Recent Comments

    IBD tagged posts

    New Therapeutic Target for Crohn’s disease

    September 21, 2016, Categories  Biology/Biotechnology, Health/Medical

    Highlights •PKCλ/ι is required for Paneth cell differentiation •PKCλ/ι reduces EZH2 stability and promotes Atoh1 and Gfi1 expression •PKCλ/ι induces intestinal epithelial cell survival through the repression of JNK •PKCλ/ι loss enhances intestinal inflammation and cancer

    Highlights •PKCλ/ι is required for Paneth cell differentiation •PKCλ/ι reduces EZH2 stability and promotes Atoh1 and Gfi1 expression •PKCλ/ι induces intestinal epithelial cell survival through the repression of JNK •PKCλ/ι loss enhances intestinal inflammation and cancer

    A promising new target for future drugs to treat inflammatory bowel disease (IBD) has been found. The study also indicates that another protein, protein kinase C (PKC) λ/ι, may serve as a biomarker of IBD severity. “The intestine is protected by specialized cells, called Paneth cells, that secrete antimicrobial peptides,” said Jorge Moscat, Ph.D., deputy director and professor in the NCI-designated Cancer Center...

    Read More

    Unlocking Secrets of Immune System could help Combat Colitis

    June 16, 2016, Categories  Biology/Biotechnology, Health/Medical

    An intrinsic complement-NLRP3 axis regulates human TH1 responses. T cell receptor activation and CD46 costimulation trigger NLRP3 expression and intracellular C5a generation. Subsequent intracellular C5aR1 engagement induces ROS production (and possibly IL1B gene transcription) and NLRP3 assembly, which in turn mediates IL-1β maturation. Autocrine IL-1β promotes TH1 induction (IFN-γ production) but restricts TH1 contraction (IL-10 coexpression). C5aR2 cell surface activation by secreted C5a negatively controls these events via undefined mechanisms. Dysfunction of this system contributes to impaired TH1 responses in infection or increased TH17 responses during intestinal inflammation.

    An intrinsic complement-NLRP3 axis regulates human TH1 responses. T cell receptor activation and CD46 costimulation trigger NLRP3 expression and intracellular C5a generation. Subsequent intracellular C5aR1 engagement induces ROS production (and possibly IL1B gene transcription) and NLRP3 assembly, which in turn mediates IL-1β maturation. Autocrine IL-1β promotes TH1 induction (IFN-γ production) but restricts TH1 contraction (IL-10 coexpression). C5aR2 cell surface activation by secreted C5a negatively controls these events via undefined mechanisms. Dysfunction of this system contributes to impaired TH1 responses in infection or increased TH17 responses during intestinal inflammation.

    Researchers have unlocked secrets of our ancient immune system...

    Read More

    Green Tea and Iron, bad combination

    March 8, 2016, Categories  Biology/Biotechnology, Health/Medical

    egcggreen-tea

    Green tea has great antioxidants, but experiments in a lab mouse model of IBD suggest that consuming green tea along with dietary iron may actually lessen green tea’s benefits. “If you drink green tea after an iron-rich meal, the main compound in the tea will bind to the iron,” said Matam Vijay-Kumar, assistant professor of nutritional sciences, Penn State. “When that occurs, the green tea loses its potential as an antioxidant. In order to get the benefits of green tea, it may be best to not consume it with iron-rich foods.” Iron-rich foods include red meat and dark leafy greens, such as kale and spinach, iron supplements.

    Vijay-Kumar and colleagues found that EGCG – the main compound in green tea – potently inhibits myeloperoxidase, a pro-inflammatory enzyme released by white blood cells...

    Read More
    Single treatment with curli fibres ameliorates TNBS colitis. Colitis was induced in 6–8-week female Balb/c (n=6–7) mice by intrarectal instillation of 1% TNBS in 50% ethanol or 50% ethanol as a vehicle control. Day 1 post TNBS enema, mice were administered treatments as follows: 0.1 mg curli (oral), 0.4 mg curli (oral), 0.1 mg anti-TNFα (i.p.) or no treatment. (a) survival (n=6), (b) histopathological scores at day 6 post TNBS induction were plotted and (c) H&E images were taken. (d) Stool consistency scores were determined at day 3 post TNBS induction. It should be noted that larger areas of immune cell infiltration and lymphoid follicles in the submucosa was determined in the colonic tissue of mice treated with TNBS alone as compared with the groups that received curli treatment (*P<0.05; **P<0.01; ****P<0.0001). H&E, hematoxylin and eosin; i.p., intraperitoneal; TNBS, 2,4,6-trinitrobenzene sulphonic acid; TNF, tumour necrosis factor; Tx, treatment.

    Single treatment with curli fibres ameliorates TNBS colitis. Colitis was induced in 6–8-week female Balb/c (n=6–7) mice by intrarectal instillation of 1% TNBS in 50% ethanol or 50% ethanol as a vehicle control. Day 1 post TNBS enema, mice were administered treatments as follows: 0.1 mg curli (oral), 0.4 mg curli (oral), 0.1 mg anti-TNFα (i.p.) or no treatment. (a) survival (n=6), (b) histopathological scores at day 6 post TNBS induction were plotted and (c) H&E images were taken. (d) Stool consistency scores were determined at day 3 post TNBS induction...

    Read More