A Review of “Oral NaHCO3 Activates a Splenic Anti-Inflammatory Pathway Evidence That Cholinergic Signals Are Transmitted via

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Date:A Review of “Oral NaHCO3 Activates a Splenic Anti-Inflammatory Pathway: Evidence That Cholinergic Signals Are Transmitted via Mesothelial Cells.”

The article is a report on an experiment that describes how oral NaHCO3 intake normally invigorate anti-inflammatory pathways. To illustrate how splenic anti-inflammatory pathways are stimulated by the intake of oral NaHCO3, scientists’ experiment by loading oral NaHCO3 then shifting macrophage polarization from inflammatory (M1) to regulatory phenotypes (M2) and FOXP3+ CD4+T-lymphocytes increased in the blood, kidneys and spleen of laboratory mice. The scientists then clearly prove that the same anti-inflammatory changes that were observed in the macrophage polarization in the laboratory mice was the same as those observed in human beings’ blood following the ingestion of NaHCO3.

The scientists used cytometry flow as well as mRNA markers in splenic macrophages that are isolated so as to determine whether M2 macrophage polarization in the both the spleen and the kidney is promoted by the intake of oral NaHCO3. The scientists also investigated the effects of acute NaHCO3 loading on cell profiles in the human blood. They found out that gentle manipulation so as to visualize the spleen at midline during sham splenectomy was necessary to abolish the oral NaHCO3 anti-inflammatory response. The scientists then investigated the pathways in which NaHCO3 intake signaling can be transmitted to the splenic parenchyma. In addition, the scientists use both anatomical and functional evidence in which signals that mediate for these responses are transmitted to the kidney and the spleen through a neural-like function of the mesothelial cells. The study shows how the mesothelial cells have a role in transmitting signals at distal sites and how it combines with the secretion of gastric acid in promoting an anti-inflammatory response to oral NaHCO3.

This study is important as it details how anti-inflammatory response macrophage polarization; including both M1 and M2 are promoted by the intake of oral NaHCO3. The study also explains how intake of oral NaHCO3 increases FOXP3 +CD4+ T regulatory cells within the kidney and the spleen. The scientists were able to confirm that such phenotypic changes are associated with anti-inflammatory effects of using MLR. They were able to examine tissues from the Ls-fed Dahl mice and normotensive Spragie Dawley rats. The scientists also explained how the Dahl mouse model develops both renal injury and hypertension when fed with an HS diet.

The data from the study indicates that the effect of NaHCO3 on macrophage polarization is independent of elevated blood pressure and salt diets. This agrees with the findings of the mice, that oral NaHCO3 promotes anti-inflammatory response in blood. Indeed, the data was a demonstration that NaHCO3 ingested orally can promote powerful anti-inflammatory responses in both human beings and rats. The scientists however speculated that the cholinergic anti-inflammatory pathway activated the ingestion of oral NaHCO3.

The next experiment that scientists should undertake should involve testing the efficacy of the intakes of oral NaHCO3 to regulate injury in inflammatory disease models in determining the potential of this therapeutic stimuli. This is because, the scientists in this study have only provided a cost effective and a safe method of activating splenic anti-inflammatory pathways in human beings thus may have an important therapeutic potential for the inflammatory disease.