Nav: Home

Research at MDI Biological Laboratory examines role of early-life stress in adult illness

October 24, 2016

BAR HARBOR, MAINE -- Scientists have long known that chronic exposure to psychosocial stress early in life can lead to an increased vulnerability later in life to diseases linked to immune dysfunction and chronic inflammation, including arthritis, asthma, cancer, diabetes, heart disease and even mental illness. But the molecular mechanisms underlying the negative effects of early exposure to stress are unknown.

Using the common aquarium fish, the zebrafish, as a model, developmental biologist James A. Coffman, Ph.D., of the MDI Biological Laboratory in Bar Harbor, Maine, and his team are beginning to elucidate these mechanisms.

In a paper recently published in Biology Open, they reported that zebrafish embryos that are chronically exposed to the stress hormone cortisol for just the first few days of life develop into adults with abnormal immune systems and signs of chronic inflammation.

"Inflammation is a normal response to protect the body from harmful stimuli, but if the inflammation is chronic, it is destructive and can cause disease," Coffman explained. "Chronic psychosocial stress increases the level of cortisol circulating in the body, and if this happens early in life it can influence how the body develops. So our research helps explain why young children who experience chronic psychosocial stress, due for example to low socioeconomic status, economic insecurity, abuse or neglect, are more vulnerable as adults to health problems associated with inflammation and immune dysfunction."

The paper was co-authored by Elli I. Hartig, Shusen Zhu and Benjamin L. King, Ph.D., all of the MDI Biological Laboratory.

"These findings contribute to the growing body of knowledge about the effects of environmental conditions before and immediately after birth on adult health," said Kevin Strange, Ph.D., president of the MDI Biological Laboratory. "Research in this emerging field suggests that interventions to mitigate the effects of early-life stress could one day lead to significant improvements in public health."

Coffman's interest in studying the molecular mechanisms underlying the contribution of stress to aging was piqued by the observation that the rate of aging is often accelerated in chronically stressed individuals, he said.

In the study, Coffman's team treated zebrafish embryos with cortisol, a hormone that is naturally produced by the body in response to stress. They then let those fish grow to adulthood and examined their ability to regenerate their tailfins following surgical removal. Specifically, the team looked at gene expression during the early stages of regeneration, when the innate immune system mounts an inflammatory response to the injury that is then rapidly resolved.

Zebrafish were used because of their extraordinary regenerative ability, and because both the cortisol-mediated stress response and innate immune system are essentially the same in zebrafish as they are in humans.

In adult zebrafish derived from cortisol-treated embryos, inflammatory genes displayed a strikingly abnormal response to the tailfin injury, which correlated with impaired regeneration. It was also found that the innate immune system failed to mount a normal response to molecular signals that are presented by infectious bacteria.

Coffman believes the aberrant immune gene regulation that his team observed in the adults derived from cortisol-treated embryos is due to glucocorticoid-induced developmental programming. In other words, early-life exposure to chronically elevated cortisol results in lasting developmental changes that affect processes critical for immune system function and regulation throughout adult life.

The next step is to identify the specific ways that development of the immune system is altered by chronically elevated cortisol, and dissect the molecular mechanisms underlying those alterations, Coffman said.
His research is supported by Institutional Development Awards (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health, grant numbers P20-GM104318 and P20-GM103423.

The MDI Biological Laboratory, located in Bar Harbor, Maine, is an independent, non-profit biomedical research institution focused on increasing healthy lifespan and increasing our natural ability to repair and regenerate tissues damaged by injury or disease. The institution develops solutions to complex human health problems through research, education and ventures that transform discoveries into cures. For more information, please visit

Mount Desert Island Biological Laboratory

Related Immune System Articles:

The immune system may explain skepticism towards immigrants
There is a strong correlation between our fear of infection and our skepticism towards immigrants.
New insights on how pathogens escape the immune system
The bacterium Salmonella enterica causes gastroenteritis in humans and is one of the leading causes of food-borne infectious diseases.
Understanding how HIV evades the immune system
Monash University (Australia) and Cardiff University (UK) researchers have come a step further in understanding how the human immunodeficiency virus (HIV) evades the immune system.
Carbs during workouts help immune system recovery
Eating carbohydrates during intense exercise helps to minimise exercise-induced immune disturbances and can aid the body's recovery, QUT research has found.
A new model for activation of the immune system
By studying a large protein (the C1 protein) with X-rays and electron microscopy, researchers from Aarhus University in Denmark have established a new model for how an important part of the innate immune system is activated.
Guards of the human immune system unraveled
Dendritic cells represent an important component of the immune system: they recognize and engulf invaders, which subsequently triggers a pathogen-specific immune response.
How our immune system targets TB
Researchers have seen, for the very first time, how the human immune system recognizes tuberculosis (TB).
How a fungus inhibits the immune system of plants
A newly discovered protein from a fungus is able to suppress the innate immune system of plants.
A new view of the immune system
Pathogen epitopes are fragments of bacterial or viral proteins. Nearly a third of all existing human epitopes consist of two different fragments.
TB tricks the body's immune system to allow it to spread
Tuberculosis tricks the immune system into attacking the body's lung tissue so the bacteria are allowed to spread to other people, new research from the University of Southampton suggests.

Related Immune System Reading:

Best Science Podcasts 2019

We have hand picked the best science podcasts for 2019. Sit back and enjoy new science podcasts updated daily from your favorite science news services and scientists.
Now Playing: TED Radio Hour

Jumpstarting Creativity
Our greatest breakthroughs and triumphs have one thing in common: creativity. But how do you ignite it? And how do you rekindle it? This hour, TED speakers explore ideas on jumpstarting creativity. Guests include economist Tim Harford, producer Helen Marriage, artificial intelligence researcher Steve Engels, and behavioral scientist Marily Oppezzo.
Now Playing: Science for the People

#524 The Human Network
What does a network of humans look like and how does it work? How does information spread? How do decisions and opinions spread? What gets distorted as it moves through the network and why? This week we dig into the ins and outs of human networks with Matthew Jackson, Professor of Economics at Stanford University and author of the book "The Human Network: How Your Social Position Determines Your Power, Beliefs, and Behaviours".