Chronic exposure to indoxacarb and pulmonary expression of toll-like receptor-9 in mice

Kaur, Simranpreet; Mukhopadhyay, Chandra Sekhar; Sethi, R. S.

doi:10.14202/vetworld.2016.1282-1286

Cited by 10 publications

(5 citation statements)

References 36 publications

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“…Microscopic investigation of the lung tissue from INDOX-administered animals showed a proliferation in fibrous tissue bundles around lung capillaries and interstitial tissues associated with inflammatory cells. Our histopathology data agreed with the findings of Kaur et al (2016) who reported that exposure to 2-mg INDOXinduced peribronchial infiltration of inflammatory cells and thickening of alveolar septa. Also, Liu et al (2016) showed considerable inflammatory cell infiltration damage and thickening in the alveolar walls in the lung sections from PQ-exposed rats.…”

Section: Discussionsupporting

confidence: 92%

“…In the present setup, we demonstrated severe immunopositive COX-2 expression in bronchial epithelium regions of INDOX-administered rat lungs when compared with control animals. These findings correlated with those of Yeh et al (2006) who concluded that PQ-exposure upregulated COX-2 expression and hypothesized that INDOX, by disturbing the antioxidant status, increased pro-inflammatory factors, such as NO, which in turn led to lung cell inflammation ( Kaur et al 2016). Our findings supported the hypothesis that significant positive COX-2 expression in INDOX-administered rat lungs confirmed that inflammation was associated with histopathological, inflammatory, and biochemical changes.…”

Section: Discussionsupporting

confidence: 90%

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The targeted delivery of chitosan nanoparticles to treat indoxacarb: induced lung fibrosis in rats

et al. 2022

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Background This study evaluated the effects of chitosan nanoparticles (Ch-NPs) on indoxacarb (INDOX)-induced pulmonary fibrosis in in vivo and in vitro models. In in vivo studies, 40 male albino rats were randomly divided into four groups (10 rats/group): Group 1, normal control; Group 2, INDOX (600 mg/kg b.w.); Group 3, Ch-NPs (2 mg/kg b.w.); and Group 4, Ch-NPs + INDOX. Characterization of Ch-NPs was done measuring dynamic light scattering, zeta potential, Fourier-transform infrared spectroscopy, transmission electron microscopy, and antioxidant activity studies after various Ch-NPs treatments. From in vitro studies, the impact of Ch-NPs on A549 lung carcinoma cell proliferation was also examined. Results Our data indicated that INDOX provoked considerable lung damage as indicated by decreased antioxidant enzyme levels of superoxide dismutase and glutathione peroxidase, increased production of nitric oxide and malondialdehyde serum levels, elevated myeloperoxidase activity, increased hydroxyproline and cytokeratin-19 serum levels, and significantly upregulated matrix metallopeptidase-9 and microRNA-101 gene expression levels when compared with controls. Furthermore, histopathological and immunohistochemical investigations of cyclooxygenase-2 in the lung tissue revealed marked inflammation, severe fibrosis, and neutrophil infiltration. Critically, Ch-NPs treatment significantly reversed INDOX-induced changes in lung biochemical, histopathological, and immunohistochemical outcomes. Conclusion Therefore, Ch-NPs may function as potential therapeutic drugs for lung fibrosis owing to their antioxidant, anti-inflammatory, and antifibrotic activities with neutrophil infiltration.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 90%

The targeted delivery of chitosan nanoparticles to treat indoxacarb: induced lung fibrosis in rats

et al. 2022

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“…Herbicide 2,4-D had been previously reported to cause lung injury [ 46 ]. Our previous work also showed long term dietary exposure to pesticide such as fipronil [ 17 , 47 ], ethion [ 20 ], lindane [ 19 ], imidacloprid [ 16 ] and indoxacarb [ 48 ] cause lung injury. In addition, similar to observations made with other pesticides [ 16 , 49 , 50 ], there was increase in blood TLC, neutrophils and lymphocytosis with the high and low dose without LPS to indicate systemic immune response.…”

Section: Discussionmentioning

confidence: 99%

Exposures to 2,4-Dichlorophenoxyacetic acid with or without endotoxin upregulate small cell lung cancer pathway

