Calpastatin upregulation in Mycoplasma hyorhinis-infected cells is promoted by the mycoplasma lipoproteins via the NF-κB pathway.

摘要: Mycoplasma hyorhinis frequently contaminates cultured cells, with effects on synthetic and metabolic pathways. We demonstrated for the first time that contamination of cells by a strain M. (NDMh) results in increased levels calpastatin (the endogenous inhibitor ubiquitous Ca(2+) -dependent protease calpain). now show upregulation NDMh neuroblastoma SH-SY5Y resides lipoprotein fraction (LPP), via NF-κB transcription pathway. activation requires dissociation cytoplasmic NF-κB/IκB complex followed translocation to nucleus. NDMh-LPP induced RelA subunit nucleus upregulated calpastatin. elevation were prevented when was inhibited either transfection non-phosphorylatable IκB mutant ΔNIκBα, or using PS1145, an kinase (IKK complex). Increased attenuate calpain-related amyloid-β-peptide -toxicity (these are central pathogenesis Alzheimer's Disease). LPP-induced provides example non-inflammatory intracellular proteins, outcome being significant alterations host cell functions. Since level is important control calpain activity, mycoplasmal LPP may be interest treating some pathological processes involving excessive activation.