Importance of CCL25 in the attraction of T cells and the role of IL-7 on the signaling pathways in intestinal epithelial cells.
We have demonstrated an inflammatory process triggered by a dietary antigen accompanied with an increase of TNF-α in an experimental model of secondary immunodeficiency. TNF-α regulates the increase of γδ T subpopulation both in lamina propria and in the intestinal intraepithelium, where IL-7 influences γδ T cells development. TECK (CCL25)is important in the attraction and generation of T and B lymphocytes to the small intestine, lamina propria and intraepithelium. In the present study we evaluate CCL25 and IL-7 mRNA levels, by semiquantitative RT-PCR in intestinal epithelial cells. Lower levels of CCL25 mRNA were detected in animals after re-feeding compared to the well-nourished ones (P< 0.05), whereas an increase of 1.5 fold of IL-7 mRNA was registered in the experimental group (P < 0.05).When studying the intestinal epithelial cell distribution of the transcriptional factors NF-kB and Stat3,they were predominantly accumulated in the nucleus of cells isolated from the malnourished group, whereas they remain in the cytosol of the control one. The finding of an apoptosis decrease in intestinal epithelial cells isolated from malnourished animals was in agreement with the increased amount of Bcl-2 found in the mitochondrial fraction of this experimental group. All the above findings may lead us to conclude that we are in the presence of a mechanism by which γδ + T cells are increased in the intestinal villi, through different signaling path ways mediated by CCl25 and IL-7.
Calabrese
Graciela C
GC
Cátedra de Biología Celular, Facultad de Farmacia y Bioquıímica, Universidad de Buenos Aires,Junín 956, Primer Piso, (C1113AAD) Ciudad Autónoma de Buenos Aires, Argentina.  gcalabe@ffyb.uba.ar
Luczak
Erica N
EN
Roux
M Estela
ME
D000818:Animals; D017209:Apoptosis; D019742:Chemokines, CC / Q000235:genetics / Q000378:metabolism*; D002634:Chemotaxis, Leukocyte; D007153:Immunologic Deficiency Syndromes / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D015851:Interleukin-7 / Q000235:genetics / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D008297:Male; D044342:Malnutrition / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism
C575676:Ccl25 protein, rat; D019742:Chemokines, CC; D015851:Interleukin-7; D016328:NF-kappa B; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D016692:Receptors, Antigen, T-Cell, gamma-delta; D050796:STAT3 Transcription Factor; C494088:Stat3 protein, rat