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We observed a significantly increased proportion of Akkermansia muciniphila, Ruthenibacterium lactatiformans, Hungatella hathewayi, and Eisenbergiella tayi and decreased Faecalibacterium prausnitzii and Blautia species.
originally posted by: tamusan
a reply to: rickymouse
It's not specifically the bacteria that breakdown plants but the byproducts of that which have been associated with MS. This is going to be a small part once we see the big picture. It is being found that there is a multitude of gut bacteria that are either overexpressed or underexpressed in those with MS and other inflammatory diseases. If I were to speculate, I would think that there is likely a bacteria that cleans up the byproducts from breaking down plants that is lacking in those who have MS.
There are also going to be some genetic and environmental factors involved with a healthy individual microflora. In the past, when most people lived in the same location as our ancestors, people were born with some of the right microflora in their gut and gained the rest from breastfeeding. Many people no longer live in the regions of their ancestors or eat the traditional diets associated with those regions, and many are also no longer breastfed. As you pointed out in my other thread, our food has lots of stuff in it that kills off the bacteria in our gut and many medications do as well, not just antibiotics.
All cyanide foods, both isothiocyanates or anthrocyanates
Anti-inflammatory activity
The therapeutic potential of sulforaphane has also been linked to its capacity to target pro-inflammatory pathways. Sulforaphane was found to attenuate pancreatic injury in a mouse model of acute pancreatitis by stimulating Nrf2-induced antioxidant enzymes (18). Concomitantly, sulforaphane significantly reduced the nuclear translocation of the pro-inflammatory transcription factor nuclear factor (NF)-κB in pancreatic acinar cells, downregulating the expression of NF-κB target genes that code for pro-inflammatory mediators, such as tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1β), and IL-6 (Figure 3) (18). Through inhibiting the NF-κB pathway, sulforaphane also targets other mediators of the inflammatory response, including the enzymes cyclooxygenase-2 (COX-2), prostaglandin E (PGE) synthase, and inducible nitric oxide synthase (iNOS). Sulforaphane exhibited anti-inflammatory effects in the lungs of mice with lipopolysaccharide (LPS)-induced acute respiratory distress syndrome (ARDS) by downregulating the expression of NF-κB, IL-6, TNF-α and COX-2, as well as decreasing production of nitric oxide (NO) and PGE2 (19). Other isothiocyanates have been shown to prevent the degradation of the NF-κB inhibitor, IκB, the nuclear translocation of NF-κB, and/or the transcriptional activity of NF-κB in vitro or in cultured cells (Figure 3) (20), which all can lead to a decrease in inflammatory responses.
The modulation of Nrf2 and NF-κB signaling pathways by isothiocyanates is especially relevant to the prevention of cancer because both oxidative stress and inflammation are significant contributors in the development and progression of cancer.