The role of dendritic cell subsets in 2,4,6-trinitrobenzene sulfonic acid-induced ileitis

Serotonin (5-HT) regulates peristaltic and secretory reflexes in the gut. The serotonin reuptake transporter (SERT; SLC6A4), which inactivates 5-HT, is expressed in the intestinal mucosa and the enteric nervous system. Stool water content is increased and colonic motility is irregular in mice with a targeted deletion of SERT. We tested the hypotheses that 5-HT plays a role in regulating intestinal inflammation and that the potentiation of serotonergic signaling that results from SERT deletion is proinflammatory. Rectal installation of 2,4,6-trinitrobenzene sulfonic acid (TNBS) was used to induce an immune-mediated colitis, which was compared in SERT knockout mice and littermate controls. Intestinal myeloperoxidase and histamine levels were significantly increased, whereas the survival rate and state of health were significantly decreased in TNBS-treated mice that lacked SERT. Deletion of SERT thus increases the severity of TNBS colitis. These data suggest that 5-HT and its SERT-mediated termination play roles in intestinal immune/inflammatory responses in mice.

Download Full-text

Pathogenic role of cyclooxygenase-2 expression in the initiation of experimental inflammatory bowel disease induced by trinitrobenzene sulfonic ACID in rats

Gastroenterology ◽

10.1016/s0016-5085(00)83479-4 ◽

2000 ◽

Vol 118 (4) ◽

pp. A345

Author(s):

Xin Guo ◽

Joshua K. Ko ◽

Ben C. Wong ◽

Chi-Hin Cho

Keyword(s):

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Sulfonic Acid ◽

Cyclooxygenase 2 ◽

Trinitrobenzene Sulfonic Acid ◽

Pathogenic Role ◽

Experimental Inflammatory Bowel Disease ◽

Inflammatory Bowel

Download Full-text

The Role of Human Dendritic Cell Subsets in Antitumor Immunity

Advances in Clinical Medicine ◽

10.12677/acm.2020.103037 ◽

2020 ◽

Vol 10 (03) ◽

pp. 232-238

Author(s):

莉莉马

Keyword(s):

Dendritic Cell ◽

Antitumor Immunity ◽

Human Dendritic Cell ◽

Dendritic Cell Subsets

Download Full-text

Leishmaniasis, contact hypersensitivity and graft-versus-host disease: understanding the role of dendritic cell subsets in balancing skin immunity and tolerance

Experimental Dermatology ◽

10.1111/j.1600-0625.2010.01116.x ◽

2010 ◽

Vol 19 (8) ◽

pp. 760-771 ◽

Cited By ~ 9

Author(s):

Kordula Kautz-Neu ◽

Ralf G. Meyer ◽

Björn E. Clausen ◽

Esther Von Stebut

Keyword(s):

Dendritic Cell ◽

Graft Versus Host Disease ◽

Contact Hypersensitivity ◽

Host Disease ◽

Graft Versus Host ◽

Skin Immunity ◽

Dendritic Cell Subsets ◽

Disease Understanding

Download Full-text

The effect of trinitrobenzene sulfonic acid on gut-derived smooth muscle cell arachidonic acid metabolism: role of endogenous prostanoids

Mediators of Inflammation ◽

10.1080/09629359791749 ◽

1997 ◽

Vol 6 (3) ◽

pp. 237-240

Author(s):

W. E. Longo ◽

G. S. Smith ◽

Y. Deshpande ◽

C. Reickenberg ◽

D. L. Kaminski

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Sulfonic Acid ◽

Muscle Cells ◽

Arachidonic Acid Metabolism ◽

Trinitrobenzene Sulfonic Acid ◽

Eicosanoid Production

The contribution of smooth muscle cells as a potential source of eicosanoid production during inflammatory states remains to be elucidated. We investigated the effect of trinitrobenzene sulfonic acid (TNB), a known pro-inflammatory agent, on jejunal smooth muscle cell eicosanoid production. Human gut-derived smooth muscle cells (HISM) were incubated with TNB for 1 hour. Additionally, some cells were preincubated with either dimethylthiourea, or indomethacin for 1 hour before exposure to identical concentrations of TNB. Incubation with TNB led to significant increases in PGE2and 6-keto PGF-1αrelease, but not leukotriene B4release; responses which were both inhibited by dimethylthiourea and indomethacin treatment. Our results suggest that gutderived smooth muscle cells may represent an important source of proinflammatory prostanoids but not leukotrienes during inflammatory states of the intestine. The inhibition of prostanoid activity by thiourea may be mediated by suppression of cyclooxygenase activity in this cell line.

Download Full-text