Mycoplasma gallisepticum (MG) is dependent on its host for many nutrients due to the loss of many important metabolic pathways.
Ceramide is a
sphingolipid that regulates multiple cellular processes in eukaryotic cell. Several studies highlighted the crucial role of
ceramide on the pathogenesis of various pathogens. This study aimed to determine whether
ceramide plays a crucial role in the pathogenesis of MG. Based on an MG
infection model in DF-1 cells, the results revealed that MG
infection induced
ceramide accumulation in DF-1 cells. Inhibiting the de novo synthesis of
ceramide significantly inhibited MG proliferation and inflammatory injury caused by MG in DF-1 cells. Meanwhile, MG
infection led to endoplasmic reticulum stress, and pharmacologic inhibition of endoplasmic reticulum stress prevented
ceramide accumulation and MG proliferation in DF-1 cells, alleviating the inflammatory injury caused by MG. In addition, MG
infection significantly promoted expression level of
stromal interaction molecule 1 (STIM1), thus induced
calcium overload and oxidative stress. Furthermore, inhibition of STIM1 expression partially restored
calcium homeostasis and mitigated oxidative stress, thus alleviated endoplasmic reticulum stress. Importantly, the inflammatory injury caused by MG were partially ameliorated by
baicalin treatment (20 µg/mL) through downregulating STIM1 expression. In summary, these results suggests that
ceramide accumulation through the de novo pathway plays an important role to promote MG proliferation and
baicalin can alleviate MG
infection induced inflammatory injury via regulating STIM1-related oxidative stress, endoplasmic reticulum stress and
ceramide accumulation in DF-1 cells.