Kaur

Kumar

Singh

et al. 2021

J Occup Med Toxicol

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Background Pesticide residues in food and environment along with airborne contaminants such as endotoxins pose health risk. Although herbicide 2,4-Dichlorophenoxyacetic acid (2,4-D) has been associated with increased risk of lung cancers such as small cell lung cancer (SCLC) among agricultural workers, there are no data on the SCLC signaling pathway upon 2,4-D exposure without LPS or in combination with endotoxin. Methods We exposed Swiss albino mice (N = 48) orally to high (9.58 mg kg− 1) and low (5.12 mg kg− 1) dosages of 2,4-D dissolved in corn oil for 90 days followed by E. coli lipopolysaccharide (LPS) or normal saline solution (80 μl/animal). Lung samples and broncho-alveolar fluid (BALF) were subjected to Total histological score (THS) and total leucocyte count (TLC) and differential leucocytes count (DLC) analyses, respectively. We used microarray and bioinformatics tools for transcriptomic analyses and differentially expressed genes were analyzed to predict the top canonical pathways followed by validation of selected genes by qRT-PCR and immunohistochemistry. Results Total histological score (THS) along with BALF analyses showed lung inflammation following long term dietary exposure to high or low doses of 2,4-D individually or in combination with LPS. Microarray analysis revealed exposure to high dose of 2,4-D without or with LPS upregulated 2178 and 2142 and downregulated 1965 and 1719 genes, respectively (p < 0.05; minimum cut off 1.5 log fold change). The low dose without or with LPS upregulated 2133 and 2054 and downregulated 1838 and 1625 genes, respectively. Bioinformatics analysis showed SCLC as topmost dysregulated pathway along with differential expression of Itgb1, NF-κB1, p53, Cdk6 and Apaf1. Immunohistological and quantitative real time PCR (qRT-PCR) analyses also supported the transcriptomic data. Conclusions Taken together, the data show exposures to high and low dose of 2,4-D with/without LPS induced lung inflammation and altered pulmonary transcriptome profile with the involvement of the SCLC pathway. The data from the study provide the insights of the potential damage on lungs caused by 2,4-D and help to better understand the mechanism of this complex relation.

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“…Herbicide 2,4-D had been previously reported to cause lung injury [37]. Our previous work also showed long term dietary exposure to pesticide such as fipronil [7,38], ethion [10], lindane [9], imidacloprid [6] and indoxacarb [39] cause lung injury. In addition, similar to observations made with other pesticides [6,40,41], there was increase in blood TLC, neutrophils and lymphocytosis with the high dose alone Interestingly, integrin β1 promotes cell adhesion to the extracellular matrix and is associated with highly invasive and metastatic behaviour in SCLC [18].…”

Section: Discussionmentioning

confidence: 67%

Exposures to 2,4-Dichlorophenoxyacetic Acid With or Without Endotoxin Upregulate Small Cell Lung Cancer Pathway

Kaur

Kumar

Singh

et al. 2020

Preprint

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Background: Pesticide residues in food and environment along with airborne contaminants such as endotoxins pose health risk. Although herbicide 2,4-Dichlorophenoxyacetic acid (2,4-D) has been associated with increased risk of lung cancers such as small cell lung cancer (SCLC) among agricultural workers, there are no data on the SCLC signaling pathway upon 2,4-D exposure alone or in combination with endotoxin. Methods: We exposed Swiss albino mice (N=48) orally to high (9.58 mg kg -1 ) and low (5.12 mg kg -1 ) dosages of 2,4-D dissolved in corn oil for 90 days followed by E. coli lipopolysaccharide (LPS) or normal saline solution (80µl/animal. Lung samples and broncho-alveolar fluid (BALF) were subjected to Total histological score (THS) and TLC and DLC analyses, respectively. We used microarray and bioinformatics tools for transcriptomic analyses and differentially expressed genes were analyzed to predict the top canonical pathways followed by validation of selected genes qPCR and immunohistochemistry. Results: Total histological score (THS) along with broncho-alveolar fluid (BALF) analyses showed lung inflammation following long term dietary exposure to high or low doses of 2,4-D individually or in combination with LPS. Microarray analysis revealed exposure to high dose of 2,4-D alone or with endotoxin upregulated 2178 and 2142 and downregulated 1965 and 1719 genes, respectively (p<0.05; minimum cut off 1.5 log fold change). The low dose alone or with LPS upregulated 2133 and 2054 and downregulated 1838 and 1625 genes, respectively. Bioinformatics analysis showed SCLC as topmost dysregulated pathway along with differential expression of Itgb1, NF-kB1, p53, Cdk6 and Apaf1. Immunohistological and qPCR analyses also supported the transcriptomic data. Conclusions: Taken together, the data show exposures to high and low dose of 2,4-D with/without LPS induced lung inflammation and altered pulmonary transcriptome profile with the involvement of the SCLC pathway. The data from the study provides the insights of the potential damage on lungs caused by 2,4-D and endotoxin interaction and helps to better understand the mechanism of this complex relation.

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Chronic exposure to indoxacarb and pulmonary expression of toll-like receptor-9 in mice

Cited by 10 publications

References 36 publications

The targeted delivery of chitosan nanoparticles to treat indoxacarb: induced lung fibrosis in rats

The targeted delivery of chitosan nanoparticles to treat indoxacarb: induced lung fibrosis in rats

Exposures to 2,4-Dichlorophenoxyacetic acid with or without endotoxin upregulate small cell lung cancer pathway

Exposures to 2,4-Dichlorophenoxyacetic Acid With or Without Endotoxin Upregulate Small Cell Lung Cancer Pathway

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