Role of Th2 cytokines on the onset of asthma induced by meta‐xylene in mice

Abstract

meta‐Xylene (m‐xylene) is one of three isomers of xylene, which is widely used as a solvent and detergent in various industries and medical technology. Exposure to volatile organic compounds, such as m‐xylene, causes pulmonary inflammation and airway inflammation, thereby contributing to the onset of asthma. Exposure to m‐xylene increases acute wheezing and intensity of asthma symptom. However, the mechanism of the onset of asthma by m‐xylene has not been studied yet. C57BL/6 mice were sensitized and challenged by m‐xylene at 100 or 300 mg/kg. The mice were then sacrificed after the last challenge. Exposure to m‐xylene increased the total number of inflammatory cells and the production of interleukin (IL)‐4, IL‐5, IL‐13, and immunoglobulin E related to the Th2 immune response. In contrast, the production of interferon‐γ related to the Th1 immune response was decreased. In addition, the airway resistance increased according to the airway hyper‐responsiveness measurements. Finally, a histological analysis revealed infiltration of inflammatory cells, mucus production, and lung fibrosis. These results suggest that m‐xylene is a potential risk factor for asthma and the onset of asthma is caused by TH2 cytokines.

The urinary metabolites of volatile organic compounds and asthma in young children: NHANES 2011–2018

“…Additionally, prolonged exposure to acrolein leads to increased mast cell toxicity, increased release of allergenic media, the key components of asthma, and activation of calcium-dependent degranulation pathways [ 27 ]. Xylene is the parent compound of 2MHA, which can further induce type 2 helper t cells to participate in the immune response by inducing mast cells and other immune cells to secrete IL4, IL-5, IL-13 and other cytokines [ 28 ]. In turn, type 2 helper t cells are the main cells that cause type 1 hypersensitivity reactions such as asthma [ 29 ].…”

The urinary metabolites of volatile organic compounds and asthma in young children: NHANES 2011-2018

“…Additionally, acrolein exposure leads to high levels of mast cell toxicity and activation of calcium-dependent degranulation pathways in mast cells, while mast cell-derived histamine, leukotrienes and cytokines are key components of allergic in ammation and asthma [23]. Xylene, the parent compound of 2MHA, induces a type 2 helper T-cell (Th2) immune response by increasing the production of IL-4, IL-5, IL-13 and total IgE [24]. Th2 cell dominance is consistent with immune response patterns found in type 1 hypersensitivity disorders such as asthma [25].…”

Blimp1 suppressed CD4+ T cells‐induced activation of fibroblast‐like synoviocytes by upregulating IL‐10 via the rho pathway

“…Synovial inflammation is a hallmark of RA and consists of a mass of activated CD4 + T cells, showing that CD4 + T cell homeostasis exerts a crucial effect in the process of RA 15,16 . Naive CD4 + T cells can differentiate into different T cell subsets (Th1, Th2, Th17 and Treg) 17,18 . Th1 and Th17 promote synovial inflammation and osteoclast formation, which is the culprit leading to the destruction of bone and cartilage 19 .…”

“…15,16 Naive CD4 + T cells can differentiate into different T cell subsets (Th1, Th2, Th17 and Treg). 17,18 Th1 and Th17 promote synovial inflammation and osteoclast formation, which is the culprit leading to the destruction of bone and cartilage. 19 Tregs are a heterogeneous population of thymic and extrathymic origins with distinct immunosuppressive functions.…”