aha----=apologies tires...... replace ways for raise....
as we seem for the moment to have exhausted other areas so then i turned to probiotics as i recall some inflammation effects from a lot of probiotics - see
below- also i recall topicals work as well as internally so a combination of all three OR perhaps to to probiotic strain dominace keeping them separate and a rotation schedule
1 Lactobacillus reuteri
https://link.springer.com/article/10.1007/s12602-016-9246-6
Abstract
Emerging evidence suggests that probiotic therapy can play a role in the prevention and management of oral inflammatory diseases through immunomodulation and down-regulation of the inflammatory cascade. The aim of this in vitro study was to investigate the viability of human gingival fibroblasts (HGF) and its production of prostaglandin E2 (PGE2), when exposed to supernatants of two mixed Lactobacillus reuteri strains (ATCC PTA 5289 and DSM 17938). The experiments were conducted in the presence and absence of the pro-inflammatory cytokine IL-1β. L. reuteri strains were grown and the bacterial supernatant was collected. The cell-free supernatant was diluted to concentrations equivalent to the ones produced by 0.5 to 5.0 × 107 CFU/mL bacteria. Cell viability was assessed with the MTT colorimetric assay and the amount of PGE2 in the cell culture medium was determined using the monoclonal enzyme immune assay kits. Our findings showed that none of the L. reuteri supernatants were cytotoxic or affected the viability of HGF. The most concentrated bacterial supernatant stimulated the production of PGE2 by the gingival cells in a significant way in the presence of IL-1β (p < 0.05), suggesting that bacterial products secreted from L. reuteri might play a role in the resolution of inflammation in HGF. Thus, our findings justify further investigations on the influence of probiotic bacteria on gingival inflammatory reactions.
2 Lactobacillus rhamnosus - pge2
3 L. gasseri
From http://www.ncbi.nlm....les/PMC4188884/
" Increased levels of 6-ketoprostaglandin F1-α, epidermal growth factor (EGF) and b-fibroblast growth factor have been implicated in the protective effect displayed by peculiar bifidobacterial strains such as Bifidobacterium brevis (B. brevis)and B. bifidum against gastric ulceration induced by acetic acid or ethanol in rats[55]. Pre-treatment of rats with Lactobacillus rhamnosus GG (L. GG) at 109 CFU/mL twice daily for three consecutive days was able to markedly lessen the suppressive actions of ethanol on mucus-secreting layer and trans-mucosal resistance along with an increase in the basal mucosal prostaglandin E2 (PGE2) levels and a concomitant reduction of cellular apoptosis[56]. In a more recent study aimed at determining the role of viable lactobacilli in the healing of acetic acid-induced chronic gastric ulcer, Uchida et al[57] reported that a yogurt containing L. gasseri OLL 2716 inhibits the formation of HCl-induced acute gastric lesions through the generation of PGE2. Overall, these findings suggested that the up-regulation of prostaglandins could stimulate the mucus secretion and increase the transmucosal resistance in the gastric mucosa."
as we seem for the moment to have exhausted other areas so then i turned to probiotics as i recall some inflammation effects from a lot of probiotics - see
below- also i recall topicals work as well as internally so a combination of all three OR perhaps to to probiotic strain dominace keeping them separate and a rotation schedule
1 Lactobacillus reuteri
https://link.springer.com/article/10.1007/s12602-016-9246-6
Abstract
Emerging evidence suggests that probiotic therapy can play a role in the prevention and management of oral inflammatory diseases through immunomodulation and down-regulation of the inflammatory cascade. The aim of this in vitro study was to investigate the viability of human gingival fibroblasts (HGF) and its production of prostaglandin E2 (PGE2), when exposed to supernatants of two mixed Lactobacillus reuteri strains (ATCC PTA 5289 and DSM 17938). The experiments were conducted in the presence and absence of the pro-inflammatory cytokine IL-1β. L. reuteri strains were grown and the bacterial supernatant was collected. The cell-free supernatant was diluted to concentrations equivalent to the ones produced by 0.5 to 5.0 × 107 CFU/mL bacteria. Cell viability was assessed with the MTT colorimetric assay and the amount of PGE2 in the cell culture medium was determined using the monoclonal enzyme immune assay kits. Our findings showed that none of the L. reuteri supernatants were cytotoxic or affected the viability of HGF. The most concentrated bacterial supernatant stimulated the production of PGE2 by the gingival cells in a significant way in the presence of IL-1β (p < 0.05), suggesting that bacterial products secreted from L. reuteri might play a role in the resolution of inflammation in HGF. Thus, our findings justify further investigations on the influence of probiotic bacteria on gingival inflammatory reactions.
2 Lactobacillus rhamnosus - pge2
3 L. gasseri
From http://www.ncbi.nlm....les/PMC4188884/
" Increased levels of 6-ketoprostaglandin F1-α, epidermal growth factor (EGF) and b-fibroblast growth factor have been implicated in the protective effect displayed by peculiar bifidobacterial strains such as Bifidobacterium brevis (B. brevis)and B. bifidum against gastric ulceration induced by acetic acid or ethanol in rats[55]. Pre-treatment of rats with Lactobacillus rhamnosus GG (L. GG) at 109 CFU/mL twice daily for three consecutive days was able to markedly lessen the suppressive actions of ethanol on mucus-secreting layer and trans-mucosal resistance along with an increase in the basal mucosal prostaglandin E2 (PGE2) levels and a concomitant reduction of cellular apoptosis[56]. In a more recent study aimed at determining the role of viable lactobacilli in the healing of acetic acid-induced chronic gastric ulcer, Uchida et al[57] reported that a yogurt containing L. gasseri OLL 2716 inhibits the formation of HCl-induced acute gastric lesions through the generation of PGE2. Overall, these findings suggested that the up-regulation of prostaglandins could stimulate the mucus secretion and increase the transmucosal resistance in the gastric mucosa."
