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Autoimmune Disease, Bioengineering, Immunology, Research, Stanford News

Adult humans harbor lots of risky autoreactive immune cells, study finds

Adult humans harbor lots of risky autoreactive immune cells, study finds

dangerIf a new study published in Immunity is on the mark, the question immunologists may start asking themselves will be not “Why do some people get autoimmune disease?” but “Why doesn’t everybody get it?”

The study, by pioneering Stanford immunologist Mark Davis, PhD, and colleagues, found that vast numbers of self-reactive immune cells remain in circulation well into adulthood, upending a long-established consensus among immunologist that these self-reactive immune cells are weeded out early in life in an organ called the thymus.

A particular type of immune cell, called “killer T cells,” is particularly adept at attacking cells showing signs of harboring viruses or of becoming cancerous. As I wrote in my news release about Davis’s study:

[The human immune system generates] a formidable repertoire of such cells, collectively capable of recognizing and distinguishing between a vast array of different antigens – the biochemical bits that mark pathogens or cancerous cells (as well as healthy cells) for immune detection. For this reason, pathogenic invaders and cancerous cells seldom get away with their nefarious plans.

Trouble is, I wrote:

[This repertoire includes] not only immune cells that can become appropriately aroused by any of the billions of different antigens characteristic of pathogens or tumors, but also immune cells whose activation could be triggered by myriad antigens in the body’s healthy tissues. This does happen on occasion, giving rise to autoimmune disease. But it happens among few enough people and, mostly, late enough in life that it seems obvious that something is keeping it from happening to the rest of us from day one.

It’s been previously thought that the human body solves this problem by eliminating all the self-reactive T cells during our early years via a mysterious select-and-delete operation performed in a mysterious gland called the thymus that’s nestled between your heart and your breastbone. Sometime in or near your early teens, the thymus mysteriously begins to shrink, eventually withering and largely turning to useless fat. (Is that mysterious enough for you? It sure creeps me out.)

But Davis and his team used some sophisticated technology – some of it originally invented by Davis, some of it by Stanford bioengineering professor and fellow study co-author Stephen Quake, PhD – to show that, contrary to prevailing dogma, tons of self-reactive killer T-cells remain in circulation well into adulthood. Then the scientists proceeded to explore possible reasons why the immune system keeps these risky cells around (it boils down to: just in case a pathogen from Mars comes along and we need to throw the kitchen sink at it) and why (at least most of the time) they leave our healthy tissues alone: A still-to-be-fully-elucidated set of molecular mechanisms keeps these self-reactive cells locked in the biochemical equivalent of parking gear, shifting out of which requires unambiguous signs of an actual pathogen’s presence: bits of debris from a bacterial cell wall, or stretches of characteristically viral DNA.

That’s our immune system, folks. Complicated, mysterious, and yet somehow incredibly efficient. You really don’t want to leave home – or even the womb – without it.

Previously: In human defenses against disease, environment beats heredity, study of twins shows, Knight in lab: In days of yore, postdoc armed with quaint research tools found immunology’s Holy Grail, In men, a high testosterone count can mean a low immune response and Deja vu: Adults’ immune systems “remember” microscopic monsters they’ve never seen before
Photo by Frederic Bisson

Big data, Emergency Medicine, Genetics, Infectious Disease, Research, Stanford News

Study means an early, accurate, life-saving sepsis diagnosis could be coming soon

Study means an early, accurate, life-saving sepsis diagnosis could be coming soon

image.img.320.highA blood test for quickly and accurately detecting sepsis, a deadly immune-system panic attack set off when our body wildly overreacts to the presence of infectious pathogens, may soon be at hand.

Sepsis is the leading cause of hospital deaths in the United States and is tied to the early deaths of at least 750,000 Americans each year. Usually caused by bacterial rather than viral infections, this intense, dangerous and rapidly progressing whole-body inflammatory syndrome is best treated with antibiotics.

The trouble is, sepsis is exceedingly difficult to distinguish from its non-infectious doppelganger: an outwardly similar but pathogen-free systemic syndrome called sterile inflammation, which can arise in response to traumatic injuries, surgery, blood clots or other noninfectious causes.

In a recent news release, I wrote:

[H]ospital clinicians are pressured to treat anybody showing signs of systemic inflammation with antibiotics. That can encourage bacterial drug resistance and, by killing off harmless bacteria in the gut, lead to colonization by pathogenic bacteria, such as Clostridium difficile.

