Feeling hungry doesn’t just make you reach for a snack – it may also change your immune system.
In a recent study in mice, researchers found that simply perceiving hunger can alter the number of immune cells in the blood, even without actual fasting. This discovery highlights the impact of the brain’s interpretation of hunger on immune system adaptation.
The study, published in Science Immunology, challenges the conventional belief that changes in nutrition, such as blood sugar or nutrient levels, primarily shape immunity. Instead, the research indicates that perception alone can reshape immunity.
The focus of the study was on two specialized brain cells, AgRP neurons, and POMC neurons, which sense the body’s energy status and regulate feelings of hunger and fullness. AgRP neurons stimulate hunger in response to low energy levels, while POMC neurons signal fullness after eating.
Using genetic tools, the researchers artificially activated hunger neurons in well-fed mice, triggering a strong urge to seek food. This experiment confirmed previous studies showing the impact of hunger signals on behavior.
Surprisingly, the synthetic hunger state led to a significant decrease in specific immune cells called monocytes in the blood. Monocytes are crucial for regulating inflammation and form part of the immune system’s initial defense.
Conversely, activating fullness neurons in fasting mice normalized monocyte levels, even without food intake. This experiment demonstrated that the brain’s perception of hunger or fullness alone could influence immune cell numbers in the blood.
Further investigation revealed a direct link between hunger neurons and the liver through the sympathetic nervous system, which regulates various bodily functions. Activation of hunger neurons reduced nutrient sensing in the liver, leading to a decrease in CCL2, a chemical that attracts monocytes to the blood.
Additionally, hunger signals triggered the release of corticosterone, a stress hormone that acted as an amplifier for immune changes. While modest levels of corticosterone alone did not affect immune cells significantly, it played a crucial role in coordinating the response with brain signals.
The study suggests that the brain’s ability to modulate immune responses based on perceived energy needs may have evolved to anticipate and prepare for potential shortages. This mechanism could have implications for diseases characterized by immune dysregulation, such as cardiovascular diseases, multiple sclerosis, and cachexia in cancer patients.
Understanding the brain’s influence on the immune system could lead to new brain-targeted approaches for immune-modulatory therapies. However, more research is needed to confirm these findings in humans, as precise neuronal activation in the human brain remains a challenge.
The study’s findings underscore the intricate connection between the brain and immune system, shedding light on how conditions like stress and eating disorders may impact inflammation and disease. The mind-body relationship observed in this study aligns with early observations from a century ago, highlighting the profound influence of the brain on physiological responses.
In conclusion, the study emphasizes the brain’s role in shaping immune responses and raises important questions about the interplay between mental and physical health. If confirmed in humans, these findings could pave the way for innovative approaches to immune-related disorders.
