Showing posts with label inflammatory bowel disease. Show all posts
Showing posts with label inflammatory bowel disease. Show all posts

Tuesday, October 5, 2010

Cellular Immune Processes in IBD Activated By Smoke, Burning and More!

"Modulation of AhR signaling pathway via the diet, cessation of smoking, or administration of AhR antagonists could be viable strategies for the treatment of IBD."

Arsenescu, R., Arsenescu, V., Zhong, J., Nasser, M., Melinte, R., Dingle, C. W., Swanson, H., and de Villiers, W. J. (2010). Role of the xenobiotic receptor in inflammatory bowel disease. Inflammatory bowel diseases.
http://www.citeulike.org/user/HEIRS/article/7950224

Saturday, August 28, 2010

AMPK agonist downregulates innate and adaptive immune responses in TNBS-induced murine acute and relapsing colitis.

"AICAR-initiated AMPK activation may act as a central downregulator in ongoing innate and adaptive immune responses of murine colitis, providing a novel therapeutic approach in the treatment of IBD."



Read more: CiteULike: AMPK agonist downregulates innate and adaptive immune responses in TNBS-induced murine acute and relapsing colitis.:

For further reading: AMPK


Sunday, August 15, 2010

Gut Inflammation and Changes in Intestinal Function From Loss of NO Neurons~!

In a recent study the author writes "enteric neurons are supported by glial cells, the ENS counterparts of astrocytes of the CNS, that can modulate enteric neuron function. Enteric neurons are known to control virtually all GI functions, including motility, secretion, blood flow, mucosal growth and aspects of the local immune system. Consequently, permanent or even transient structural alterations in the ENS, as occur in IBD, disrupt normal GI function. Structural changes in the ENS are predictive of disease evolution suggesting that neuroprotection would decrease disease severity and may play a role in recurrence in CD." Further he continues that under conditions of experimental trichinosis infection in the murine "that in this animal model of colitis, there was a significant loss of nitric oxide synthase- (NOS-) immunoreactive neurons in the myenteric plexus of infected rats. Moreover, the selective loss of NOS-positive neurons appears to underlie changes in motility." (Lakhan) Recent reports also suggest that hormones such as serotonin influences gut regulation and may activate inflammatory cytokines in the intestine leading to alterations in gut function. (Khan) Inflammatory activity such as Tnf-a in the periphery such as the gut may influence production of cytokines and changes in gene expression in the brain that change behavior and have other unexpected health effects.




Khan, W. I. and Ghia, J. E. (2010). Gut hormones: emerging role in immune activation and inflammation. Clinical and experimental immunology, 161(1):19-27.
http://www.citeulike.org/user/HEIRS/article/7323747

Lakhan, S. E. and Kirchgessner, A. (2010). Neuroinflammation in inflammatory bowel disease. Journal of neuroinflammation, 7:37+.
http://www.citeulike.org/user/HEIRS/article/7471133

Thursday, July 1, 2010

Plant Extract May be Effective Against Inflammatory Bowel Disease

"Newswise — A South Dakota State University scientist’s research shows an extract made from a food plant in the Brassica family was effective in alleviating signs of ulcerative colitis, an inflammatory bowel condition, in mice......The ongoing study by associate professor Moul Dey in SDSU’s Department of Health and Nutritional Sciences — funded by the National Institutes of Health — moves on now to examine the potential use of the plant extract against colon cancer."


Read more:Plant Extract May be Effective Against Inflammatory Bowel Disease:

Sunday, February 21, 2010

Researchers Find Gut Protein that Protects Against Infection

A signaling protein that is key in orchestrating the body’s overall immune response has an important localized role in fighting bacterial infection and inflammation in the intestinal tract, according to a study by UC San Diego School of Medicine investigators, published in the journal Cell Host and Microbe. Further the author says, "diminished levels may be potentially an underlying factor in the severe illness caused by pathogens such as E. coli, and inflammation of the intestine by diseases such as Crohn’s disease


Researchers Find Protein that Protects Gut from Infection: "Researchers Find Protein that Protects Gut from Infection"

Thursday, December 31, 2009

Monday, November 2, 2009

Nitric Oxide Production by the Human Intestinal Microbiota by Dissimilatory Nitrate Reduction to Ammonium

Summary: "the human fecal microbiota were shown to produce NO from trace levels of nitrate under gastrointestinal conditions. Moreover, our data indicate that NO was produced by DNRA and not by denitrification or the L-arginine pathway. Studying the interaction between bacterially produced NO and the host epithelial cells might be pivotal in the etiology of inflammatory diseases of the gastrointestinal tract."


Vermeiren, J., Van de Wiele, T., Verstraete, W., Boeckx, P., and Boon, N. (2009). Nitric oxide production by the human intestinal microbiota by dissimilatory nitrate reduction to ammonium. Journal of Biomedicine and Biotechnology.http://www.citeulike.org/user/HEIRS/article/6056766

Monday, October 26, 2009

Microbial induction of IBD Through Protein Expression By TLR Signaling

HEIRS Environmental Illness Research Blog: Why Endotoxin Can Increase Pain,Chemical and Mold Sensitivity and Causes Sickness Behavior!


Summary: A number of gram negative, gram positive and other anaerobes stimulate protein that contributes to IBD. This process is dependant on TLR signaling and can be inhibited by blocking the P38 pathway. In an earlier study showed that the levels of TL1A and number of cells that expressed it correlated with the level of inflammation, especially in Crohn's disease.

Title:Microbial induction of inflammatory bowel disease associated gene tl1a (tnfsf15) in antigen presenting cells.
Shih, D. Q., Kwan, L. Y., Chavez, V., Cohavy, O., Gonsky, R., Chang, E. Y., Chang, C., Elson, C. O., and Targan, S. R. (2009). Microbial induction of inflammatory bowel disease associated gene tl1a (tnfsf15) in antigen presenting cells. European Journal of Immunology, 9999(9999):NA+. http://www.citeulike.org/user/HEIRS/article/6009014
Bamias, G., Martin, C., Marini, M., Hoang, S., Mishina, M., Ross, W. G., Sachedina, M. A., Friel, C. M., Mize, J., Bickston, S. J., Pizarro, T. T., Wei, P., and Cominelli, F. (2003). Expression, localization, and functional activity of tl1a, a novel th1-polarizing cytokine in inflammatory bowel disease. Journal of immunology (Baltimore, Md. : 1950), 171(9):4868-4874. http://www.citeulike.org/user/HEIRS/article/6009138