Contribution of free radicals to Pseudomonas aeruginosa induced acute pyelonephritis

Abstract

Pyelonephritis induces an inflammatory process in the renal parenchyma, which may occur as a result of excessive reactive nitrogen intermediates (RNI) and reactive oxygen species (ROS) and/or impaired antioxidant capacity. In the present investigation, contribution of free radicals to the development of acute pyelonephritis induced by planktonic and biofilm cells of Pseudomonas aeruginosa was studied. Increase in production of RNI and ROS in urine, bladder and renal tissue following infection with P. aeruginosa was observed which correlated with bacterial load, neutrophil recruitment and malondialdehyde (MDA). Evaluation of the data revealed that excessive production of free radicals causes tissue damage leading to bacterial persistence in host's tissues. Treatment of mice with N-acetylcysteine (NAC), a potent antioxidant, lead to significant amelioration of oxidative stress and subsequent decrease in bacterial titer, neutrophil influx, MDA as well as tissue pathology highlighting important role of free radicals in P. aeruginosa induced pyelonephritis. Results of the present study bring out that production of RNI and ROS contributes to the pathophysiology of pyelonephritis. These findings may be relevant for the better understanding of host–parasite interactions and may be of clinical importance in the development of preventive intervention against P. aeruginosa induced pyelonephritis.