Not ideal. When a patient has a sterile inflammation, antibiotics not only don’t help but are counterproductive. However, the occasion for my news release was the identification, by Stanford biomedical informatics wizard Purvesh Khatri, PhD, and his colleagues, of a tiny set of genes that act differently under the onslaught of sepsis from they way they behave when a patient is undergoing sterile inflammation instead.

In a study published in Science Translational Medicine, Khatri’s team pulled a needle out of a haystack – activity levels of more than 80 percent of all of a person’s genes change markedly, and in a chaotically fluctuating manner over time, in response to both sepsis and sterile inflammation. To cut through the chaos, the investigators applied some clever analytical logic to a “big data” search of gene-activity results on more than 2,900 blood samples from nearly 1,600 patients in 27 different data sets containing medical information on diverse patient groups: men and women, young and old, some suffering from sterile inflammation and other experiencing sepsis,  and (as a control) healthy people.

The needle that emerged from that 20,000-gene-strong haystack of haywire fluctuations in gene activity consisted of an 11-gene “signature” that, Khatri thinks, could serve up a speedy, sensitive, and specific diagnosis of sepsis in the form of a simple blood test.

The 11-gene blood test still has to be validated by independent researchers, licensed to manufacturers, and approved by the FDA. Let’s hope for smooth sailing. Every hour saved in figuring out a possible sepsis sufferer’s actual condition represents, potentially, thousands of lives saved annually in the United States alone, not to mention billions of dollars in savings to the U.S. health-care system.

Previously: Extracting signal from noise to combat organ rejection and Can battling sepsis in a game improve the odds for material world wins?
Photo by Lightspring/Shutterstock

Big data, Ethics, Genetics, Science Policy, Stanford News

Stanford panel: Big issues will loom when everyone has their genomic sequence on a thumb drive

Stanford panel: Big issues will loom when everyone has their genomic sequence on a thumb drive

When I was a biology grad student in the early 1980s, we used to joke about people who were getting their PhDs by spending six long years sequencing a single gene. They worked around the clock seven days a week – and seven nights, too, sleeping on their lab benches when they slept at all.

A few years later the Human Genome Project came along and sped things up quite a bit. But it still took 13 years and a billion dollars to fully sequence a single human genome.

It’s a different story now. With a one-day, $1,000 genome sequence in sight, a 20-minute, $100 sequence can’t be far off. It appears that within 15 years or so, the average individual’s genomic sequence will be just another lengthy, standard supplemental addition to that person’s electronic medical record.

That raises a lot of questions. Last Saturday, I had the great privilege of asking a few of them to a panel of three tier-one Stanford experts: Mildred Cho, PhD, associate director of the Stanford Center for Biomedical Ethics; Hank Greely, JD, director of the Center for Law and the Biosciences, and Mike Snyder, MD, PhD, chair of Stanford’s genetics department and director of the Center for Genomics and Personalized Medicine. (I was the moderator.)

The panel, titled “Genetic Privacy: The Right (Not) to Know,” was a lively one, part of a day-long Alumni Day event sponsored by the Stanford Medical Center Alumni Association. (Here’s a link to the video above). Cho, Greely and Snyder have their own well-developed perspectives and policy preferences on the utility of mass genomic-sequence availability, and they articulated those views with passion and aplomb.

The 300 people in the audience, most of them doctors, had plenty of questions of their own. Several were ones I’d hoped to ask but hadn’t had time.

By the time I walked away from this consciousness-raising clash of perspectives, newly aware of just how fast the future is coming at us, I had another question: Once everyone has the equivalent of a thumb drive with their complete genome on it, can you imagine a kind of online matchmaking service in which you upload your genome to a server, which then picks out a date or a mate for you? The selection is guided by what you say you’re looking for: short-term mutual attraction, an enduring monogamous relationship, robust offspring … Is that now thinkable?

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Bioengineering, Imaging, Neuroscience, Research, Stanford News, Stem Cells

New way to watch what stem cells transplanted into the brain do once they get there

New way to watch what stem cells transplanted into the brain do once they get there

binocularsStem cell replacement therapy is a promising but problem-plagued medical intervention.

In a recent news release detailing a possible way forward, I wrote:

Many brain disorders, such as Parkinson’s disease, are characterized by defective nerve cells in specific brain regions. This makes disorders such as Parkinson’s excellent candidates for stem cell therapies, in which the defective nerve cells are replaced. But the experiments in which such procedures have been attempted have met with mixed results, and those conducting the experiments are hard put to explain them.

