Propionibacterium overabundance could equal PFS

Im just throwing this out there for now.
Ive had quite a time recovering after trialing Propionibacterium freudenreichii on and off on a few different occasions.
I think some of its effects could be predicated on the intense production of the scfa propionate.

Doxycycline could be the most potent antibiotic to knock down this bacteria similar as in its treatment for the closely related p. acnes.

Maximum treatment would be for a duration of 3 months.
I see some have mentioned Doxy on here.
This might not be the whole story though as im still looking at natural production of retinoic acid to possibly keep this bacteria in check.

Ill get back to this.

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How does it change the immune system? Intense production of propionate, isnt this anti inflammatory like butyrate? Why do you want to reduce Propionibacterium freudenreichii?

When you think anti-inflammatory also think immune suppression. I believe propionate could be capable of immune suppression. Its about a balance or proper regulation between immune activation and tolerance.

Elevated Gut Microbiome-Derived Propionate Levels Are Associated With Reduced Sterile Lung Inflammation and Bacterial Immunity in Mice

^Reduced immunity.
I think I want to boost immunity.

Ah, ok I get it, very interesting studyā€¦

Very interesting, i will get this done too.

Get what done?

Sorry, wrong thread I think. I was thinking about a microbiome analysis

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A is for antimicrobial.
I believe this would go beyond the skin as well. I would also immediately start thinking about the sinuses and any exposed mucus membranes.
I think problems here could maybe lead to thinning of the skin or loss of thickness/protection.
They also mention what sounds like Accutane.

Molecule that protects skin from infections needs vitamin A to work

What is already known on this topic

People with a low dietary vitamin A intake are highly susceptible to skin infections, but little is known about how this vitamin affects skin immunity.

What this research adds

Researchers have identified a previously unknown skin protein that kills bacteria by breaking up their cell membrane. The protein requires vitamin A to work.

Conclusions

The study provides an insight into how diet impacts the ability of the skin to protect itself from bacterial infection.

The team identified a gene whose product is called resistin-like molecule Ī± (RELMĪ±). This protein is known to be produced by some types of immune cells, fat tissue, and lung cells, but it had not been described in skin epithelium.

Like other skin antimicrobial molecules, RELMĪ± is able to kill bacteria including Streptococcus pyogenes, Pseudomonas aeruginosa, Escherichia coli and Propionibacterium acnes .

The bacteria-killing effects of RELMĪ± are due to the proteinā€™s ability to make holes into the bacterial cell membrane, the researchers found. However, RELMĪ± is expressed only in the presence of vitamin A or its derivatives, like retinol .

Whatā€™s more, mice fed a diet lacking vitamin A made no RELMĪ±, but they did start to produce the protein in their skin when treated with a vitamin A derivative that is used for severe acne.

Although more research is needed to determine how these findings will impact people with inflammatory skin conditions such as acne and psoriasis, the study provides an insight into how diet impacts the ability of the skin to protect itself from bacterial infections . It also helps to define the molecules that create a healthy relationship between the skin and its microbiota , the scientists say.

The work shows how vitamin A analogs so effectively treat skin conditions such as acne and psoriasis.

Sidenote,
The pathogenesis of acne centres around follicular dyskeratosis.
Topical retinoids such as tretinoin, adapalene or tazarotene are included in almost all acne treatment regimens because they are ā€œarguably the only agents to normalise the abnormal follicular differentiation seen in acneā€ and by targeting the microcomedones ā€œretinoids can not only treat but can also prevent the development of new lesions,ā€ she said.

In an article on vitamin A therapy in cases of Darierā€™s disease Carleton and Steven1 stated that it occurred to Peck that ā€œsince the chief pathologic change is a follicular dyskeratosis, the disease might possibly be due to vitamin A deficiency.ā€ They listed follicular hyperkeratosis as one of the diseases associated with vitamin A deficiency which is amenable to vitamin A therapy.

Follicular hyperkeratosis , also known as keratosis pilaris (KP), is a skin condition characterized by excessive development of keratin in hair follicles , resulting in rough, cone-shaped, elevated papules. The openings are often closed with a white plug of encrusted sebum.

^im thinking clogged pores and hair follicles that could also lead to hair loss.
Funny I might have had some of this going on before Accutane, meaning Accutane could have been just sort of a bandaid.

