Increased Fecal Levels of Chromogranin A, Chromogranin B, and Secretoneurin in Collagenous Colitis

被引:19
作者
Wagner, Michael [1 ]
Stridsberg, Mats [2 ]
Peterson, Christer G. B. [1 ]
Sangfelt, Per [1 ]
Lampinen, Maria [1 ]
Carlson, Marie [1 ]
机构
[1] Uppsala Univ, Dept Med Sci, Gastroenterol Res Grp, S-75185 Uppsala, Sweden
[2] Uppsala Univ, Dept Clin Chem, S-75185 Uppsala, Sweden
基金
瑞典研究理事会;
关键词
collagenous colitis; inflammatory bowel disease; chromogranin A; chromogranin B; secretoneurin; fecal samples; INFLAMMATORY-BOWEL-DISEASE; RAT ENTEROCHROMAFFIN CELLS; ENTERIC NERVOUS-SYSTEM; ULCERATIVE-COLITIS; SECRETOGRANIN-II; SUBSTANCE-P; MUCOSAL PERMEABILITY; BUDESONIDE TREATMENT; TERMINAL FRAGMENT; ADRENAL-MEDULLA;
D O I
10.1007/s10753-013-9612-4
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Interactions between the enteric nervous system and the immune system are suggested to play an important role in the pathophysiology of inflammatory bowel disease (IBD). This study aims to determine if chromogranin A (CgA), chromogranin B (CgB), and secretoneurin (SN) are detectable in feces (F) from patients with collagenous colitis (CC) and to compare the levels found in patients with ulcerative colitis (UC) and Crohn's disease (CD) before and during treatment. Patients with CC (n = 12) were studied before and after 3, 7, 28, and 56 days of treatment. Patients with IBD (UC, n = 21; CD, n = 11) were studied before and after 28 and 56 days of treatment. Clinical data were recorded, and fecal samples were collected at each occasion. F-CgA, F-CgB, and F-SN were measured by RIA. Eleven patients with CC, 21 with UC, and 10 with CD achieved remission. On inclusion, CC patients had higher levels of F-CgA, F-CgB, and F-SN than patients with IBD and controls. Patients with IBD expressed markedly lower levels of F-SN than controls. During treatment, F-SN in CC patients decreased to control levels but remained low in IBD patients. No change was found in F-CgA or F-CgB in any of the groups. In conclusion, CgA, CgB, and SN are detectable in feces, and CC patients express higher values than patients with IBD and controls. During treatment, F-SN decreased to control levels in CC. These findings suggest that the enteric nervous system is clearly involved in the pathophysiology of CC.
引用
收藏
页码:855 / 861
页数:7
相关论文
共 58 条
[1]   Rectal carcinoid arising in ulcerative colitis associated with rectal adenocarcinoma [J].
Aoki, S ;
Watanabe, M ;
Hasegawa, H ;
Nishibori, H ;
Mukai, M ;
Kitajima, M .
JOURNAL OF GASTROENTEROLOGY, 2004, 39 (07) :697-698
[2]   New antimicrobial activity for the catecholamine release-inhibitory peptide from chromogranin A [J].
Briolat, J ;
Wu, SD ;
Mahata, SK ;
Gonthier, B ;
Bagnard, D ;
Chasserot-Golaz, S ;
Helle, KB ;
Aunis, D ;
Metz-Boutigue, MH .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2005, 62 (03) :377-385
[3]   Mechanisms of diarrhea in collagenous colitis [J].
Bürgel, N ;
Bojarski, C ;
Mankertz, J ;
Zeitz, M ;
Fromm, M ;
Schulzke, JD .
GASTROENTEROLOGY, 2002, 123 (02) :433-443
[4]   Increased substance P responses in dorsal root ganglia and intestinal macrophages during Clostridium difficile toxin A enteritis in rats [J].
Castagliuolo, I ;
Keates, AC ;
Qiu, BS ;
Kelly, CP ;
Nikulasson, S ;
Leeman, SE ;
Pothoulakis, C .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (09) :4788-4793
[5]   The immunomodulation of enteric neuromuscular function: Implications for motility and inflammatory disorders [J].
Collins, SM .
GASTROENTEROLOGY, 1996, 111 (06) :1683-1699
[6]   Localization of eosinophils to airway nerves and effect on neuronal M-2 muscarinic receptor function [J].
Costello, RW ;
Schofield, BH ;
Kephart, GM ;
Gleich, GJ ;
Jacoby, DB ;
Fryer, AD .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1997, 273 (01) :L93-L103
[7]   Secretoneurin, a novel neuropeptide, is a potent chemoattractant for human eosinophils [J].
Dunzendorfer, S ;
Schratzberger, P ;
Reinisch, N ;
Kähler, CM ;
Wiedermann, CJ .
BLOOD, 1998, 91 (05) :1527-1532
[8]   Colonic endocrine cells in inflammatory bowel disease [J].
El-Salhy, M ;
Danielsson, Å ;
Stenling, R ;
Grimelius, L .
JOURNAL OF INTERNAL MEDICINE, 1997, 242 (05) :413-419
[9]   Neutrophil-mediated gastrointestinal injury [J].
Elliott, SN ;
Wallace, JL .
CANADIAN JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, 1998, 12 (08) :559-568
[10]  
FLEJOU JF, 1984, ARCH PATHOL LAB MED, V108, P977