Chronic inflammation underlies many autoimmune and inflammatory diseases, including rheumatoid arthritis, lupus, and inflammatory bowel disorders. In these conditions, the immune system remains locked in a persistent “attack mode,” leading to tissue damage and progressive loss of function. Although modern immunosuppressive drugs can be effective, they are often expensive and associated with significant side effects. Consequently, researchers have shown growing interest in simple, low-cost interventions that might safely modulate immune activity. A study published in The Journal of Immunology provides intriguing evidence that sodium bicarbonate—commonly known as baking soda—may induce a systemic anti-inflammatory immune shift.

The research was conducted by scientists at the Medical College of Georgia at Augusta University and investigated how ingestion of a modest dose of sodium bicarbonate affects immune signaling. Rather than acting directly on immune cells in the bloodstream, bicarbonate was found to influence immune behavior through an unexpected organ: the spleen. The spleen plays a critical role in filtering blood and coordinating immune responses, particularly those involving macrophages and lymphocytes.

According to the study, drinking sodium bicarbonate sends a biochemical signal to specialized mesothelial cells that line the spleen. These cells act as communicators between the circulatory system and the immune system. When exposed to bicarbonate, mesothelial cells altered the chemical environment sensed by immune cells, effectively signaling that the body was not under threat. As a result, white blood cells—especially macrophages—shifted from a pro-inflammatory phenotype, often described as an aggressive or “attack” mode, to a more regulatory, anti-inflammatory state.

This immune reprogramming had two major effects. First, macrophages reduced their production of inflammatory mediators, lowering signals that typically amplify immune responses. Second, there was an increase in regulatory T cells (Tregs), a subset of immune cells essential for maintaining immune tolerance and preventing excessive or misdirected inflammation. Tregs are often deficient or dysfunctional in autoimmune diseases, so their expansion represents a meaningful anti-inflammatory adaptation.

Importantly, this immune shift did not resemble generalized immune suppression. Instead, it appeared to selectively dampen harmful inflammation while preserving immune balance. This distinction is crucial, as broad immunosuppression can leave patients vulnerable to infections and cancer. The findings suggest that bicarbonate acts more like an immune “reset signal” rather than a blunt inhibitory agent.

The authors proposed that this mechanism could help explain why sodium bicarbonate has long been used empirically to relieve inflammatory symptoms in certain conditions, despite limited scientific understanding of its effects. By promoting an anti-inflammatory immune profile, bicarbonate ingestion may help reduce the destructive immune activity characteristic of autoimmune diseases such as rheumatoid arthritis. Because sodium bicarbonate is inexpensive, widely available, and already consumed by humans in various contexts, its potential clinical relevance is particularly appealing.

However, the researchers were careful to emphasize the limitations of their work. The study focused on mechanistic immune changes rather than long-term clinical outcomes. While the immune shifts observed are consistent with reduced inflammation, it remains unknown whether regular bicarbonate consumption can meaningfully improve symptoms, slow disease progression, or reduce medication requirements in patients with autoimmune disorders. Large, well-controlled clinical trials will be necessary to determine optimal dosing, safety with long-term use, and real-world therapeutic benefit.

In conclusion, the study published in The Journal of Immunology demonstrates that sodium bicarbonate ingestion can trigger a systemic anti-inflammatory response by signaling through splenic mesothelial cells and reprogramming immune cell behavior (The Journal of Immunology, year of publication). Although preliminary, these findings open the door to the possibility that a simple, over-the-counter substance could one day serve as a supportive, low-cost strategy for managing chronic inflammatory and autoimmune diseases—pending rigorous clinical validation.