That’s because there’s been no good way to evaluate what those transplanted stems cells are doing once you’ve put them inside a living individual. I mean, you’re not gonna break into someone’s brain every couple of days to take a peek, right? Instead, you have to look for behavioral changes. Is the patient or experimental animal walking better (if you’re trying to treat Parkinson’s), or (if it’s Alzheimer’s) remembering better ? Then, even when you see those changes, you still don’t know whether new nerve cells derived from the newly transplanted cells integrated into the proper brain circuits and are now functioning correctly there, or whether the originally transplanted cells are just sitting around secreting some kind of feel-good factor to pep up ailing cells in the vicinity, juicing their  performance. Or maybe it was a placebo effect.

It’s hard to improve on a procedure when you don’t really know what went wrong – or even what went right – on the last attempt. Optimizing the regimen becomes a matter of guesswork and luck.

But in a new study in NeuroImage, neuroscientist/bioengineer Jin Hyung Lee, PhD, and her colleagues came up with a way to peer deep into the living brain and view the results of a stem-cell transplant procedure. They combined an established brain-imaging technique with a newer but increasingly widespread one, called optogenetics, that lets researchers stimulate specific cells.

The first step in optogenetics is to genetically modify the cells you want to stimulate, so that their surfaces become coated by a photosensitive protein that generates electric current in response to laser light. Lee’s team performed this operation on the stem cells before transplanting them into rats’ brains. This way, they could selectively stimulate nerve cells derived from those stem cells and,  using the brain-imaging technique, see if doing so triggered nerve-cell activity at the site of the transplant as well as other places in the brain with which the new cells had established connections.

In these experiments, the stem-cell-derived nerve cells survived, matured into nerve cells, integrated into targeted brain circuits and, most important, fired on cue and ignited activity in downstream nerve circuits. But had all that not happened, at least the researchers would have been able to pinpoint the weak link in the chain.

In principle, the new approach should be possible to use for all kinds of stem-cell therapies, and in humans as well as animals. As Lee told me when I interviewed her for my release on her new study, “If we can watch the new cells’ behaviors for weeks and months after we’ve transplanted them, we can learn – much more quickly and in a guided way rather than a trial-and-error fashion – what kind of cells to put in, exactly where to put them, and how.”

If this light-driven stem-cell-monitoring technique or some others I’ve reported on hold up, brave explorers may no longer have to poke around in the dark.

Previously: Alchemy: From liposuction fluid to new liver cells, Iron-supplement-slurping stem cells can be transplanted, then tracked to make sure they’re making new knees, You’ve got a lot of nerve! Industrial-scale procedure for generating plenty of personalized nerve cells and Nano-hitchhikers ride stem cells into heart, let researchers watch in real time and weeks later
Photo by Nicki Dugan Pogue

Autoimmune Disease, Cancer, Infectious Disease, Microbiology, Nutrition, Stanford News

Getting to the good gut: how to go about it

Getting to the good gut: how to go about it

In a blog post a few years ago I wrote, The Good Gutwith misplaced parenthetical self-assuredness:

Anybody who’s ever picked up an M&M off the sidewalk and popped it into his or her mouth (and, really, who among us hasn’t?) will be gratified to learn that the more germs you’re exposed to, the less likely you are to get asthma … hay fever and eczema.

I soon learned to my surprise, if not necessarily to my embarrassment, that virtually nobody – at least nobody over 6 – cops to having stooped-and-scooped as I routinely did as a kid on what I called my “lucky-sidewalk” days.

But those M&Ms may have been the best pills I ever took.

Stanford microbiologists Justin Sonnenburg, PhD, and Erica Sonnenburg, PhD, (they’re married) have written a new book, The Good Gut, about the importance of restocking our germ-depleted lower intestines.

Massive improvements in public sanitation and personal hygiene, the discovery of antibiotics and the advent of sedentary lifestyles have taken a toll on the number and diversity of microbes that wind up inhabiting our gut. According to The Good Gut, we need more, and more varieties, of them. And we need to treat them better. The dearth of friendly microorganisms in the contemporary colon is due not just to a lack of bug intake but to a lack of fiber in the modern Western diet. Indigestible to us, roughage is the food microbes feast on.

The Good Gut packages that message for non-scientists. “We wanted to convey the exciting findings in our field to the general public,” Justin Sonnenberg recently told me. “We’d noticed we were living our life differently due to our new understanding. We were eating differently and had modified both our own lifestyle and the way we were raising our children.”

