CONICET | Buscador de Institutos y Recursos Humanos

Acoustic stimuli (AS) induces long term severe intestine inflammation in the mouse. Rial Hawila M. R., Bottero E., Roux M.E. andMiranda S. Background: Noiseis a stressful factor that may cause deleterious effects on health. In thisstudy we analyzed the effects of AS exposure on mouse gut. Methods: CBA/J,BALB/c and DBA/2 mice were exposed to a 24 hour AS (300 Hz-70 dB) and dividedinto groups (each one, n=10): 1) mice were killed after AS; 2) mice were killed3 weeks after AS; 3) mice were submitted to AS once a week during a month and thenwere killed. Control animal groups received equal treatment without ASexposition. Sections from small intestine were employed for stainings (H&E,May Grünwald-Giemsa and PAS/Hematoxylin), immunohistochemical (for detecting TNFα, TGF-β ad Ki67) and immunofluorescence studies(for CCL25, IL-17 and IL-22).Results: Group1 displayed fragmented intestinal villi, diminished lamina propria cells, neutrophilsinfiltration and increased number of goblet cells. IL-17 represented the maincytokine, followed by IL-22 and TNF-α with a mild increase of TGF-β. Expression of CCL25 and Ki67 were upregulated.Histological alterations exacerbatedin group 2. IL-17 and leukocyte infiltration were not detected; IL-22expression diminished, TNF-α and TGF-β expression increased moderately. Additionally, many villi zones showed CCL25multilayers expressing Ki67 as epithelial proliferative foci.In group 3 severe histologicalalterations were observed (short and broken villi invaded by crypts, abundantfoci of cell proliferation). TGF-β and IL-22 were moderately expressed and TNFαincreased. IL-17 expression was not detected. Conclusions: AS induced profound inflammationand histological alterations in mouse small intestine suggesting that it couldbe considered a Crohn´s disease animal model.

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