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Pregnant women may pass on the effects of stress to their fetus by way of bacterial changes in their vagina, suggests a study in mice. It may affect how well their baby’s brain is equipped to deal with stress in adulthood.

The bacteria in our body outnumber our own cells by about 10 to 1, with most of them found in our gut. Over the last few years, it has become clear that the bacterial ecosystem in our body – our microbiome – is essential for developing and maintaining a healthy immune system.

Our gut bugs also help to prevent germs from invading our bodies, and help to absorb nutrients from food.

A baby gets its first major dose of bacteria in life as it passes through its mother’s birth canal. En route, the baby ingests the mother’s vaginal microbes, which begin to colonise the newborn’s gut.

Chris Howerton, then at the University of Pennsylvania in Philadelphia, and his colleagues wanted to know if this initial population of bacteria is important in shaping a baby’s neurological development, and whether that population is influenced by stress during pregnancy.

Stressful pregnancy

The first step was to figure out what features of the mother’s vaginal microbiome might be altered by stress, and then see if any of those changes were transmitted to the offspring’s gut.

To do this, the team exposed 10 pregnant mice to a different psychologically stressful experience, such as exposing them to fox odour, keeping their cages lit at night, or temporarily restraining them every day for what would be the equivalent of the first trimester of their pregnancy. Another 10 pregnant mice were housed normally during the same time.

The team took samples of their vaginal bacteria throughout the pregnancy and again just after the mice had given birth. These samples were genetically sequenced to see what types of bacteria were present.

The microbiomes of the stressed mice were remarkably different to those of the unstressed mice after they had each given birth. There were more types of bacteria present, and the proportion of one common gut bacteria, Lactobacillus, was significantly reduced.

Like mother, like pup

To see whether these changes had been passed on to the pups, a few days after birth the pups’ nascent gut bacteria was removed from their colon and sequenced. Sure enough, the same bacterial patterns were seen in the pups of stressed mothers.

By analysing tissue from the pups’ hypothalamus – a brain area involved in hormone control, behaviour and sleep, among other things – the team was able to infer which genes were affected by the stress-induced changes in each mother’s microbiome.

They found that the expression of 20 genes was affected by the decrease in Lactobacillus, including genes related to the production of new neurons and the growth of synaptic connections in the brain.

These genetic outcomes in the brain are probably a result of a different suite of nutrients and metabolites circulating in the “stressed” pup’s blood, thanks to the altered gut flora they inherited. Indeed, when the team analysed the blood of the pups of the stressed mothers, they found that there were fewer molecules present necessary for the formation of essential neurotransmitters – chemicals that transmit signals to the brain. Furthermore, there were lower levels of a molecule thought to protect the brain from harmful oxidative stress.

“These changes are significant and are likely to be important for determining how the brain initially develops and how it will respond in the future to things like stress or changes in the environment,” says Tracy Bale, Howerton’s supervisor during the research and director of the University of Pennsylvania lab.

As well as changing the nutrients available, the microbiome could also affect the brain via the immune system or by innervating the nerves in the gut that connect to it. “These three mechanisms aren’t mutually exclusive. It’s likely that they all play a role,” says Howerton.

Human angle

If the same effects are seen in humans, there may be a straightforward solution. “We can easily manipulate the bacteria we have inside of us,” says Howerton. For example, if a certain cocktail of bacteria is found to be beneficial to the newborns of stressed mothers, we could give it to them right after birth, he suggests. This approach could also benefit babies born via C-section, who do not pass through their mother’s birth canal, or those born to mothers whose gut bacteria has been disrupted as a result of antibiotic use during pregnancy.

Bale is now investigating the link between bacteria and brain development in pregnant women who have been through several traumatic experiences to analyse the effects on their babies’ gut bacteria. She also intends to follow their children’s behaviour as they grow up.

Resource rationale

“This is a remarkable trans-disciplinary study in how it bridged multiple organ systems to illuminate a complex question,” says Catherine Hagan from the University of Missouri in Columbia. She says that more work needs to be done to show a causal link. “Mice are not tiny people – people are not big mice – more data is needed to understand how stress in mothers affects brain development in children,” she says. “That said, mice and people have enough in common that this study provides a rationale for allocating resources to address such a concern.”

“At the end of the day, most of what makes you ‘you’, and what drives your quality of life, comes down to the brain,” says Bale. “It’s this very important, vulnerable tissue that is susceptible to many perturbations. If the microbiome is proven to be one of these driving forces, then it’s essential we know just how factors in our environment can change it and can reprogram the brain.”

The research was presented this week at the Society for Neuroscience conference in San Diego, California.

Read more: https://www.newscientist.com/article/dn24586-pregnant-mothers-stress-affects-babys-gut-and-brain/#ixzz5vqZCynkf

The earliest evidence that the gut might be involved in Parkinson’s emerged more than 200 years ago. In 1817, the English surgeon James Parkinson reported that some patients with a condition he termed “shaking palsy” experienced constipation. In one of the six cases he described, treating the gastrointestinal complaints appeared to alleviate the movement-related problems associated with the disease.

Since then, physicians have noted that constipation is one of the most common symptoms of Parkinson’s, appearing in around half the individuals diagnosed with the condition and often preceding the onset of movement-related impairments. Still, for many decades, the research into the disease has focused on the brain. Scientists initially concentrated on the loss of neurons producing dopamine, a molecule involved in many functions including movement. More recently, they have also focused on the aggregation of alpha synuclein, a protein that twists into an aberrant shape in Parkinson’s patients. A shift came in 2003, when Heiko Braak, a neuroanatomist at the University of Ulm in Germany, and his colleagues proposed that Parkinson’s may actually originate in the gut rather than the brain.