In simple language, the Sonnenburgs explain how the pieces of our intestinal ecosystem fit together, what can go wrong (obesity, cancer, autoimmunity, allergy, depression and more), and how we may be able to improve our health by modifying our inner microbial profiles. Their book includes everything from theories to recipes, along with some frank discussion of digestive processes and a slew of anecdotes capturing their family’s knowledge-altered lifestyle.

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Ebola, Global Health, Infectious Disease, Microbiology, Research

Can a single drug outsmart many kinds of viral invaders?

Can a single drug outsmart many kinds of viral invaders?

blue virus

We’ve got plenty of effective antibiotics – maybe even too many– to knock off bacteria we don’t like. But when it comes to viruses, it’s a different story, Stanford infectious-disease specialist Shirit Einav, MD, and postdoc Elena Bekerman, PhD, write in a recently published perspective piece in Science.

“Although hundreds of viruses are known to cause human disease, antiviral therapies are approved for fewer than 10,” the authors write, before going on:

[Antiviral drugs that interfere with crucial viral enzymes] have shown considerable success in the treatment of HIV and hepatitis C virus… infections. However, this approach does not scale easily and is limited particularly with respect to emerging viruses against which no vaccines or antiviral therapies are approved.

Which is too bad, because viruses can be nasty. Not to mention creepy: They’re master puppeteers when it comes to manipulating us into submission. They can’t even replicate on their own. The little body-snatchers need our own cells, which they break into, bamboozle, and bully into producing copies of themselves and then squirting them out so they can infect other cells and, with luck, other people.

A partial list of merging and re-emerging viruses for which there are no decent treatments includes dengue, estimated to infect 400 million people each year; SARS and MERS, responsible for outbreaks of severe acute respiratory syndromes; and Ebola, which, as everybody now knows, caused an ongoing epidemic in Africa.

Developing antiviral drugs is a huge challenge. It takes, on average, more than $2 billion and about a decade, plus or minus a couple of years, to develop a new drug targeting just one single type of virus, Bekerman and Einav write. To make things worse, these nano-villains evolve even faster than bacteria do.

Einav’s research has been taking a different tack. She’s working on drugs that, instead of gumming up this or that viral enzyme (at least until it mutates into a form the drug can’t gum up), interfere with the activity of components in our cells that the viruses absolutely depend on for their own survival and replication. There are already drugs, many of them already approved for far different indications such as cancer, that can do just that – without, however, disabling our own cells so much that the cure becomes worse than the disease.

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Imaging, Research, Stanford News, Stroke, Technology

Image-interpretation software could open window of treatment for stroke

Image-interpretation software could open window of treatment for stroke

open windowRestoring blood flow to the brain quickly after a stroke is key to damage control as well as to optimal recovery. But restoring blood flow to brain tissue that is already dead can cause problems, like swelling and hemorrhage.

That makes the treatment of choice – an intravenous dose of a substance called tPA, which dissolves clots – a double-edged sword. The consensus in the medical community is that tPA is not a good idea once 4-1/2 hours have elapsed since a patient has suffered a stroke.

But the consensus is based on averages, derived from numerous studies. Clinicians have tended to treat that 4-1/2 hour time-point as analogous to a window slamming shut. Yet every stroke, and every patient who experiences one, is unique.

A new study published in the New England Journal of Medicine joins three earlier ones that show improved results when tPA administration is combined with the insertion of a device – a so-called stent retriever – that can mechanically break up clots in the brain.

Even more exciting, two of the four studies, including the new one, employed software called RAPID – designed and developed at Stanford at the instigation of Stanford neurologist Greg Albers, MD – that quickly interprets brain scans of patients and helps clinicians decide which patients will benefit from supplementing the standard intravenous tPA infusion with the stent retrieval procedure. In both of these two studies, substantial majorities of patients selected as good candidates for the combination had extremely high rates of solid recovery as measured three months after their stroke – the best results ever obtained in stroke studies.

Albers, who is also one of the co-authors of the new NEJM study, hopes to move stroke care away from the clock on the wall and instead focus on a biological clock – what the brain image shows to be going on inside this patient’s brain, now – so that each patient’s care can be individualized and optimized. It could turn out that for some patients, 4-1/2 hours after a stroke is already too late for aggressive clot-busting treatment, while for others the window remains wide open for 6, 7, 8 hours or longer.

