The story so far, according to the Creationists Gospel:
Once upon a time, just a few thousand years ago, a magic man in the sky magicked a small flat planet with a dome over it in the Middle East, and then made some people to live on it.
It also made lots of harmful bacteria and other parasites to live in them and make them sick, but luckily, it also gave the humans an immune system to stop the parasites it made to make them sick, from doing what it designed them to do.
The only problem was that the ramshackle immune system it designed, which often doesn't do what it was designed to do, is also a little hypersensitive and prone to treating other things like the body it should be protecting as a parasite and mounting an attack on it so we suffer from all sorts of 'autoimmune' diseases that require another layer of complexity to keep in check. The other thing about it is that it needs training and until that's complete, it will treat all manner of things as parasites, including the food babies eat - and that could result in food allergies that would make life miserable!
But rather than do the simple thing and design the immune system to be able to tell the difference between food and harmful parasites, creationism's version of William Heath-Robinson went for one of the most bizarre solutions you can imagine. Rather like William Heath-Robinson's solution to an every-day problem, it co-opted things in the baby's environment to perform functions they were never intended to perform, like an upright piano being used to stand a step-ladder on to give it enough height, or a stick and some string being used to mend a broken spoke in a wheel, creationism's designer co-opted some of the bacteria that live in a baby's gut.
How it did this is explained in a free access paper in Science Immunology by a team of researchers from the Department of Pediatrics at Weill Cornell Medicine, led by Assistant Professor Dr. Melody Zeng of the Gale and Ira Drukier Institute for Children's Research. Their work is described in a Weill Cornel Medicine news item:
Weill Cornell Medicine investigators discovered that unique bacteria colonize the gut shortly after birth and make the neurotransmitter serotonin to educate gut immune cells. This prevents allergic reactions to food and the bacteria themselves during early development. The preclinical study, published in Science Immunology on Mar. 15, showed that bacteria abundant in the guts of newborns produce serotonin, which promotes the development of immune cells called T-regulatory cells or Tregs. These cells suppress inappropriate immune responses to help prevent autoimmune diseases and dangerous allergic reactions to harmless food items or beneficial gut microbes.
Gut Bacteria in Babies Provide a Helping HandThe gut is now known as the second human brain as it makes over 90 percent of the neurotransmitters in the human body. While neurotransmitters such as serotonin are best known for their roles in brain health, receptors for neurotransmitters are located throughout the human body.
Assistant Professor Dr. Melody Zeng, senior author
Gale and Ira Drukier Institute for Children's Research
and the Department of Pediatrics
Weill Cornell Medicine.
The researchers observed that the neonatal mouse gut had much higher levels of neurotransmitters, including serotonin, than the adult gut.
This was also confirmed in babies through a human infant stool biobank that the Zeng lab has established in collaboration with the Neonatal Intensive Care Unit in the New York-Presbyterian Alexandra Cohen Hospital for Women and Newborns. These samples were obtained with parental consent and deidentified.So far, almost all studies of gut neurotransmitters were conducted in adult animals or human subjects, where a specific gut cell type called enterochromaffin cells produce neurotransmitters. However, we discovered that this isn't the case in the newborn gut where most of the serotonin is made by bacteria that are more abundant in the neonatal gut.
Assistant Professor Dr. Melody Zeng
The study results suggest that before the neonatal gut is mature enough to make its own neurotransmitters, unique gut bacteria may supply neurotransmitters that are needed for critical biological functions during early development.
The high serotonin levels shift the balance of immune cells by increasing the number of Tregs, which helps prevent the immune system from overreacting and attacking gut bacteria or food antigens.We found that gut bacteria in young mice not only directly produce serotonin but also decrease an enzyme called monoamine oxidase that normally breaks down serotonin, thus keeping gut serotonin levels high.
The neonatal gut needs these serotonin-producing bacteria to keep the immune system in check.
Dr. Katherine Sanidad, lead author
Weill Cornell Medicine.
Healthy Immune System Helps Later in Life
Dr. Zeng noted that this work underscores the importance of having the right types of beneficial bacteria soon after birth. Babies in developed countries have better access to antibiotics, less exposure to diverse microbes in their clean environments and potentially unhealthy diets that may significantly impact the abundance of serotonin-producing bacteria in their intestines.
As a result, these babies may have fewer Tregs and develop immune reactions to their own gut bacteria, or allergies to food. This may be one reason food allergies have become increasingly common in children, particularly in developed countries.
The team next plans to look at bacteria in human infant stool samples to measure their production of serotonin, other neurotransmitters and molecules that may help train the immune system to prevent future immune-related diseases, such as allergies, infections and cancer.If educated properly, the immune system in babies would recognize that things like peanuts and eggs are okay, and it doesn't have to attack them. [This may also have an impact on developing autoimmune diseases—when the immune system attacks the body's own healthy cells—later in life.]
Assistant Professor Dr. Melody Zeng
It's essential to understand how the immune system is trained during early life, but this is understudied in newborns and children. Further studies of these developmental periods may hopefully lead us to mitigation approaches to reduce the risk of inflammatory diseases like food allergies and inflammatory bowel disease later in life.
