Evaluation of Tumour Necrosis Factor-Alpha and Interleukin-1beta in an Experimental Pyelonephritis Model Induced with Planktonic and Biofilms Cells of Pseudomonas aeruginosa

Urinary tract infections may induce severe inflammation, transient impairment in renal function and scar formation, ranging in severity from acute symptomatic pyelonephritis to chronic pyelonephritis, and have the potential to lead to renal failure and death. In the present study, the relationship b...

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Main Authors: Rahul Mittal, Saroj Sharma, Sanjay Chhibber, Kusum Harjai
Format: Article
Language:English
Published: Wiley 2009-01-01
Series:Canadian Journal of Infectious Diseases and Medical Microbiology
Online Access:http://dx.doi.org/10.1155/2009/810791
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author Rahul Mittal
Saroj Sharma
Sanjay Chhibber
Kusum Harjai
author_facet Rahul Mittal
Saroj Sharma
Sanjay Chhibber
Kusum Harjai
author_sort Rahul Mittal
collection DOAJ
description Urinary tract infections may induce severe inflammation, transient impairment in renal function and scar formation, ranging in severity from acute symptomatic pyelonephritis to chronic pyelonephritis, and have the potential to lead to renal failure and death. In the present study, the relationship between production of tumour necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), neutrophil recruitment, bacterial colonization and tissue damage was investigated using a mouse model of acute ascending pyelonephritis induced with planktonic and biofilm cells of Pseudomonas aeruginosa. Neutrophil influx correlated with rise in TNF-α and IL-1β, indicating an association between these cytokines and neutrophil infiltration. However, biofilm cells of P aeruginosa induced higher levels of TNF-α and IL-1β leading to higher neutrophil infiltration causing tissue damage, assessed in terms of malondialdehyde, lactate dehydrogenase and glutathione content, which may have contributed to bacterial persistence compared with their planktonic counterparts. The results of the present investigation suggest that exaggerated cytokine production during P aeruginosa-induced pyelonephritis causes tissue damage operative through neutrophil recruitment leading to bacterial persistence in host tissues. The findings of the present study may be relevant for the better understanding of disease pathophysiology and for the future developments of preventive strategies against pyelonephritis based on anti-inflammatory intervention.
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spelling doaj-art-388595343f0a4c269a9fbbbdedc4e6692025-02-03T05:49:29ZengWileyCanadian Journal of Infectious Diseases and Medical Microbiology1712-95322009-01-01203e35e4210.1155/2009/810791Evaluation of Tumour Necrosis Factor-Alpha and Interleukin-1beta in an Experimental Pyelonephritis Model Induced with Planktonic and Biofilms Cells of Pseudomonas aeruginosaRahul Mittal0Saroj Sharma1Sanjay Chhibber2Kusum Harjai3Division of Infectious Diseases, Childrens Hospital Los Angeles, Los Angeles, California, USADepartment of Microbiology, Panjab University, Chandigarh, IndiaDepartment of Microbiology, Panjab University, Chandigarh, IndiaDepartment of Microbiology, Panjab University, Chandigarh, IndiaUrinary tract infections may induce severe inflammation, transient impairment in renal function and scar formation, ranging in severity from acute symptomatic pyelonephritis to chronic pyelonephritis, and have the potential to lead to renal failure and death. In the present study, the relationship between production of tumour necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), neutrophil recruitment, bacterial colonization and tissue damage was investigated using a mouse model of acute ascending pyelonephritis induced with planktonic and biofilm cells of Pseudomonas aeruginosa. Neutrophil influx correlated with rise in TNF-α and IL-1β, indicating an association between these cytokines and neutrophil infiltration. However, biofilm cells of P aeruginosa induced higher levels of TNF-α and IL-1β leading to higher neutrophil infiltration causing tissue damage, assessed in terms of malondialdehyde, lactate dehydrogenase and glutathione content, which may have contributed to bacterial persistence compared with their planktonic counterparts. The results of the present investigation suggest that exaggerated cytokine production during P aeruginosa-induced pyelonephritis causes tissue damage operative through neutrophil recruitment leading to bacterial persistence in host tissues. The findings of the present study may be relevant for the better understanding of disease pathophysiology and for the future developments of preventive strategies against pyelonephritis based on anti-inflammatory intervention.http://dx.doi.org/10.1155/2009/810791
spellingShingle Rahul Mittal
Saroj Sharma
Sanjay Chhibber
Kusum Harjai
Evaluation of Tumour Necrosis Factor-Alpha and Interleukin-1beta in an Experimental Pyelonephritis Model Induced with Planktonic and Biofilms Cells of Pseudomonas aeruginosa
Canadian Journal of Infectious Diseases and Medical Microbiology
title Evaluation of Tumour Necrosis Factor-Alpha and Interleukin-1beta in an Experimental Pyelonephritis Model Induced with Planktonic and Biofilms Cells of Pseudomonas aeruginosa
title_full Evaluation of Tumour Necrosis Factor-Alpha and Interleukin-1beta in an Experimental Pyelonephritis Model Induced with Planktonic and Biofilms Cells of Pseudomonas aeruginosa
title_fullStr Evaluation of Tumour Necrosis Factor-Alpha and Interleukin-1beta in an Experimental Pyelonephritis Model Induced with Planktonic and Biofilms Cells of Pseudomonas aeruginosa
title_full_unstemmed Evaluation of Tumour Necrosis Factor-Alpha and Interleukin-1beta in an Experimental Pyelonephritis Model Induced with Planktonic and Biofilms Cells of Pseudomonas aeruginosa
title_short Evaluation of Tumour Necrosis Factor-Alpha and Interleukin-1beta in an Experimental Pyelonephritis Model Induced with Planktonic and Biofilms Cells of Pseudomonas aeruginosa
title_sort evaluation of tumour necrosis factor alpha and interleukin 1beta in an experimental pyelonephritis model induced with planktonic and biofilms cells of pseudomonas aeruginosa
url http://dx.doi.org/10.1155/2009/810791
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