Pre-exposure to hydrogen sulfide modulates the innate inflammatory response to organic dust.
Pre-exposure to hydrogen sulfide modulates the innate inflammatory response to organic dust.
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DOI：
10.1007/s00441-020-03333-3
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发表时间：
2021-04
影响因子：
3.6
通讯作者：
Charavaryamath C
中科院分区：
文献类型：
--
作者：
Shrestha D;Bhat SM;Massey N;Santana Maldonado C;Rumbeiha WK;Charavaryamath C
动物生产单位在现场产生和储存许多污染物，包括有机粉尘（OD）和硫化氢（H2S）。在这些环境中工作的工人报告了各种呼吸道疾病症状。OD和H2S都显示出诱导肺部炎症。然而，尚未研究同时暴露于H2S和OD的影响。因此，我们测试了一个假设，即预先暴露于H2S调节肺部对有机粉尘的先天性炎症反应。在H2S和有机粉尘提取物（ODE）暴露的小鼠模型中，我们定量评估了肺部炎症。我们将人气道上皮细胞和单核细胞暴露于培养基或H2S单独或H2S随后ODE，并测量细胞活力、氧化应激和其他炎症标志物。暴露于10 ppm H2S，然后ODE增加灌洗液白细胞。然而，单独暴露于10 ppm H2S导致紧密连接蛋白的变化，tlr 2和tlr 4以及ncf 1、ncf 4、hif 1 α和nrf 2的mRNA水平增加。H2S单独或H2S和ODE暴露降低细胞活力和增加活性氮物质的产生。在体外和体内模型中，ODE暴露均增加了tlr 2和tlr 4的转录，而仅在体外模型中观察到ODE和H2S暴露后nfkbp 65转录的增加。单独H2S和H2S + ODE暴露可增加IL-1β水平。我们的结论是，预先暴露于H2S调节肺先天炎症反应ODE。
Animal production units produce and store many contaminants on-site, including organic dust (OD) and hydrogen sulfide (H2S). Workers in these settings report various respiratory disease symptoms. Both OD and H2S have shown to induce lung inflammation. However, impact of co-exposure to both H2S and OD has not been investigated. Therefore, we tested a hypothesis that pre-exposure to H2S modulates the innate inflammatory response of the lungs to organic dust. In a mouse model of H2S and organic dust extract (ODE) exposure, we assessed lung inflammation quantitatively. We exposed human airway epithelial and monocytic cells to medium or H2S alone or H2S followed by ODE and measured cell viability, oxidative stress, and other markers of inflammation. Exposure to 10 ppm H2S followed by ODE increased the lavage fluid leukocytes. However, exposure to 10 ppm H2S 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. H2S alone or H2S and ODE exposure decreased cell viability and increased reactive nitrogen species production. ODE exposure increased the transcripts of tlr2and tlr4 in both in vitro and in vivo models, whereas increased nfkbp65 transcripts following exposure to ODE and H2S was seen only in in vitro model. H2S alone and H2S followed by ODE exposure increased the levels of IL-1β. We conclude that pre-exposure to H2S modulates lung innate inflammatory response to ODE.
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影响因子：
5.2
作者：
Anantharam P;Whitley EM;Mahama B;Kim DS;Imerman PM;Shao D;Langley MR;Kanthasamy A;Rumbeiha WK
通讯作者：
Rumbeiha WK
影响因子：
4.7
作者：
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通讯作者：
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影响因子：
4.6
作者：
Jiang J;Chan A;Ali S;Saha A;Haushalter KJ;Lam WL;Glasheen M;Parker J;Brenner M;Mahon SB;Patel HH;Ambasudhan R;Lipton SA;Pilz RB;Boss GR
通讯作者：
Boss GR
影响因子：
--
作者：
Giuffrè A;Vicente JB
通讯作者：
Vicente JB
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影响因子：
3.6
作者：
Che J;Yue D;Zhang B;Zhang H;Huo Y;Gao L;Zhen H;Yang Y;Cao B
通讯作者：
Cao B