Effect of ochratoxin A on the intestinal mucosa and mucosa-associated lymphoid tissues in broiler chickens

Abstract

The immunotoxic effect of ochratoxin A (OTA) on the intestinal mucosaassociated lymphoid tissue and its cytotoxic action on the intestinal epithelium were studied in broiler chickens experimentally treated with the toxin. From the 7th day of life, 80 male broiler chickens (Ross 308) were randomly divided into four groups of 20 birds each. The three experimental groups (E1-3) were treated with OTA for 28 days (E1: 50 µg/kg body weight [bw]/day; E2: 20 µg/kg bw/day; E3: 1 µg/kg bw/day) and the fourth group served as control. Histological examination of the intestinal mucosa and immunohistochemical staining for identification of CD4+, CD8+, TCR1 and TCR2 lymphocytes in the duodenum, jejunum and ileocaecal junction were performed, and CD4+/CD8+ and TCR1/TCR2 ratios were calculated. OTA toxicity resulted in decreased body weight gain, poorer feed conversion ratio, lower leukocyte and lymphocyte count, and altered intestinal mucosa architecture. After 14 days of exposure to OTA, immunohistochemistry showed a significant reduction of the lymphocyte population in the intestinal epithelium and the lamina propria. After 28 days of exposure, an increase in the CD4+ and CD8+ values in both the duodenum and jejunum of chickens in Groups E1 and E2 was observed, but the TCR1 and TCR2 lymphocyte counts showed a significant reduction. No significant changes were observed in Group E3. The results indicate that OTA induced a decrease in leukocyte and lymphocyte counts and was cytotoxic to the intestinal epithelium and the mucosa-associated lymphoid tissue, altering the intestinal barrier and increasing susceptibility to various associated diseases.

Selenium Yeast Alleviates Ochratoxin A-Induced Apoptosis and Oxidative Stress via Modulation of the PI3K/AKT and Nrf2/Keap1 Signaling Pathways in the Kidneys of Chickens

“…The experimental period lasted for 21 days. Animal [31], and Se-Y doses were based on those reported by Bakhshalinejad et al [32].…”

Transcriptome Analysis of Ochratoxin A-Induced Apoptosis in Differentiated Caco-2 Cells

“…OTA-induced intestinal damage has been reported in both animals and in vitro intestinal models [22,23]. It has been shown to damage the intestinal epithelium in chickens and rats [24][25][26] and also shows toxicity in intestinal epithelial cells, including a porcine intestinal cell line (IPEC-J2) and human intestinal epithelial lines (HT-29-D4 cells and Caco-2 cells) [20,27,28]. Previously published studies have shown that cell apoptosis is one of the ways by which OTA exerts intestinal toxicity [20,26,29].…”

“…It has been shown to damage the intestinal epithelium in chickens and rats [24][25][26] and also shows toxicity in intestinal epithelial cells, including a porcine intestinal cell line (IPEC-J2) and human intestinal epithelial lines (HT-29-D4 cells and Caco-2 cells) [20,27,28]. Previously published studies have shown that cell apoptosis is one of the ways by which OTA exerts intestinal toxicity [20,26,29]. Wang et al [20] suggested that apoptosis induced by OTA may play a major role in the intestinal toxicity of this mycotoxin, and Bouaziz et al [30] also suggested that OTA causes toxicity through apoptosis.…”

Dietary Factors as Triggers of Low-Grade Chronic Intestinal Inflammation in Poultry

“…OTA also induces oxidative stress that might be the reason for negative findings such as the reduction of villus height: crypt depth ratio in broilers [85]. Solcan et al [86] increased OTA concentrations in the broilers feed and observed modification of the architecture of intestinal epithelia, with a decrease of villus height:crypt depth ratio in the duodenum, necrosis areas, apoptosis, altered glands of lamina propria, and taller enterocytes with big and multiple nuclei and sometimes with no brush border. In the same study, when evaluating the lymphoid associated tissue, TCR1, TCR2, CD4+ and CD8+ intraepithelial lymphocytes in epithelia were reduced and showed death signs as pyknosis and cortical hyperchromatosis.…”