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Great work. Could you go into more detail about how you took the Propionibacterium freudenreichii? Thanks

Theres only one company that puts out p.freudenreichii as a probiotic at 5 billion cfuā€™s per capsule.
They recommend 5 billion to 10 billion per day.

Ive probably taken as much as 20 billion per day, but just one pill per day is very potent and starts to build up in your system very quickly.
What I first noticed was pretty intense acid production, (Im not talking about stomach acid) and I became a little concerned of this effect on my teeth. I could also tell it was getting in my sinuses.
I tend to ride things out a little bit in an effort to learn more, but this last time had me more concerned with its lingering effects.
Im still feeling its acid production even weeks after stopping this probiotic.
It seems to be a recurring theme here, a type of shift in health that takes longer to recover from, not limited to Fin or Accutane.
Whats trying to recover?

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This I agree. But a temporary bandaid and more aggressive when the bandaid effect is gone.

Adding to this,

Resistin-like Molecule Ī± Provides Vitamin-A-Dependent Antimicrobial Protection in the Skin

https://www.sciencedirect.com/science/article/pii/S1931312819302070

Vitamin A deficiency increases susceptibility to skin infection. However, the mechanisms by which vitamin A regulates skin immunity remain unclear. Here, we show that resistin-like molecule Ī± (RELMĪ±), a small secreted cysteine-rich protein, is expressed by epidermal keratinocytes and sebocytes and serves as an antimicrobial protein that is required for vitamin-A-dependent resistance to skin infection. RELMĪ± was induced by microbiota colonization of the murine skin, was bactericidal in vitro , and was protected against bacterial infection of the skin in vivo . RELMĪ± expression required dietary vitamin A and was induced by the therapeutic vitamin A analog [isotretinoin](https://www.sciencedirect.com/topics/immunology-and-microbiology/isotretinoin), which protected against skin infection in a RELMĪ±-dependent manner. The RELM family member Resistin was expressed in human skin, was induced by vitamin A analogs, and killed skin bacteria, indicating a conserved function for RELM proteins in skin innate immunity. Our findings provide insight into how vitamin A promotes resistance to skin infection.

The vitamin A derivative retinoic acid protects against infection because it stimulates the expression of immunity-related genes that contain retinoic acid response elements (RAREs). Vitamin A deficiency is associated with an increased susceptibility to skin infections, and retinoids are effective for treating some inflammatory skin conditions. Harris et al . found that keratinocytes and sebocytes (sebaceous gland cells) of mice produced resistin-like molecule Ī±Ī± (RELMĪ±) when germ-free animals were challenged with the opportunistic pathogen Staphylococcus aureus . In vitro, RELMĪ± and its human homolog resistin (RETN) exhibited bactericidal activity against both Gram-negative and Gram-positive species, and they permeabilized liposomes, suggesting that they may act as pore-forming, antimicrobial peptides (see commentary by Schrƶder). Experiments with RELMĪ±-deficient mice indicated that RELMĪ± played a role in shaping the composition of the skin microbiome. In a human sebaceous gland cell line, the RETN promoter, which contains putative RAREs, immunoprecipitated with retinoic acid receptors (RARs), and its activity was stimulated by retinol in the presence of the proinflammatory cytokine interleukin-1Ī² unless RARs were pharmacologically inhibited. In mice fed a vitamin Aā€“deficient diet, RELMĪ± and the transcript encoding it ( Retlna ) were less abundant in the skin, and the animals were more susceptible to skin infection compared with controls. Oral administration of the synthetic retinoid isotretinoin stimulated Retlna expression in mice fed normal chow and rescued Retlna expression and susceptibility to infection in vitamin Aā€“deficient mice. Although further work will be required to determine how bacteria induce Retlna expression, these findings identify an important role for vitamin A derivatives in shaping the microbial community of the skin and protecting against colonization by pathogenic bacteria.

Another thought about this with Covid going around.

ā€œElevated propionate: acetate ratios, as seen in CLF after antibiotic exposure, strongly blunted inflammatory responses in vitro . In vivo , exposure of lungs to high dose propionate, to mimic how prior antibiotic exposure changed SCFA levels, resulted in diminished immune containment of Staphylococcus aureus pneumonia.ā€