Natural Remedies

Hyaluronic Acid for Bronchiectasis?

Posted by Gianfranco (Venezia - Italy) on 05/07/2023 2 posts

Are there benefits by using oral Hyaluronic Acid for Bronchiectasis? If so, what kind to use and what protocol to follow? in such a way as not to weaken the immune system and at the same time to reduce the lungs alveoli inflammation.

Replied by Art
California
05/07/2023
2184 posts

Gianfranco,

Most studies using HA for Bronchiectasis have used nebulized or aerosolized HA in order to obtain benefit and deliver directly to the lungs interior to afford maximum benefit. I haven't seen any studies using oral HA for the purpose.

If you aren't already using N Acetyl Cysteine (NAC), it may be a consideration as it acts as a mucolytic to thin mucus secretions and help them flow out. It also acts as a potent antioxidant and reduces lung inflammation which is very useful for Bronchiectasis.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6458826/

Here is a relevant quote from the study :

' A total of 24.7% of the N-acetylcysteine group patients and 11.3% of the control group patients remained exacerbation-free throughout the 12-month follow-up (χ2 = 4.924, P = 0.026). Compared with the control group, the volume of 24-h sputum in the N-acetylcysteine group was significantly reduced (t = − 3.091, P = 0.002). Additionally, the N-acetylcysteine group showed a significant improvement in the quality of life. No severe adverse events were reported in the intervention group. '

While not specifically for bronchiectasis, Melatonin has also shown significant anti inflammatory effects in various lung diseases as discussed here :

https://www.frontiersin.org/articles/10.3389/fimmu.2021.668002/full

Here is a relevant quote :

' Animal experiments showed that melatonin can not only alleviate chronic lipopolysaccharide (LPS)-induced mouse lung destruction and chronic lung inflammation but also reduce necroptosis (RIP1/RIP3/MLKL), a programmed cell death process in bronchial epithelial cells. The protective effect of melatonin on chronic lung inflammation was further suggested to be dependent on targeting its membrane receptor MT1/MT2. In addition, transcriptomic and metabolomic profiling in the lungs of mice indicated that LPS can induce perturbations of the mainstream metabolites associated with amino acid and energy metabolism. Melatonin may reduce the necroptosis by modifying the disordered pathways of alanine, aspartate, and glutamate metabolism caused by LPS. This study suggests that melatonin may act as a potential therapeutic agent for alleviating the chronic inflammation associated with COPD.

Art