The Anti-inflammatory baking soda effect is mediated by the splenic nerve

 This  DIY health hack was totally inknown to me, and I try to keep up with these sorts of low cost, safe solutions.

Oral sodium bicarbonate (NaHCO3), baking soda,  shows promise in treating inflammatory disorders by stimulating the inflammatory reflex (IR). Its mechanisms remain unclear. In a rat study, NaHCO3 increased anti-inflammatory markers and decreased pro-inflammatory ones in the spleen. These effects relied on the splenic nerve, crucial for NaHCO3-induced immunomodulation. Neural networks accurately distinguished NaHCO3 from water treatment in intact rats but not in splenic nerve-denervated ones, indicating the nerve’s vital role. Spleen denervation independently affected immune markers, highlighting its distinct influence.  We’ve discussed splenic nerve here. 

A summary of a similar article here.

The immunomodulatory effect of oral NaHCO3 is mediated by the splenic nerve: multivariate impact revealed by artificial neural networks
JO – Journal of Neuroinflammation
SP – 79
VL – 21
IS – 1
AB – Stimulation of the inflammatory reflex (IR) is a promising strategy for treating systemic inflammatory disorders. Recent studies suggest oral sodium bicarbonate (NaHCO3) as a potential activator of the IR, offering a safe and cost-effective treatment approach. However, the mechanisms underlying NaHCO3-induced anti-inflammatory effects remain unclear. We investigated whether oral NaHCO3’s immunomodulatory effects are mediated by the splenic nerve. Female rats received NaHCO3 or water (H2O) for four days, and splenic immune markers were assessed using flow cytometry. NaHCO3 led to a significant increase (p < 0.05, and/or partial eta squared > 0.06) in anti-inflammatory markers, including CD11bc + CD206 + (M2-like) macrophages, CD3 + CD4 + FoxP3 + cells (Tregs), and Tregs/M1-like ratio. Conversely, proinflammatory markers, such as CD11bc + CD38 + TNFα + (M1-like) macrophages, M1-like/M2-like ratio, and SSChigh/SSClow ratio of FSChighCD11bc + cells, decreased in the spleen following NaHCO3 administration. These effects were abolished in spleen-denervated rats, suggesting the necessity of the splenic nerve in mediating NaHCO3-induced immunomodulation. Artificial neural networks accurately classified NaHCO3 and H2O treatment in sham rats but failed in spleen-denervated rats, highlighting the splenic nerve’s critical role. Additionally, spleen denervation independently influenced Tregs, M2-like macrophages, Tregs/M1-like ratio, and CD11bc + CD38 + cells, indicating distinct effects from both surgery and treatment. Principal component analysis (PCA) further supported the separate effects. Our findings suggest that the splenic nerve transmits oral NaHCO3-induced immunomodulatory changes to the spleen, emphasizing NaHCO3’s potential as an IR activator with therapeutic implications for a wide spectrum of systemic inflammatory conditions.
SN – 1742-2094
UR – https://doi.org/10.1186/s12974-024-03067-x
DO – 10.1186/s12974-024-03067-x
ID – Alvarez2024