Summary: When you catch a cold or the flu, the physical symptoms—congestion, fever, chills—are often accompanied by a distinct psychological shift: a low mood, a desire to withdraw from others, and a heavy, diffuse feeling of malaise. These behavioral changes are not merely side effects of being ill. They are an active neurobiological response driven by the immune system’s activation.
This same inflammatory-driven form of depression also affects people with chronic inflammatory conditions such as rheumatoid arthritis and inflammatory bowel disease (IBD). Research led by David Engblom at Linköping University explores how inflammation in the body communicates with the brain to produce changes in mood, motivation, and social behavior.
Key Facts
- Inflammatory depression: Symptoms like social withdrawal, low mood, and generalized sickness behavior are triggered by immune activation and signaling pathways that influence the brain.
- Chronic disease overlap: Persistent activation of these pathways in conditions such as rheumatoid arthritis and IBD helps explain the high rates of co-occurring depression in these patients.
- Brain–immune communication: Engblom’s research aims to map how inflammatory molecules in the bloodstream interact with cells at the blood–brain interface to alter neuronal activity and neurotransmitter systems.
- Collaborative science: Engblom emphasizes that modern neurobiological discoveries depend on coordinated team effort—doctoral students, postdocs, and lab staff are central to experimental success.
- Teaching excellence: In addition to his research, Engblom has been recognized repeatedly by medical students at Linköping University, receiving the “Kandidat Kork” teaching award five times.
- Clinical potential: Understanding the specific molecular routes that link systemic inflammation to brain function creates opportunities to develop targeted therapies that relieve neuro-inflammatory symptoms without impairing peripheral immune defense.
Source: Linköping University
Remember the last time you had a cold or the flu. Did you feel a little down, more withdrawn, and generally unwell? That pattern—often dismissed as just feeling “sick”—reflects a coordinated biological program.
When the immune system mounts a response to infection or ongoing inflammation, it releases signaling molecules such as cytokines into the blood. Those signals influence the brain through specialized interfaces rather than by flooding it directly. The result is a conserved behavioral response sometimes called “sickness behavior”: reduced activity, social withdrawal, increased sleep, and loss of interest in normal rewards. From an evolutionary perspective, these changes help conserve energy for the immune response and limit disease transmission.
David Engblom has spent his career probing the precise molecular and cellular mechanisms that allow peripheral inflammation to change brain circuits. His work focuses on how barrier cells—vascular endothelial cells and certain circumventricular regions—sense circulating inflammatory markers and trigger secondary signaling cascades that alter deep brain centers governing mood and motivation.
Engblom’s path to research began during his medical studies; what started as a brief detour led to a long-term scientific career. His achievements have been recognized with prestigious awards and grants, and colleagues praise both his scientific contributions and his impact as an educator.
“It’s easy to connect this research to human suffering, which motivates efforts to develop treatments and improve care,” Engblom says. “The brain is also fascinating because it offers unique challenges in understanding how complex systems work.”
He also stresses the team nature of scientific progress: “Early in your career you do the bench work yourself. Later you shift into a coaching role. The breakthroughs come from students and laboratory colleagues executing experiments and interpreting results.”
Alongside his research record, Engblom has been repeatedly honored by the medical students he teaches. The “Kandidat Kork” award, given by students to outstanding teachers, has been awarded to him five times. The Faculty of Medicine and Health Sciences at Linköping University recently presented Engblom with its largest research prize—SEK 400,000—highlighting both his scientific excellence and his contributions to education and collegial life.
Key Questions Answered:
A: This response, known as sickness behavior, is an adaptive survival strategy. Fighting infection consumes substantial metabolic resources. By inducing lethargy, reduced social drive, and low motivation, the nervous system helps the body conserve energy, focus on immune defense, and limit the spread of pathogens to others.
A: The blood–brain barrier prevents most substances from freely entering the brain, but it also contains sensor cells and specialized regions that detect peripheral signals. Circulating cytokines bind to these barrier components, which then release secondary messengers or alter vascular and glial function. These intermediaries modulate neuronal circuits that control mood and motivation.
A: For many years, depressive symptoms in chronic inflammatory disease were seen primarily as psychological reactions to long-term illness. Engblom’s findings reframe these symptoms as biologically driven consequences of sustained inflammation acting on brain systems. Mapping the exact molecular pathways opens the possibility of treatments that block neuroinflammatory signaling to the brain, potentially relieving depression without weakening immune defenses elsewhere in the body.
Editorial Notes:
- This article was edited by a neuroscience news editor.
- Referenced journal papers were reviewed in full.
- Additional explanatory 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: Image credit listed as Neuroscience News