The multidrug resistance gene product,
P-glycoprotein, may act as a defense mechanism against natural and man-made environmental toxins. Like mammals, chickens show high levels of
P-glycoprotein expression in the liver, small intestine, and kidney. Expression of
P-glycoprotein rapidly increased with age in the liver and kidney reaching a plateau by 2 and 4 days of age, respectively; however, expression of
P-glycoprotein in the duodenum did not significantly change with age. Addition of dietary
antibiotics (
monensin,
bacitracin), as models for dietary toxins, altered
P-glycoprotein expression.
Monensin increased
P-glycoprotein expression in the liver and duodenum.
Bacitracin reduced
P-glycoprotein expression by 45% in the liver, but did not alter expression in the duodenum.
Intraperitoneal injection of E. coli
lipopolysaccharide, a model for acute
inflammation, rapidly increased expression of Pgp
protein in the liver ( approximately 2-fold). Expression then declines to pre-induction levels by 24 h. Similar responses were observed in the spleen and kidney but not the duodenum. These results confirm the presence of an avian
P-glycoprotein homologue and suggest that dietary constituents regulate the expression of
P-glycoprotein. Changes in
P-glycoprotein expression may represent an important physiological response to foods containing toxins and an important component of the acute phase immune response.