Previously: Targeted stimulation of specific brain cells boosts stroke recovery in mice, Calling all pharmacologists: Stroke-recovery mechanism found, small molecule needed and Stanford neuroscientists uncover potential drug treatment for stroke
Photo by glasseyes view

Neuroscience, Research, Sleep, Stanford News

New findings on exactly why our “idle” brains burn so much fuel

New findings on exactly why our "idle" brains burn so much fuel

1959 Cadillac

“The human brain is a greedy organ,” I wrote in my release describing a new Stanford study before elaborating:

Accounting for only 2 percent of the body’s weight, it consumes 20 percent of the body’s energy. Yet the rate at which the brain gobbles glucose (the fuel our brain cells run on) barely budges when we cease performing a physical or mental activity. Even at rest, the brain seems engaged in a blizzard of electrical activity, which neuroscientists have historically viewed as useless “noise.”

The study, which appears today in in Neuron, sheds light on why the brain paradoxically appears to exhaust so much energy in what at first glance seems akin to the idling of a car’s engine. Although you wouldn’t know it from just staring at it, the human brain is a complicated orchestra of electrical circuits constantly humming along with one another over the comparatively long distances that separate one part of the organ from another.

Over the past decade, neuroscientists using brain-imaging methods have identified dozens of distributed, collaborative clusters of brain regions working in concert and dedicated to various mental activities from solving math problems to recalling what one ate for breakfast.

Now a team led by Stanford neuroscientist Josef Parvizi, MD, PhD, has tracked the electrical activity within and between these simultaneously pulsing clusters (or, in Neurospeak, “networks”) with more precision than has previously been possible, and shown that these closely coordinated firing patterns persist even during sleep. This, in turn, may go a long way to explaining why when it comes to how fast the brain guzzles energy, the most intense thoughts, emotions or actions on our part barely budge the needle.

In their study, Parvizi and his colleagues were able to dig deeper than brain-imaging studies can usually go, because they could directly record electrical activity in selected areas in living human subjects’ brains.

The areas in question are distinct parts of a well-studied brain network called the default mode network, which is perhaps the most energetic of the dozens that have so far been discovered. That’s because the default mode network is most active when a person is at rest — lying still with eyes closed or just staring off into space  — or is retrieving an autobiographical memory (“What did I eat for breakfast?”).

Parvizi and his associates showed that the same pattern of coordinated electrical activity observed in the default mode network regions when experimental subjects were performing an autobiographical-memory task persisted even when those individuals were sound asleep.

It adds up to this, Parvizi told me: “The vast amount of energy consumption by our brain is due to its spontaneous activity at all times when we are not consciously involved in a specific task.”

It may be that, all through the night, the brain’s circuits are talking to each other, taking each other’s measure, and staying tuned for optimal function when day breaks. An idling engine puts you just one gas-pedal pump away from a fast take-off.

Previously: In a human brain, knowing a human face and naming it are separate worries, Mind-reading in real life: Study shows it can be done (but they’ll have to catch you first), We’ve got your number: Exact spot inbrainwhere numeral recognition takes place revealed, Metamorphosis: At the push of a button, a familiar face becomes a strange one and Why memory and math don’t mix: They require opposing states of the same brain circuitry
Photo by Don O’Brien

Aging, Immunology, Infectious Disease, Research, Stanford News

Frenemies: Chronic cytomegalovirus infection boosts flu vaccination efficacy (IF you’re young)

Frenemies: Chronic cytomegalovirus infection boosts flu vaccination efficacy (IF you're young)

cheapo boost“The enemy of my enemy is my friend.” This phrase, or at least the thinking it embodies, is at least 2,400 years old. So, there must be something to it, right?

Of course, it’s arguably a vast oversimplification. The more nuanced and much newer term “frenemy,” dating back merely to the early 1950s, is more apt in the case of infection by the microbe known as cytomegalovirus (CMV, for short). If the name is unfamiliar, brace yourself: You’ve probably already been introduced. It’s ubiquitous.

“Between 50 percent and 80 percent of adults in the United States have had a CMV infection by age 40,” states a page on the National Institutes of Health’s website. (Worldwide, the proportion of people infection exceeds 90 percent.) Once CMV is in a person’s body, it stays there for life,” the page soberly adds.

For the most part in healthy people, CMV pretty much sits there inside of cells (particularly in the salivary glands), pretty much biding its time and getting slapped down by the immune system if it tries to act up.

