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Published on: April 2, 2014
Imidacloprid induced histomorphological changes and expression of TLR-4 and TNFα in lung
Arif Ahmad Pandit1, Shanti Choudhary1, Ramneek1
1School of Animal Biotechnology, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, Punjab 141 004, India.
Abstract:
The imidacloprid is used worldwide as a pesticide and has been linked with endocrine disturbances and reduced pulmonary function. However, effects of imidacloprid alone or in combination with microbial molecules on lungs are not fully understood. Because the pulmonary effects of interactions of endotoxins with imidacloprid are unknown, we designed a study to investigate that in a mouse model. Mice (N=14) were given imidacloprid orally @ 1/20(th) of LD50 dissolved in corn oil for 30days. After the treatments, six animals from each group were challenged with E. coli lipopolysaccharide (LPS) @ 80μg/animal via intranasal route and remaining animals were challenged with normal saline solution @ 80μl/animal via same route. Imidacloprid in combination with LPS led to significant increase in total cell and neutrophil counts in BAL and peripheral blood. Semi-quantitative histopathology revealed lung injury in imidacloprid treatment group and injury was more marked in animal receiving both imidacloprid and LPS. There was no change (p<0.05) in the expression of TLR-4 and TNF-α both at mRNA and protein levels following exposure to imidacloprid alone or in combination with LPS. The data show that imidacloprid alone or in combination with LPS resulted changes in lung morphology without altering the expression of TLR-4 and TNF-α. Furthermore, pre-treatment with imidacloprid didn't affect response to LPS.
Insights
Imidacloprid pesticide exposure caused lung injury in mice, worsening when combined with bacterial endotoxins (LPS). This lung damage occurred without changes in key inflammatory markers like TLR-4 and TNF-α.
Area of Science:
- Environmental Toxicology
- Pulmonary Medicine
- Immunology
Background:
- Imidacloprid is a widely used pesticide with suspected links to endocrine disruption and reduced lung function.
- The specific pulmonary effects of imidacloprid, especially in combination with microbial molecules like endotoxins, remain poorly understood.
- Investigating these interactions is crucial for understanding pesticide-related respiratory health risks.
Purpose of the Study:
- To investigate the pulmonary effects of imidacloprid alone and in combination with Escherichia coli lipopolysaccharide (LPS) in a mouse model.
- To determine if imidacloprid alters the lung's response to bacterial endotoxins.
- To examine the expression of Toll-like receptor 4 (TLR-4) and Tumor Necrosis Factor-alpha (TNF-α) following these exposures.
Main Methods:
- Mice were orally administered imidacloprid (1/20th LD50) for 30 days.
- Following treatment, mice were intranasally challenged with either E. coli lipopolysaccharide (LPS) or saline.
- Bronchoalveolar lavage (BAL) fluid, peripheral blood, and lung tissues were analyzed for cell counts, histopathology, and gene/protein expression (TLR-4, TNF-α).
Main Results:
- Imidacloprid combined with LPS significantly increased total cell and neutrophil counts in BAL fluid and peripheral blood.
- Histopathological analysis revealed lung injury in the imidacloprid group, which was more severe in mice exposed to both imidacloprid and LPS.
- No significant changes in mRNA or protein levels of TLR-4 and TNF-α were observed in any treatment group.
Conclusions:
- Imidacloprid exposure, alone or with LPS, induces lung morphological changes without altering TLR-4 and TNF-α expression.
- Pre-treatment with imidacloprid did not modulate the inflammatory response to LPS challenge.
- These findings suggest that imidacloprid may cause lung injury through mechanisms independent of TLR-4 and TNF-α pathways.
