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Effects of AP‑1 and NF‑κB inhibitors on colonic endocrine cells in rats with TNBS‑induced colitis.

El-Salhy M, Umezawa K - Mol Med Rep (2016)

Bottom Line: The density of cells expressing CgA, PYY and PP was significantly lower in the TNBS group compared with in the control group, whereas the density of cells expressing serotonin, oxyntomodulin and somatostatin was significantly higher in the TNBS group compared with in the control group.None of the endocrine cell types differed significantly between the control group and either the DTCM‑G or DHMEQ groups.These results indicated that the immune system and enteroendocrine cells interact in IBD.

View Article: PubMed Central - PubMed

Affiliation: Division of Gastroenterology, Department of Medicine, Stord Helse‑Fonna Hospital, 5416 Stord, Norway.

ABSTRACT
Interactions between intestinal neuroendocrine peptides/amines and the immune system appear to have an important role in the pathophysiology of inflammatory bowel disease (IBD). The present study investigated the effects of activator protein (AP)‑1 and nuclear factor (NF)‑κB inhibitors on inflammation‑induced alterations in enteroendocrine cells. A total of 48 male Wistar rats were divided into the following four groups (n=12 rats/group): Control, trinitrobenzene sulfonic acid (TNBS)‑induced colitis only (TNBS group), TNBS‑induced colitis with 3‑[(dodecylthiocarbonyl)-methyl]-glutarimide (DTCM‑G) treatment (DTCM‑G group), and TNBS‑induced colitis with dehydroxymethylepoxyquinomicin (DHMEQ) treatment (DHMEQ group). A total of 3 days following administration of TNBS, the rats were treated as follows: The control and TNBS groups received 0.5 ml vehicle (0.5% carboxymethyl cellulose; CMC), respectively; the DTCM‑G group received DTCM‑G (20 mg/kg body weight) in 0.5% CMC; and the DHMEQ group received DHMEQ (15 mg/kg body weight) in 0.5% CMC. All injections were performed intraperitoneally twice daily for 5 days. The rats were sacrificed, and tissue samples obtained from the colon were examined histopathologically and immunohistochemically. Inflammation was evaluated using a scoring system. In addition, the sections were immunostained for chromogranin A (CgA), serotonin, peptide YY (PYY), oxyntomodulin, pancreatic polypeptide (PP) and somatostatin, and immunostaining was quantified using image‑analysis software. The density of cells expressing CgA, PYY and PP was significantly lower in the TNBS group compared with in the control group, whereas the density of cells expressing serotonin, oxyntomodulin and somatostatin was significantly higher in the TNBS group compared with in the control group. None of the endocrine cell types differed significantly between the control group and either the DTCM‑G or DHMEQ groups. All of the colonic endocrine cell types were affected in rats with TNBS‑induced colitis. The expression density of these endocrine cell types was restored to control levels following treatment with AP‑1 or NF‑κB inhibitors. These results indicated that the immune system and enteroendocrine cells interact in IBD.

No MeSH data available.


Related in: MedlinePlus

Serotonin-expressing cells in the colon of rats in the (A) control, (B) trinitrobenzene sulfonic acid, (C) 3-[(dodecylthiocarbonyl)-methyl]-glutarimide and (D) dehydroxymethylepoxyquinomicin groups.
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f3-mmr-14-02-1515: Serotonin-expressing cells in the colon of rats in the (A) control, (B) trinitrobenzene sulfonic acid, (C) 3-[(dodecylthiocarbonyl)-methyl]-glutarimide and (D) dehydroxymethylepoxyquinomicin groups.

Mentions: Cells expressing CgA, serotonin, PYY, oxyntomodulin, PP and somatostatin were detected in all colonic tissues from all of the groups. The endocrine cells were predominantly located at the crypts of Lieberkühn. These cells were flask-shaped and occasionally contained a long basal cytoplasmic process, often known as a 'neuropod' (43–46) (Figs. 2 and 3).