On the other hand, the virus can cause serious trouble if you’re immune-compromised: say, getting a bunch of immune-suppressing drugs pending or after a transplantation operation, or carrying another virus, the infamous immune-deficiency-causing HIV (which as far as we know is nothing but an enemy, plain and simple.)

But in a new study published in Science Translational Medicine, Stanford immunology expert Mark Davis, PhD, and his colleagues show that carriers of CMV mount a more robust immune response to seasonal influenza vaccinations, increasing the chances that the annual vaccine will be more effective in those people.

That’s the good news. The not-so-great news is that this only holds for young people (20-30 years old), not the older ones (age 60 and up) who could really use a boost: The older you get, it’s well known, the less effective the standard seasonal flu vaccine is in helping you fight off an influenza infection.

Experimenting with mice, Davis and his associates went a step farther. They actually infected the animals with influenza itself. Sure enough, young mice who were carrying CMV fought off the bug better than the non-infected mice did.

That’s the good news. The not-so-great news is that the old mice didn’t.

And although the study didn’t say so, one wonders whether in young people whose immune systems are going strong, that extra rocket fuel CMV seems to provide may have a dark side, for example a tendency to autoimmunity. Women’s immune systems tend to be more robust than those of men (very possibly due to the effects of testosterone, as Davis and his crew found a little over a year ago. And they have several times the rate of many autoimmune diseases that men do.

Previously: In human defenses against disease, environment beats heredity, study of twins shows, Why do flu shots work in some but not others? Stanford researchers are trying to find out, In men, a high testosterone count can mean a low immune response and Mice to men: Immunological research vaults into the 21st century
Photo by Joe Lillibridge

Immunology, Microbiology, Research, Stanford News

Drugs for bugs: Industry seeks small molecules to target, tweak and tune up our gut microbes

Drugs for bugs: Industry seeks small molecules to target, tweak and tune up our gut microbes

bacterial cytoplasmMy first encounter with microbiologist Justin Sonnenburg, PhD, came when I was researching “Caution: Do Not Debug,” an article I wrote five years ago for Stanford Medicine about the astonishing microbiotic superorganism that beats within the human gut.

According to the Human Microbiome Project, the typical healthy person is inhabited with trillions of intestinal microbes. A person typically hosts 160 or so species of gut bacteria. This bug collection carries its own “shadow genome” consisting of hundreds of times as many genes, in all, than our own measly 20,000 or so human ones.

In exchange for the three square meals a day we provide them, our microbial moochers do lots of good things: From my article:

[O]ur commensal microbes work hard for their living. They synthesize biomolecules that manipulate us in ways that are helpful to both them and us. They produce vitamins, repel pathogens, trigger key aspects of our physiological development, educate our immune system, help us digest our food and for the most part get along so well with us and with one other that we forget they’re there.

Since I wrote that piece, the list of microbial good deeds has continued to grow. As Sonnenburg pointed out recently in a review article in CELL Metabolism, “Starving our Microbial Self,” our resident microbes are producing hundreds or thousands of little drug-like compounds. For example: Short-chain fatty acids, generated by our gut bacteria from starches and fiber in our diet, downregulate inflammation.

Quoted in a just-published feature in Nature Biotechnology, “Drugging the Microbiome,” Sonnenburg elaborates:

Might a lack of dietary fiber lead directly to autoimmune and inflammatory diseases? That’s the view of Justin Sonnenburg, a Stanford microbiologist. “A reduction in short-chain fatty acid production… is what happens when you get rid of dietary fiber, and [leads to] increasing inflammatory responses of the host immune system,” he says. “And it’s this simmering state of inflammation that the Western immune system exists in that’s really the cause of all the diseases that we’ve been talking about. … You can just imagine that if you get rid of these important regulatory molecules, and the immune system becomes a little bit pro-inflammatory across a large population, you’re going to see increases in things like cancer, heart disease, allergies, asthma and inflammatory bowel disease.”

While they’re indispensable, our gut microbes can do bad things, too. Research has implicated them in the production of certain metabolites implicated in deleterious effects, with potential involvement in conditions ranging from heart disease to autism to Parkinson’s to colon and liver cancer, according to the Nature Biotechnology feature.

Either way, it’s going to be well worth our while to learn everything we can about the details of the ecosystem of one-celled creatures who call us “home.”

Previously: Civilization and its dietary (dis) contents: Do modern diets starve out our gut-microbial community?, The future of probiotics and Researchers manipulate microbes in the gut
Photo by Duncan Hull

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