Abstract
Repeated exposure to fungi-contaminated dust can lead to multiple adverse effects on the lung, such as hypersensitivity pneumonitis, granuloma even irreversible fibrosis. 1,3-β-glucan, a major cell wall component of fungi, is considered as its exposure biomarker. Existing studies showed that a series of Th responses were involved in 1,3-β-glucan induced hypersensitivity pneumonitis, in which macrophages, Treg, and IL-10 producing B cells were reported to participate. The reciprocal interaction among those critical immune cells in 1,3-β-glucan induced inflammation was not investigated yet. To clarify the regulatory mechanism of IL-10 producing B cells on Th and Treg, the current study set up a primary cell co-culture system. The anti-CD22 antibody was injected intraperitoneally to generate IL-10 producing B cells deficiency mouse model. Cells were isolated and purified from C57BL∖6 mice in different groups. Flow cytometry was used to check the phenotype of different cell subtypes. CBA assay and real-time PCR were used to examine the levels of multiple cytokines. Our results indicated that IL-10 producing B cells could modulate the 1,3-β-glucan induced inflammatory response. The modulation of IL-10 producing B cells on Th response after 1,3-β-glucan treatment was cell contact independent. What's more, the modulation pattern of IL-10 producing B cells might be impaired without Treg response. IL-10-producing B cells regulated 1,3-β-glucan induced Th responses in co-ordination with Treg cells.
Highlights
The Inhalation of the fungal or bacteria polluted organic dust could induce various inflammatory disease, such as hypersensitivity pneumonitis (HP)
Our results indicated that IL-10 producing B cells were involved in modulating 1,3-β-glucan induced inflammatory response
Our results showed that IL-10-producing B cells were involved in modulating the inflammatory response after 1,3-β-glucan treatment in vitro
Summary
The Inhalation of the fungal or bacteria polluted organic dust could induce various inflammatory disease, such as hypersensitivity pneumonitis (HP). The gradually increased morbidity of those organic dust-induced disease was related to its wildly existence in living environment, and because more and more occupational environments were at risk of organic dust exposure. Some previously ignored occupations took risk to organic dust exposure Study showed that both the fungal load and the bacteria load in air in veterinary environment exceeded the WHO limit [7]. Repeated exposure to fungi contaminated dust can lead to multiple adverse effect on lung, such as hypersensitivity pneumonitis, granuloma even irreversible fibrosis. Existing studies showed that series of Th response were involved in 1,3-β-glucan induced hypersensitivity pneumonitis, in which macrophages, regulatory T cells (Treg) and IL-10 producing B cells were reported to participate. The reciprocal interaction among those critical immune cells in 1,3-β-glucan induced inflammation were not investigated yet
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