Open AccessPre-exposure to hydrogen sulfide modulates the innate inflammatory response to organic dust
Author(s) -
Denusha Shrestha,
Sanjana Mahadev Bhat,
Nyzil Massey,
Cristina Santana Maldonado,
Wilson K. Rumbeiha,
Chandrashekhar Charavaryamath
Publication year - 2021
Publication title -
cell and tissue research/cell and tissue research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.64
H-Index - 137
eISSN - 1432-0878
pISSN - 0302-766X
DOI - 10.1007/s00441-020-03333-3
Subject(s) - hydrogen sulfide , inflammation , tlr4 , innate immune system , chemistry , oxidative stress , tlr2 , in vivo , immunology , biology , biochemistry , immune system , sulfur , microbiology and biotechnology , organic chemistry
Animal production units produce and store many contaminants on-site, including organic dust (OD) and hydrogen sulfide (H 2 S). Workers in these settings report various respiratory disease symptoms. Both OD and H 2 S have shown to induce lung inflammation. However, impact of co-exposure to both H 2 S and OD has not been investigated. Therefore, we tested a hypothesis that pre-exposure to H 2 S modulates the innate inflammatory response of the lungs to organic dust. In a mouse model of H 2 S and organic dust extract (ODE) exposure, we assessed lung inflammation quantitatively. We exposed human airway epithelial and monocytic cells to medium or H 2 S alone or H 2 S followed by ODE and measured cell viability, oxidative stress, and other markers of inflammation. Exposure to 10 ppm H 2 S followed by ODE increased the lavage fluid leukocytes. However, exposure to 10 ppm H 2 S alone resulted in changes in tight junction proteins, an increase in mRNA levels of tlr2 and tlr4 as well as ncf1, ncf4, hif1α, and nrf2. H 2 S alone or H 2 S and ODE exposure decreased cell viability and increased reactive nitrogen species production. ODE exposure increased the transcripts of tlr2 and tlr4 in both in vitro and in vivo models, whereas increased nfkbp65 transcripts following exposure to ODE and H 2 S was seen only in in vitro model. H 2 S alone and H 2 S followed by ODE exposure increased the levels of IL-1β. We conclude that pre-exposure to H 2 S modulates lung innate inflammatory response to ODE.