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Immune system promotes digestive health by fostering community of 'good' bacteria
Loss of MyD88 disturbs the microbial community because it disrupts production of IgA. This class of antibody works like a gatekeeper that controls which types of bacteria, and how many, are allowed to inhabit the gut. By performing inventories of total gut bacteria compared to species that bind IgA, the scientists determined that without MyD88, IgA failed to recognize species that it can otherwise.
When the immune system functions properly (MyD88 is active), IgA antibodies bind multiple species of bacteria, keeping the numbers and types of 'good' bacteria that inhabit the gut under control. When the immune system is disrupted (MyD88 is inactive), IgA binds bacteria less effectively, and the bacterial community becomes imbalanced, jeopardizing digestive health.
MYD88 is a gene found on 23&Me, neither good or bad category on Promethease report. I apparently have a normal microbiome and IgA production (from stool and blood tests) and my SNPs are rs7744(A;G) and rs6853 (A;A). The rs1244(A;G) is associated with ulcerative colitis!
The *1244 A>G polymorphism of MyD88 (rs7744) is closely associated with susceptibility to ulcerative colitis
Toll‑like receptor activation intitially recruits the myeloid differentiation primary response gene (88) (MyD88) protein. A polymorphism *1244 A>G (rs7744) in the 3'‑untranslated region of MyD88 has been identified. In the present study, the association of this polymorphism with ulcerative colitis (UC) was investigated. The population studied comprised 922 individuals, including patients with UC (UC cases) and without (controls). Genotyping of rs7744 was performed by PCR single-strand conformation polymorphism and the rs7744 G allele frequencies in the controls and UC cases were 32.8 and 43.5%, respectively (P<0.0001). The results showed that the genotype frequency of the AA homozygote was significantly lower and that of the GG homozygote was significantly higher in the UC cases compared with those in the controls (P=0.0012 for both groups). The rs7744 minor allele variants were significantly associated with susceptibility to UC as indicated by dominant and recessive genetic models. The minor allele variants were associated with an increased risk for UC in the male individuals but not the female individuals. The rs7744 was also associated with a non‑continuous phenotype of UC and steroid unused/independent UC. This minor allele homozygote was associated with the disease severity of UC, hospitalization and response to steroid treatment. The results of the present study provided evidence that MyD88 polymorphism rs7744 was significantly associated with the development of UC and that this polymorphism may be associated with the response to treatment therapies for UC.
LONDON: Researchers have found that the colonisation of the gut by certain types of bacteria may lead to immune responses later in life that are linked to autoimmune disease. Research on mice studies found that increases in the levels of segmented filamentous bacteria can trigger changes in the lymphoid tissue of the mouse gut that result in the production of antibodies that attack components of the cell nucleus.
Segmented filamentous bacteria are clostridia-related microorganisms found in the gut of many animals including mice, rats and humans.
This type of damage is a hallmark of autoimmune diseases like systemic lupus erythematosus and systemic sclerosis where organs throughout the body are damaged by wayward immune responses, researchers said.
"Our results demonstrate how gut health in young animals may be linked to autoimmune disease in older animals," said Dirk Elewaut, Professor at Ghent University Hospital in Belgium.
"The microbiome of the young mouse impacts a loss of tolerance of the secondary immune system against proteins in the nucleus of the cell. The attack of certain proteins by the body's own immune system can subsequently lead to disease," Elewaut said.
Hmmmm. That doesn't correlate with their UC risk analysis very well, does it.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
