Researchers from a renowned French institute have shown that smoking impairs the body’s ability to produce key signaling molecules called cytokines, which are central to mounting effective immune responses. The findings were published in Nature, a leading scientific journal.
Cytokines are small, soluble proteins that coordinate immune activity by guiding how cells communicate, divide, differentiate, and recruit defenders to sites of infection or injury. To understand why people vary in their immune responses, scientists focused on cytokines as a core part of the immune network. The study analyzed blood samples from thousands of donors with diverse health statuses, body weights, and smoking histories, tracking a range of cytokines and related markers. Among the molecules measured were CXCL5, granulocyte colony-stimulating factor CSF2, interferon gamma, and several interleukins including IL-1 beta, IL-2, IL-6, IL-8, IL-10, IL-12p70, IL-13, IL-17, and IL-23, along with tumor necrosis factor. Blood samples were stimulated for about 22 hours using methods that mimic immune activation, and responses were categorized by the type of stimulus, such as microbial or viral triggers, activation by T lymphocytes, and cytokine production profiles.
The results indicate that smoking dampens both innate and adaptive immune responses. Analysis showed that smoking elevates inflammatory signals and increases susceptibility to bacterial infections, particularly Staphylococcus aureus and Escherichia coli, in part by altering cytokine expression patterns.
Moreover, the research suggests that some of the negative effects of smoking on innate immunity can be reversed after cessation. Yet the impact on adaptive immunity, the kind learned through exposure to pathogens or vaccines, may persist for years in former smokers, indicating long-lasting changes in how the immune system responds to familiar antigens.
Earlier work has highlighted the benefits of quitting smoking at a young age, demonstrating improved immune function and reduced risk of disease later in life. The current findings add a nuanced view, showing that stopping smoking can restore certain immune functions, while some adaptive responses may take longer to rebound. These insights help explain why former smokers sometimes experience lingering differences in infection risk and vaccine responsiveness compared with never-smokers.