Open AccessMultiple exposures to poultry barn air and lipopolysaccharide synergistically increase the pulmonary expression of TLR‐4 and IL‐1β
Author(s) -
Kaur Gaganpreet,
Sethi Ram Saran
Publication year - 2019
Publication title -
journal of occupational health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 59
ISSN - 1348-9585
DOI - 10.1002/1348-9585.12094
Subject(s) - barn , bronchoalveolar lavage , tlr4 , lipopolysaccharide , medicine , histopathology , lung , immunology , real time polymerase chain reaction , respiratory system , andrology , pathology , inflammation , biology , gene , biochemistry , civil engineering , engineering
Objective Poultry farm workers are exposed to barn air and suffer from various respiratory disorders. Due to frequent prevalence of endotoxin in the farm settings workers can get co‐exposed to barn air and endotoxin. The study was aimed to explore the pulmonary damage following long‐term multiple exposures to poultry barn air with or without endotoxin. Methods We studied the pulmonary expression of Toll‐like receptor 4 (TLR4) and Interleukin‐1β (IL‐1β) by exposing Swiss albino mice to poultry barn air for 6 days (Monday‐Saturday) in a week for 5 and 10 weeks. At the end of exposure, animals were challenged with lipopolysaccharide (LPS) or normal saline solution @80 μg/mouse intranasally. Histopathology, bronchoalveolar lavage (BAL) fluid and blood analysis were used to characterize lung damage. mRNA and protein expression of TLR4 and IL‐1β were evaluated using quantitative polymerase chain reaction (qPCR) and immunohistochemistry, respectively. Results Histopathology along with TLC and DLC of blood and BAL fluid revealed lung damage following multiple exposures and damage was severe in combination with LPS. Exposures altered mRNA and protein expression of TLR‐4 and IL‐1β and the expression was more marked following 30 days of exposure. Further LPS co‐challenge showed a synergistic effect on the expression of TLR4 and IL‐1β. Conclusions The data suggest that long‐term exposures with or without LPS caused lung damage and altered the pulmonary expression of TLR4 and IL‐1β.