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Lipopolysaccharide is a commonly used inflammation promoter in several environmental and occupational air pollutant conditions that are known to cause airway inflammation. DBA1/J mice were assigned to either sham, CIA, LPS, or CIA + LPS for 5 weeks by combining repeated LPS inhalation exposures with the collagen induced arthritis model. Bone loss in CIA and CIA+LPS has been documented in CIA and CIA + LPS, but not in LPS alone. Increased infiltrates of activated CD11b+ macrophages and transitioning CD11c+CD11b+ monocyte-macrophage populations with CIA + LPS, potentially signaling a change to pro-fibrotic processes. With CIA + LPS with IL-33 lung staining triggered by LPS, lung homogenates' concentrations were boosted with IL-33 concentrations in lung homogenates, which was triggered by LPS. In lung tissues from patients with RA-associated lung disease patients with RA-associated lung disease compared to controls, there was also a significant rise in IL-33 expression in lung tissues. Following airborne biohazard exposures elevated in LPS, patients with RA may be more likely to experience interstitial lung disease. These findings show that patients with RA may be more likely to experience interstitial lung disease.
Source link: https://doi.org/10.1016/j.intimp.2021.108069
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