccine

Tuberculosis kills upwards of a million people worldwide every year. This airborne bacterial infection is contagious and often resists treatment. While the illness disproportionally affects developing nations, it’s a threat even in wealthy countries–especially for people with compromised immune systems, such as those with AIDS. Rates of TB infection and death have increased with the prevalence of Covid 19, due to overwhelmed healthcare systems that cause delays in diagnosis and treatment. 

The tuberculosis vaccine, called the Bacillus Calmette–Guérin (BCG) vaccine, is given to infants in areas with high rates of infection. The BCG vaccine is not always effective, however, and even where it’s readily available, infection remains a significant driver of mortality. Researchers at Colorado State University, though, have found that the BCG vaccine’s efficacy could potentially be boosted by exposure to bacteria in the same family. 

Tuberculosis is caused by mycobacterium tuberculosis. Like leprosy, m. tuberculosis is one member among hundreds in the mycobacteriaceae family of bacteria. Most of the members of this family do not cause disease, fortunately–mycobacteria are extremely common in water and soil.

The CSU researchers found that mice who were consistently exposed to non-TB mycobacteria after vaccination showed a 50 percent increase in prolonged protection against tuberculosis. 

Using spatial transcriptomics technology (similar to the INVADEseq method mentioned earlier), the researchers identified a robust immune response comprising B cells, antibodies, and new growth of lymphatic structures in the lungs of the mice with vaccine plus exposure. 

These results contradict the widely-held opinion that exposure to mycobacteria leads to decreased protection against tuberculosis after vaccination; this hypothesis makes sense, given the greater populations of mycobacteria in areas with high rates of infection. However, other environmental factors in these areas, such as parasitic infections, could factor into decreased vaccine efficacy. 

In the future, intentional mycobacteria exposure could offer an inexpensive means of increasing the efficacy of the BCG vaccine in humans. While we can’t jump to conclusions from a single mouse-model experiment, the CSU study offers a welcome advance in our understanding of this deadly disease. 

Lactose Tolerance Could Explain Size Increases in Ancient Northern European Populations 

“Drink your milk so you can grow up big and strong!” was once a frequent refrain in pediatrician offices and at dinner tables throughout the Western Hemisphere. While this advice is far less prevalent today, recent studies suggest that milk consumption could have led to size increases among ancient European populations in a period when the average size was decreasing globally. 

The earliest evidence of widespread dairy production dates from Western Asia about 9,000 years ago before spreading globally. Dairy production reached Europe around 7,400 years ago at the latest. 

Today, about 68 percent of adult humans are lactose intolerant. Like other mammals, most of us lose the ability to digest lactose, a sugar heavily concentrated in milk, after infancy. The percentage of lactose intolerance was even higher among the first dairy farmers, who continued to consume milk in spite of the symptoms. At some point, a few of our ancestors began to hang onto their ability to produce lactase, the enzyme that allows us to comfortably drink milk well into adulthood. This is called lactase persistence. 

Lactase persistence did not become common worldwide until the last 7,000 years. In central and northern Europe, this development occurred rapidly alongside long periods of acute famine. This coincidence led researchers to believe that the features of lactose intolerance–diarrhea, gas, and gastric pain–became deadly for many, meaning that lactase persistence provided a survival advantage in these areas. Those with the genetic mutation for lactase persistence would have then gone on to survive and bear young who would continue to spread the mutation (natural selection). 

Testing this hypothesis, researchers at Western University in Ontario, Canada recently examined 3,507 skeletons from 366 archeological sites in the Mediterranean region, southern, central, and northern Europe, the Nile Valley, South Asia, and China. They measured the skeletons’ height and the size of their weight-bearing joints, finding that the average height for men and women began declining about 30,000 years ago. 

The average height reached its minimum around 8,000 and 6,000 years ago–except in central and northern Europe, where both height and body mass increased. This correlates with discoveries about the development of widespread lactase persistence in these areas. The study’s authors postulate that lactase persistence contributed to this size increase while populations elsewhere were becoming smaller. 

Others are skeptical of this hypothesis. Mark Thomas, a Professor of Evolutionary Genetics at University College London, says that while the study’s scope is impressive, it fails to deliver numeric data supporting these hypotheses. 

Either way, this brings us closer to understanding how our ancient ancestors evolved–and it may one day help us understand how we are still evolving.

That’s it for this week, folks. Thank you for reading. We’ll be back next week with more groundbreaking discoveries! Until then, be safe and stay curious.