Effects of AP‑1 and NF‑κB inhibitors on colonic endocrine cells in rats with TNBS‑induced colitis.

El-Salhy M, Umezawa K - Mol Med Rep (2016)

Serotonin-expressing cells in the colon of rats in the (A) control, (B) trinitrobenzene sulfonic acid, (C) 3-[(dodecylthiocarbonyl)-methyl]-glutarimide and (D) dehydroxymethylepoxyquinomicin groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4940105&req=5

f3-mmr-14-02-1515: Serotonin-expressing cells in the colon of rats in the (A) control, (B) trinitrobenzene sulfonic acid, (C) 3-[(dodecylthiocarbonyl)-methyl]-glutarimide and (D) dehydroxymethylepoxyquinomicin groups.
Mentions: Cells expressing CgA, serotonin, PYY, oxyntomodulin, PP and somatostatin were detected in all colonic tissues from all of the groups. The endocrine cells were predominantly located at the crypts of Lieberkühn. These cells were flask-shaped and occasionally contained a long basal cytoplasmic process, often known as a 'neuropod' (43–46) (Figs. 2 and 3).

Bottom Line: The density of cells expressing CgA, PYY and PP was significantly lower in the TNBS group compared with in the control group, whereas the density of cells expressing serotonin, oxyntomodulin and somatostatin was significantly higher in the TNBS group compared with in the control group.None of the endocrine cell types differed significantly between the control group and either the DTCM‑G or DHMEQ groups.These results indicated that the immune system and enteroendocrine cells interact in IBD.

View Article: PubMed Central - PubMed

Affiliation: Division of Gastroenterology, Department of Medicine, Stord Helse‑Fonna Hospital, 5416 Stord, Norway.

ABSTRACT
Interactions between intestinal neuroendocrine peptides/amines and the immune system appear to have an important role in the pathophysiology of inflammatory bowel disease (IBD). The present study investigated the effects of activator protein (AP)‑1 and nuclear factor (NF)‑κB inhibitors on inflammation‑induced alterations in enteroendocrine cells. A total of 48 male Wistar rats were divided into the following four groups (n=12 rats/group): Control, trinitrobenzene sulfonic acid (TNBS)‑induced colitis only (TNBS group), TNBS‑induced colitis with 3‑[(dodecylthiocarbonyl)-methyl]-glutarimide (DTCM‑G) treatment (DTCM‑G group), and TNBS‑induced colitis with dehydroxymethylepoxyquinomicin (DHMEQ) treatment (DHMEQ group). A total of 3 days following administration of TNBS, the rats were treated as follows: The control and TNBS groups received 0.5 ml vehicle (0.5% carboxymethyl cellulose; CMC), respectively; the DTCM‑G group received DTCM‑G (20 mg/kg body weight) in 0.5% CMC; and the DHMEQ group received DHMEQ (15 mg/kg body weight) in 0.5% CMC. All injections were performed intraperitoneally twice daily for 5 days. The rats were sacrificed, and tissue samples obtained from the colon were examined histopathologically and immunohistochemically. Inflammation was evaluated using a scoring system. In addition, the sections were immunostained for chromogranin A (CgA), serotonin, peptide YY (PYY), oxyntomodulin, pancreatic polypeptide (PP) and somatostatin, and immunostaining was quantified using image‑analysis software. The density of cells expressing CgA, PYY and PP was significantly lower in the TNBS group compared with in the control group, whereas the density of cells expressing serotonin, oxyntomodulin and somatostatin was significantly higher in the TNBS group compared with in the control group. None of the endocrine cell types differed significantly between the control group and either the DTCM‑G or DHMEQ groups. All of the colonic endocrine cell types were affected in rats with TNBS‑induced colitis. The expression density of these endocrine cell types was restored to control levels following treatment with AP‑1 or NF‑κB inhibitors. These results indicated that the immune system and enteroendocrine cells interact in IBD.

No MeSH data available.


Related in: MedlinePlus