Dr. Katherine Sanidad.
AbstractAnd after all that, as you might expect of creationism's incompetent designer, even that added layer of complexity often fails because people still develop serious food allergies to practically any food you can imagine, but especially to nuts, eggs, shellfish and gluten in wheat.
The gut microbiota promotes immune system development in early life, but the interactions between the gut metabolome and immune cells in the neonatal gut remain largely undefined. Here, we demonstrate that the neonatal gut is uniquely enriched with neurotransmitters, including serotonin, and that specific gut bacteria directly produce serotonin while down-regulating monoamine oxidase A to limit serotonin breakdown. We found that serotonin directly signals to T cells to increase intracellular indole-3-acetaldehdye and inhibit mTOR activation, thereby promoting the differentiation of regulatory T cells, both ex vivo and in vivo in the neonatal intestine. Oral gavage of serotonin into neonatal mice resulted in long-term T cell–mediated antigen-specific immune tolerance toward both dietary antigens and commensal bacteria. Together, our study has uncovered an important role for specific gut bacteria to increase serotonin availability in the neonatal gut and identified a function of gut serotonin in shaping T cell response to dietary antigens and commensal bacteria to promote immune tolerance in early life.
INTRODUCTION
Bacterial colonization of the gut in early life is a critical driver of intestinal maturation and the development of the immune system (1–3), and this is mediated in part by the gut metabolome. Unlike the adult gut, the maturing neonatal gut is enriched with sugars and milk oligosaccharides, colonized by a dynamically changing gut microbiota, and inhabited by maturing immune cells under the influence of microbial and metabolic signals. Recent studies have reported altered gut microbiotas and metabolomes in children with food allergies, asthma, and neurodevelopmental defects (4–6). Early life is also a crucial time window for the establishment of immune tolerance toward gut commensal bacteria as well as dietary and environmental antigens (7, 8). However, it remains poorly understood whether or how the neonatal metabolome influences the development of immune tolerance in early life.
The gut has emerged as a major site of neurotransmitters, including dopamine and serotonin, which are produced mainly by epithelial enterochromaffin cells (ECs) and exert both local and systemic effects on the enteric and central nervous systems (CNSs) (9). Germ-free (GF) mice exhibit abnormal stress responses and fear extinction learning (10–12), in part because of altered availability of metabolites or neurotransmitters for neuronal signaling in the absence of critical gut bacterial to facilitate this process. More evidence has emerged in recent years to shed light on gut bacteria as a critical regulator of neuroinflammation that underlies neurodevelopmental disorders (13–15). Our understanding of the regulation of neurotransmitters in the gut during early development, however, remains limited.
Serotonin (5-hydroxytryptamine or 5-HT) is an essential neurotransmitter known to control gut motility, platelet function, and mood regulation. It is also implicated in gut inflammatory diseases, such as inflammatory bowel disease (IBD) or inflammatory bowel syndrome (8), in part because of indirect effects of 5-HT on enteric neurons. However, it remains unclear whether there is direct cross-talk between 5-HT and gut immune cells. Currently, our understanding of 5-HT synthesis in the gut is solely based on studies of adult animals; the regulation and immune functions of 5-HT in the neonatal gut remain undefined.
This study aimed to elucidate how the neonatal gut metabolome shapes immune response in early life. We identify that the gut metabolome is enriched with neurotransmitters in the mouse neonatal small intestine (SI). Futher, we show that gut bacteria maximize 5-HT availability in the neonatal gut through three independent mechanisms: directly producing 5-HT, inducing host tryptophan hydroxylase 1 (TPH1) to promote the conversion of tryptophan to 5-HT, and limiting the breakdown of 5-HT by down-regulating monoamine oxidase A. In addition, our in vitro and in vivo studies demonstrate that 5-HT directly alters T cell metabolism by increasing intracellular indole-3-acetaladehyde to inhibit mammalian target of rapamycin (mTOR) activation. This promotes the differentiation of regulatory T cells (Tregs) while dampening helper T cell activation both in vitro and in vivo in the neonatal SI. Lastly, we show that 5-HT exposure in the neonatal gut leads to antigen-specific Tregs that confer long-term immune tolerance to both dietary antigens and gut commensal bacteria. Collectively, this work has uncovered a unique neurotransmitter-enriched metabolome in the neonatal gut and a mechanism by which gut bacteria–derived 5-HT promotes oral immune tolerance in early life.
Someone really needs to teach creationism's putative designer the basic elements of good design - minimal complexity, minimal waste and fitness for purpose. It's almost exactly like it's a mindless, utilitarian natural process with no hindsight, no foresight, no plan and no ability to scrap a bad design and start again. But for some reason, creationists seem to regard its efforts as evidence of a supreme intelligence and to prefer it that people think of it as an incompetent fool that couldn't be trusted to design a functional door stop.
The evolutionary explanation for this phenomenon is naturally to be found in the selfish gene theory because it is in the gut microbiome's interest that the infant gut should not produce antibodies to them. Promotion of immune tolerance is thus also beneficial to the gut bacteria. An example of the sort of co-operative co-evolutionary alliance that the selfish gene theory of evolution predicts.
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