So your kind of playing the same game here that has been done with androgens over the years, but with retinoic acid instead.
Such as androgen disruption leads to dysbiosis,
or is it dysbiosis leads to retinoic acid disruption?
Cause leads to consequence.
The question im looking at, is it the microbiome itself that could lead to vitamin a or retinoic acid status?
I know this is something a few of us have noticed over the years including myself.
A key thought from this study,
Whether dysbiosis is a cause or consequence of chronic respiratory conditions, or whether retinoic acid (RA) - the bioactive metabolite of Vitamin A - is essential for lung microbiome homeostasis,
Vitamin A Deficiency and the Lung Microbiome
Vitamin A is an essential micronutrient responsible for lung morphogenesis, respiratory function,
and innate immunity. While vitamin A deficiency (VAD) alters gene expression and tissue
morphology, the microbiome has been shown to play an intimate role in the metabolic regulation,
pathogen inhibition, and inflammatory responses in the lung. Once believed to be sterile, recent
studies now show microbes inhabiting healthy lungs that are dysregulated in patients with
chronic obstructive pulmonary disease (COPD), asthma, and tuberculosis (TB). Whether
dysbiosis is a cause or consequence of chronic respiratory conditions, or whether retinoic acid
(RA) - the bioactive metabolite of Vitamin A - is essential for lung microbiome homeostasis,
remains unknown. We hypothesize dysregulation of host-microbe interactions in VAD lungs that
are associated with chronic respiratory conditions. To characterize this association, we obtained
a preliminary metatranscriptomic signature profile and H&E stains of paraffin-embedded tissue
samples to compare the morphology and changes in gene expression in the lungs of these two
groups. Histology results provide evidence of an inflammatory-like pathology in VAD lungs that
are absent in VAS lungs. Our computational results show an increase of COPD-associated
microbial expression and dysregulation of the host immune pathways, indicating a possible
correlation between lung dysbiosis and the alteration of granulocyte and macrophage function in
the absence of vitamin A. By using our combined molecular-metatranscriptomics approach to
compare mammalian and microbial gene expression profiles, we aim to identify novel host microbe interactions that will prove invaluable for treating chronic respiratory diseases.