The Complexity of Fevers: Exploring the Intricate Causes Beyond ‘Heat Kills Bugs’
In the midst of battling a fever induced by the flu, one may wonder why the body would subject itself to the uncomfortable symptoms of chills, sweats, and aches. Recent research sheds light on the underlying processes at play. A study published in the journal Science Immunology on September 20 delves into how fever-like temperatures influence the behavior of immune cells, enhancing the activity of key infection-fighting cells while diminishing the suppression of regulatory cells by altering their metabolism.
Understanding the mechanisms behind fevers has long been a mysterious biological process, but this new research provides partial explanations on how fevers combat infections. However, the findings also highlight a potential darker side of our immune response. The biological pathways identified in the study could contribute to the heightened cancer risk associated with prolonged inflammation. According to senior study author Jeff Rathmell, a professor of immunobiology at Vanderbilt University Medical Center (VUMC), “A little bit of fever is good, but a lot of fever is bad.”
A fever is characterized by a systemic rise in body temperature, often occurring as a response to infection. Inflammation, on the other hand, involves a localized increase in body temperature due to injury or illness. While temperature has been recognized as a crucial variable in various biological processes, the exact impact of heat on the immune system remains poorly understood. Rathmell notes that while it has been assumed that heat makes the body less hospitable to invading microbes, the pathogens that cause illness, the precise mechanisms are still unknown.
The new research challenges the simplistic notion that heat merely repels pathogens, revealing a more intricate interplay between temperature and immune cell responses. Previous studies have suggested that heat can boost the immune system by stimulating activity, and the latest research delves into this phenomenon at the cellular level.
Rathmell and his colleagues investigated how different types of T cells, a subset of white blood cells, respond to elevated temperatures. Through experiments on lab-cultured cells, they discovered that a moderate fever of around 102 degrees Fahrenheit enhances the metabolism, proliferation, and activity of generalist T cells, which can differentiate into various immune functions. Simultaneously, regulatory T cells that typically suppress immune responses were impaired, leading to a loosening of the body’s defense system.
Interestingly, while one type of helper T cells, crucial for combating viruses, experienced stress under higher temperatures and some cells perished, the surviving cells exhibited enhanced functionality. The surviving cells demonstrated adaptations that enabled them to thrive despite the stress, ultimately becoming more effective in the long run. This delicate balance between immune cell responses is vital during infections, where increased effector functions and decreased suppressor functions are beneficial.
Further experiments by the researchers focused on elucidating the mechanisms underlying these observed changes. They found that cell metabolism and mitochondria, particularly a key metabolic protein called Electron Transport Chain 1, played a critical role in the cellular responses to elevated temperatures. The protein complex responsible for fueling cells became less efficient under higher temperature conditions, leading to cellular stress and DNA damage that could potentially contribute to conditions like cancer.
The link between chronic inflammation and certain cancers, such as colon cancer associated with inflammatory bowel diseases like Crohn’s disease, raises important questions about the long-term effects of inflammation on cellular health. The researchers propose that the mitochondrial mechanisms triggered by inflammation and heat may contribute to the development of cancer-promoting mutations.
While the findings offer valuable insights into the intricate interplay between temperature, immune responses, and cellular metabolism, further research is needed to validate these hypotheses. Rathmell emphasizes the importance of studying temperature changes in living organisms to better understand the complex interactions at play.
In conclusion, the research highlights the multifaceted nature of fevers and their impact on immune responses. While fevers play a crucial role in combating infections, excessive or prolonged fever could have detrimental effects on the body. By unraveling the underlying mechanisms of fever-induced immune responses, researchers aim to better understand the balance between beneficial and harmful effects of elevated temperatures on cellular health.