National Institute for Environmental Studies, Tsukuba, Japan
Correspondence to: Ken-ichiro Inoue, MD, Inhalation Toxicology Research Team, and Pathophysiology Research Team, National Institute for Environmental Studies, 16–2 Onogawa, Tsukuba, Japan; e-mail: email@example.com
To the Editor:
We read with great interest the recent in vitro study by Tong and colleagues.1We have some comments. First, the authors implicated the possibility of pentoxifylline as a therapeutic option for pulmonary sarcoidosis. A study2 has described that pentoxifylline has no severe side effects as compared with dexamethasone. However, as Tong et al1 introduced in their discussion, pentoxifylline induces a selective suppression of interleukin-2 and interferon-γ, T-helper type 1-derived cytokines.3T-cells play a central role in cell-mediated immune responses through the production of type 1 cytokines, such as interferon-γ and interleukin-2. It has been reported that the suppression of T-helper type 1 function damages the host response to fungi.4 We should give careful consideration when using the agent, especially its long-term use in clinical stages, because it may lead to mycosis in patients.
In addition, we wonder if dexamethasone could not inhibit lipopolysaccharide-induced interleukin-1β expression in alveolar macrophages in the experiment by Tong et al.1 Glucocorticoids are potent inhibitors of immune response, inflammation, and endotoxic shock. This occurs, at least partly, through an inhibition of the synthesis of proinflammatory cytokines and chemokines.5–7 One of the target enzymes of glucocorticoids inhibition is interleukin-1β. Dexamethasone (10 nmol/L to 10 μmol/L) inhibits interleukin-1 messenger RNA in lipopolysaccharide-stimulated human monocytes in a dose-dependent fashion.8Also, dexamethasone suppresses interleukin-1β gene expression in lipopolysaccharide-stimulated RAW 264.7 cells through the inhibition of the activation of transcription factors related to endotoxin such as nuclear factor-κB and activator protein-1.9 Other mechanisms may be present in lipopolysaccharide-induced interleukin-1 production in alveolar macrophages of patients with sarcoidosis.
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