Braak’s theory was grounded in the observation that in post-mortem samples of Parkinson’s patients, Lewy bodies, clumps of alpha synuclein, appeared in both the brain and the gastrointestinal nervous system that controls the functioning of the gut. The work by Braak and his colleagues also suggested that the pathological changes in patients typically developed in predictable stages that starts in the gut and ends in the brain. At the time, the researchers speculated that this process was linked to a “yet unidentified pathogen” that travels through the vagus nerve—a bundle of fibers connecting major bodily organs to the brainstem, which joins the spinal cord to the brain.

The idea that the earliest stages of Parkinson’s disease may occur in the gastrointestinal tract has been gaining traction. A growing body of evidence supports this hypothesis, but the question of how changes in the intestines drive neurodegeneration in the brain remains an active area of investigation. Some studies propose that aggregates of alpha synuclein move from the intestines to the brain through the vagus nerve. Others suggest that molecules such as bacterial breakdown products stimulate activity along this channel, or that that the gut influences the brain through other mechanisms, such as inflammation. Together, however, these findings add to the growing consensus that “even if the pathology [of Parkinson’s] is very much driven by brain abnormalities, it doesn’t mean that the process starts in the brain,” says Michael Schlossmacher, a physician-scientist at the Ottawa Hospital Research Institute.

THE GUT-BRAIN HIGHWAY

The vagus nerve, a bundle of fibers that originates in the brain stem and innervates major organs, including the gut, may be the primary route through which pathological triggers of Parkinson’s travel from the gastrointestinal tract to the brain. Recent epidemiological examinationsof vagotomy patients whose vagus nerves were severed show that they have a lower risk of developing Parkinson’s. Researchers have also demonstrated that alpha-synuclein fibers, injected into the gastrointestinal tracts of rodents, can traverse through the vagus into the brain.

If alpha-synuclein does travel from the intestines to the brain, the question still arises: Why does the protein accumulate in the gut in the first place? One possibility is that alpha-synuclein produced in the gastrointestinal nervous system helps fight off pathogens. Last year, Michael Zasloff, a professor at Georgetown University, and his colleagues reported that the protein appeared in the guts of otherwise healthy children after norovirus infections, and that, at least in a lab dish, alpha-synuclein could attract and activate immune cells.

Microbes themselves are another potential trigger for promoting the build-up of intestinal alpha-synuclein. Researchers have found that, in mice, bacterial proteins could trigger the aggregation of the alpha-synuclein in the gut and the brain. Some proteins made by bacteria may form small, tough fibers, whose shape could cause nearby proteins to misfold and aggregate in a manner akin to the prions responsible for mad cow disease, explains Robert Friedland, a neurologist at the University of Louisville who coauthored that study.

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This experiment was conducted to investigate the effect of exposure to high altitude and low oxygen on intestinal microbial communities using mice as an animal model. Fecal microbiota from mice housed in a control environment representing 2,200 meters (NC group) above sea level with 16% Oxygen and mice that were placed in a hypobaric chamber representing 5000 meters (HC group) above sea level with 11% Oxygen for 30 days, were analyzed by the HiSeq Illumina sequencing platform. The results showed a significant difference in beta diversity observed between the two groups, while no significant difference was observed in alpha diversity.

Compared with the NC group, the relative abundance of class Epsilonproteobacteria, phlym Actinobacteria, class Erysipelotrichia and genus Helicobacter were significantly lower (P<0.05), while the relative abundance of genus Alistipes was increased in the HC group; Phenotypic analysis showed no significant difference in aerobic, anaerobic, facultatively anaerobic, potentially pathogenic, stress tolerant, mobile element, biofilms formation, gram negative and gram positive between HC group and NC group; Functional analysis results showed significant differences in 34 gene functional metabolic pathways (carbohydrate digestion and absorption, energy metabolism, arachidonic acid metabolism, flavonoid biosynthesis, RIG-I-like receptor signaling pathway, etc) between HC group and NC group.

Together, these findings suggest that exposure to high altitude and low oxygen had the potential to change the intestinal microbial communities, which potentially may modulate metabolic processes in mice.

Source: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0203701

Females and males differ in the energy consumption and nutritional requirements which are based on the interactions between environmental factors and sex hormones. The studies in early 1940s ascertained that females have enhanced capability of producing antibodies. This enhanced immune reactivity in females helps mount an effective resistance to infection and therefore females are less susceptible to viral infections, but can develop immune-pathogenic effects and predisposition to autoimmunity due to hyper immune responses. Sex hormones can also control the immune response via circadian rhythm.

Many hormones like cortisol, known to regulate T cell mediated inflammation, have a circadian rhythm with a maximum peak at 8:00 a.m. and progressively lower levels as the day progresses. Interaction between sex hormones and environmental factors like cigarette smoke and infections lead to variable responses in both genders. There is emerging evidence that sex hormones impact microbial composition and the resulting immune response via secondary metabolites binding with receptors like estrogen receptors (ERs), peroxisome proliferator-activated receptors (PPARs). These differences in immune response can lead to variability in disease phenotypes with autoimmunity occurring more often in females and cancers occurring more in males.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6119719/

Stress adjusts gut bacteria in mice

Researchers found that the social pressure/stressed group had more Bilophila and Dehalobacterium than the controls.   Researchers have also discovered more elevated amounts of these gut bacteria in individuals with MS (multiple sclerosis).

Researchers discovered that there is a chain of occasions whereby stress introduction (1), changes to gut bacteria (2), and changes to immune cells (4) lead to a higher risk of an autoimmune attack (5, result).

Source: https://www.medicalnewstoday.com/articles/325193.php