Blocking endogenous HA receptor binding in mice impairs gut development and barrier function (Riehl et al. 2015) within about 5 days, so we know that signal is generated routinely. Immunostaining of healthy human jejunum also shows intense HA in the lamina propria with no staining in the epithelial layer, so healthy guts do produce substantial HA endogenously. That doesn’t tell us whether it’s produced steadily or mainly during episodic damage and repair, or whether epithelial HA produces different effects, or whether supplement levels send an important extra signal.
The Bacteroides as pathogen shield argument is new and interesting. I’d expect hyaluronidase producing bacteria to roughly equilibrate to available HA over time, whether from endogenous production, episodic repair, or diet. Do you have specific reasons to think supplementing HA would change the ratio rather than just the levels?
Blocking endogenous HA receptor binding in mice impairs gut development and barrier function (Riehl et al. 2015) within about 5 days, so we know that signal is generated routinely. Immunostaining of healthy human jejunum also shows intense HA in the lamina propria with no staining in the epithelial layer, so healthy guts do produce substantial HA endogenously. That doesn’t tell us whether it’s produced steadily or mainly during episodic damage and repair, or whether epithelial HA produces different effects, or whether supplement levels send an important extra signal.
The Bacteroides as pathogen shield argument is new and interesting. I’d expect hyaluronidase producing bacteria to roughly equilibrate to available HA over time, whether from endogenous production, episodic repair, or diet. Do you have specific reasons to think supplementing HA would change the ratio rather than just the levels?