title: Neutrophil migration stimulates rat intestinal epithelial cell cytokine expression during helminth infection.
abstract: We are interested in understanding the role of epithelial cells during inflammation, and we previously reported that rat small intestinal epithelial cells express interleukin-1beta (IL-1beta) during infection by Trichinella spiralis. We now report that the epithelium also produces the potent neutrophil chemotactic factor, macrophage inflammatory protein-2 (MIP-2), and an IL-1 antagonist: the type II IL-1 receptor. Consequently we investigated the pattern of neutrophil infiltration into the infected intestine, which closely paralleled the epithelial cytokine expression. Speculating that neutrophil infiltration may provoke epithelial cytokine expression, neutrophil migration into the infected gut was reduced by depleting circulating cells through the use of a specific antibody, or by preventing migration through the use of a function-blocking anti-CD18 monoclonal antibody. Either treatment reduced the number of neutrophils recoverable from the small intestinal epithelium and was paralleled by reduced mRNA levels for epithelial cytokines. These results demonstrate that neutrophil infiltration of the small intestinal epithelium contributes to the stimulation of epithelial cell cytokines.
authors.affiliation: Departments of Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada. Andrew.Stadnyk@Dal.Ca
authors.forename: A W
authors.initials: AW
authors.lastname: Stadnyk
authors.forename: C D
authors.initials: CD
authors.lastname: Dollard
authors.forename: A C
authors.initials: AC
authors.lastname: Issekutz
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D018821:CD18 Antigens / Q000276:immunology; D054426:Chemokine CXCL2; D018925:Chemokines / Q000096:biosynthesis* / Q000235:genetics; D004848:Epithelium / Q000378:metabolism / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D007375:Interleukin-1 / Q000096:biosynthesis* / Q000235:genetics; D007411:Intestinal Diseases, Parasitic / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000473:pathology; D007421:Intestine, Small / Q000276:immunology* / Q000473:pathology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D020556:Neutrophil Infiltration / Q000187:drug effects; D009504:Neutrophils / Q000502:physiology*; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D011917:Rats, Inbred Lew; D017472:Receptors, Interleukin-1 / Q000096:biosynthesis* / Q000235:genetics; D053574:Receptors, Interleukin-1 Type II; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017160:Trichinella spiralis / Q000276:immunology*; D014235:Trichinellosis / Q000276:immunology* / Q000473:pathology
chemical_list: D000911:Antibodies, Monoclonal; D018821:CD18 Antigens; D054426:Chemokine CXCL2; D018925:Chemokines; C404915:Cxcl2 protein, mouse; D007375:Interleukin-1; D012333:RNA, Messenger; D017472:Receptors, Interleukin-1; D053574:Receptors, Interleukin-1 Type II