This shows the outline of a head.
A new study focuses on tracing the cellular and molecular pathways through which peripheral bodily inflammation breaches neural defenses to induce profound changes in behavior and mood. Credit: Neuroscience News

Bodily Inflammation Shapes the Brain and Behavior

Summary: When you catch a cold or the flu, the physical symptoms, congestion, fever, and chills, are often accompanied by a distinct psychological shift: a mild depression, a desire to withdraw from social company, and a heavy, diffuse sense of sickness.

This collective behavioral response is not an accidental byproduct of a virus; it is an active neurobiological state triggered by the immune system’s activation. This identical inflammatory-induced depression also plagues individuals suffering from chronic, lifelong conditions such as rheumatoid arthritis and inflammatory bowel diseases (IBD).

Key Facts

  • Inflammatory Depression: The psychological symptoms of being sick, social withdrawal, low mood, and malaise are directly driven by the immune system activating specific inflammatory signaling pathways that talk to the brain.
  • Chronic Disease Overlap: This neural pathway is continuously active in chronic inflammatory conditions like rheumatoid arthritis and IBD, explaining the high clinical rates of comorbid depression in these patients.
  • Brain-Immune Communication: Dr. Engblom’s research program focuses on decoding the exact mechanism of how inflammatory signals in the bloodstream cross the blood-brain barrier to alter neuronal firing and neurotransmitter behavior.
  • Team-Driven Science: Engblom analogizes modern neurobiological research to coaching a football team, emphasizing that breakthrough scientific milestones rely entirely on the collaborative execution of doctoral students and lab colleagues.
  • Educational Excellence: Alongside his research achievements, medical students at Linköping University have awarded Engblom the “Kandidat Kork” teaching prize five separate times for his work instructing the medical program.
  • Clinical Horizon: Unlocking these specific pathways provides critical structural knowledge necessary to develop targeted pharmaceutical treatments that can alleviate the neuro-inflammatory human suffering associated with both acute infections and chronic diseases.

Source: Linköping University

Try to remember how you felt the last time you had a cold or had the flu. Were you a little depressed, avoiding the company of others and having a diffuse sense of sickness? Probably.

This type of depression is due to the immune system being activated by the inflammation in your body, and also occurs in lifelong conditions such as rheumatoid arthritis and inflammatory bowel diseases. But why? David Engblom has devoted his research career to finding out how inflammation in the body affects our brain function and how we behave.

 “It’s very easy to link this to human suffering, which you’d want to alleviate. Research can contribute to knowledge needed for treatment and care. The brain is also unusually interesting when it comes to figuring out how it works,” says David Engblom.

Becoming a researcher was a total coincidence, he claims. He studied medicine and began doing research halfway into the programme. The idea was to go back to studying after a while, but one thing led to another. And that was lucky. According to the jury’s citation, he “represents a research achievement of exceptional scientific excellence which has resulted in a series of prestigious awards and grants.”

“On a day like this, I’m very happy that I became a scientist. I think you should keep jumping at opportunities throughout life. If you have very rigid ideas from the beginning about what to do, you might miss a lot of opportunities that pop up along the way,” says David Engblom.

In addition to his success in research, David Engblom has also been awarded as a teacher at the university. He teaches mostly on the medical programme he once attended. The medical students have awarded him the “Kandidat Kork” teacher award no less than five times.

“We’re delighted that David Engblom is awarded the Faculty of Medicine and Health Sciences’ largest and most prestigious research award. In addition to outstandingly fine research, David also makes significant contributions in education and collegial contexts,” says Lena Jonasson, Dean of the Faculty of Medicine and Health Sciences at Linköping University, who led the award committee’s nomination work.

The value of the award this year is SEK 400,000 and is given to David Engblom as a private individual. He himself highlights the doctoral students, research colleagues and students who have worked with the research over the years:

“Research is in many respects teamwork. At the beginning of your career as a researcher, you’re actively involved in the experiments and doing practical research work, but my role now is more like coaching a football team. I’m no longer the one who scores the goals; the research team does.”

Key Questions Answered:

Q: Why does the immune system intentionally make us feel depressed when we are sick?

A: This phenomenon, scientifically known as “sickness behavior,” is an evolutionary survival mechanism. When your body is fighting an infection, it requires an immense amount of metabolic energy to fuel the immune system. By altering your brain chemistry to make you feel mildly depressed, lethargic, and socially withdrawn, your nervous system forces you to rest, conserve your caloric resources, and avoid spreading pathogens to the rest of your community.

Q: How does inflammation in the body manage to change brain function if the brain is protected by the blood-brain barrier?

A: This is the core question Dr. Engblom’s career has targeted. While the blood-brain barrier shields the brain from most circulating toxins and pathogens, it contains specialized interfaces, including the brain’s vascular endothelial cells and specific circumventricular organs, that can act as sensors. When peripheral inflammatory markers like cytokines travel through the bloodstream, they bind to these barrier cells, triggering a secondary cascade of chemical signals that directly manipulate deep brain circuits responsible for mood, motivation, and social drive.

Q: What does this research mean for people suffering from long-term inflammatory diseases like arthritis?

A: For decades, psychiatric symptoms in patients with rheumatoid arthritis or Crohn’s disease were treated as mere psychological reactions to having a painful, chronic illness. Dr. Engblom’s work shifts this paradigm completely by proving that their depression is a direct, physical consequence of systemic inflammation altering their neural architecture. Understanding the specific molecular pathways involved allows pharmacology researchers to design treatments that block these inflammation signals from reaching the brain, offering relief from chronic depression without compromising peripheral immunity.

Editorial Notes:

  • This article was edited by a Neuroscience News editor.
  • Journal paper reviewed in full.
  • Additional context added by our staff.

About this neuroinflammation and behavior research news

Author: Karin Söderlund Leifler
Source: Linköping University
Contact: Karin Söderlund Leifler – Linköping University
Image: The image is credited to Neuroscience News

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