title: Induction of NGAL synthesis in epithelial cells of human colorectal neoplasia and inflammatory bowel diseases.
abstract: In inflammatory and neoplastic disorders of the colon a defect barrier function of the mucosa may result in absorption of bacterial products from the intestinal lumen. These products may further recruit inflammatory cells and thus augment the inflammatory response. A novel lipocalin in neutrophils, neutrophil gelatinase associated lipocalin (NGAL), with the ability to bind bacterial formylpeptides, has been described and therefore it is of interest to investigate the expression of this protein in diseases of the colon. Expression of NGAL was investigated by immunohistochemistry and by mRNA in situ hybridisation in normal colon and in neoplastic and inflammatory colorectal diseases. A very high expression of NGAL was seen in colonic epithelium in areas of inflammation, both in non-malignant epithelium (diverticulitis, inflammatory bowel disease, and appendicitis) as well as in premalignant and malignant neoplastic lesions of the colon. In adenocarcinoma, the NGAL expression was especially abundant in the transitional mucosa and in the superficial ulcerated area. On the other hand, no NGAL expression could be detected in lymph node metastases from these adenocarcinomas. A weak expression of NGAL in some epithelial cells was only occasionally seen in normal colon. In conclusion, NGAL synthesis is induced in epithelial cells in inflammatory and neoplastic, colorectal diseases. NGAL may serve an important anti-inflammatory function as a scavenger of bacterial products.
authors.affiliation: Department of Pathology, Sundby Hospital, Denmark.
authors.forename: B S
authors.initials: BS
authors.lastname: Nielsen
authors.forename: N
authors.initials: N
authors.lastname: Borregaard
authors.forename: J R
authors.initials: JR
authors.lastname: Bundgaard
authors.forename: S
authors.initials: S
authors.lastname: Timshel
authors.forename: M
authors.initials: M
authors.lastname: Sehested
authors.forename: L
authors.initials: L
authors.lastname: Kjeldsen
mesh_terms: D000209:Acute-Phase Proteins; D000230:Adenocarcinoma / Q000378:metabolism; D000236:Adenoma / Q000378:metabolism; D001064:Appendicitis / Q000378:metabolism; D002352:Carrier Proteins / Q000032:analysis / Q000096:biosynthesis* / Q000235:genetics; D003093:Colitis, Ulcerative / Q000378:metabolism; D003106:Colon / Q000737:chemistry / Q000378:metabolism*; D015179:Colorectal Neoplasms / Q000378:metabolism*; D003424:Crohn Disease / Q000378:metabolism; D004239:Diverticulitis, Colonic / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D015212:Inflammatory Bowel Diseases / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000737:chemistry / Q000378:metabolism*; D000071068:Lipocalin-2; D054834:Lipocalins; D009363:Neoplasm Proteins / Q000032:analysis / Q000096:biosynthesis* / Q000235:genetics; D015513:Oncogene Proteins; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger / Q000032:analysis
chemical_list: D000209:Acute-Phase Proteins; D002352:Carrier Proteins; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D009363:Neoplasm Proteins; D015513:Oncogene Proteins; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger