Summary: When you catch a cold or the flu, the physical symptoms—congestion, fever, chills—are often accompanied by a predictable psychological shift: low mood, a desire to withdraw from others, and a diffuse feeling of illness. These behavioral changes are not accidental side effects of infection but arise from a specific neurobiological state triggered by immune activation. The same inflammatory processes that produce short-term “sickness behavior” can also drive persistent mood disturbances in chronic inflammatory diseases such as rheumatoid arthritis and inflammatory bowel disease (IBD).
Researchers increasingly describe this phenomenon as inflammatory depression: a form of low mood and social withdrawal produced by immune signaling that reaches and rearranges brain circuits. Understanding how peripheral inflammation communicates with the brain is central to developing treatments that relieve the psychological burden associated with both acute infections and long-term inflammatory illness.
Key Facts
- Inflammatory depression: Symptoms commonly experienced during infections—low mood, fatigue, social withdrawal, and general malaise—are actively driven by inflammatory signaling from the immune system to the brain.
- Chronic disease overlap: The same inflammatory signaling pathways remain active in chronic conditions such as rheumatoid arthritis and inflammatory bowel disease, helping to explain the high rates of co-occurring depression in these patient groups.
- Brain-immune communication: Work led by David Engblom focuses on the mechanisms by which circulating inflammatory molecules interact with cells at the blood–brain barrier and other neural interfaces to change neuronal activity and neurotransmitter function.
- Team-driven science: Engblom emphasizes that modern neuroscience advances rely on collaborative effort—doctoral students, postdocs and lab colleagues perform the experiments that turn hypotheses into discoveries.
- Teaching recognition: In addition to his research contributions, Engblom has been repeatedly honored by medical students at Linköping University, receiving the “Kandidat Kork” teaching prize five times for his instruction in the medical program.
- Clinical potential: Mapping the precise molecular steps that carry inflammatory signals into the brain creates opportunities to design targeted therapies that block those signals and ease neuro-inflammatory symptoms without undermining peripheral immune defense.
Source: Linköping University
Recall the last time you had a cold or the flu. Were you less sociable, less motivated, and generally unwell in spirit as well as body? That low mood and desire for solitude are part of a conserved response called sickness behavior. Rather than being merely psychological, these responses are orchestrated by the immune system through inflammatory mediators that alter brain function.
David Engblom has centered his career on clarifying how inflammation in the body influences the brain and behavior. His work seeks to explain exactly how inflammatory signals in the bloodstream are detected by the brain’s protective interfaces and converted into changes in neuronal firing and neurotransmitter activity that produce mood and motivational changes.
“It’s easy to connect this work to human suffering and the need for better treatments,” Engblom says. “Research can provide the knowledge necessary for improved care. The brain is also incredibly interesting when you try to understand how it works.”
Engblom describes his path into research as serendipitous. He studied medicine and began laboratory research during his medical training. What began as a temporary detour became a career. The award committee noted that his body of work represents exceptional scientific achievement and has attracted prestigious recognition and funding.
Reflecting on career choices, Engblom advises remaining open to new opportunities: “If you have rigid ideas about a single path from the start, you might miss meaningful chances that appear along the way.”
Beyond his laboratory leadership, Engblom is a dedicated educator. He primarily teaches in the medical program at Linköping University and has been honored with the student-voted “Kandidat Kork” teaching award five times, demonstrating consistent impact in the classroom.
Lena Jonasson, Dean of the Faculty of Medicine and Health Sciences at Linköping University, commented on Engblom’s recognition: “We are delighted that David Engblom receives our faculty’s most prestigious research award. In addition to outstanding research, he contributes significantly to education and collegial life.”
The award this year is valued at SEK 400,000 and was presented to Engblom as a private individual. He highlights that research is a collective effort: “At the start of a research career you are deeply involved in hands-on experiments, but over time my role has shifted toward coaching. I’m no longer the one scoring the goals—the team does.”
Key Questions Answered:
A: This response, known as sickness behavior, is an adaptive survival mechanism. Fighting infection demands high metabolic resources. By inducing lethargy, reduced social interaction, and lowered motivation, the nervous system promotes rest and energy conservation and helps limit pathogen spread to others. The behavioral change supports recovery and reduces transmission.
A: Although the blood–brain barrier restricts many circulating molecules, it contains specialized structures and cell types that sense peripheral inflammation. Circulating cytokines and other inflammatory mediators interact with vascular endothelial cells or specialized brain regions that monitor the blood. Those interactions trigger secondary signaling cascades—chemical messengers released at the brain side of the barrier—that modify the activity of neural circuits involved in mood, motivation and social behavior.
A: For many years, depressive symptoms in patients with chronic inflammatory conditions were often viewed as understandable reactions to pain and disability. Engblom’s work reframes some of that burden as a direct, biological consequence of systemic inflammation acting on the brain. By identifying the molecular routes that transmit inflammatory signals into neural circuits, researchers can pursue targeted treatments that block those signals and potentially relieve depression without undermining normal immune defense in the body.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- The referenced journal paper was reviewed in full.
- Additional context was provided by editorial staff.
About this neuroinflammation and behavior research news
Author: Karin Söderlund Leifler
Source: Linköping University
Contact: Karin Söderlund Leifler – Linköping University
Image credit: Neuroscience News