Cholesterol exacerbates Mycoplasma hyopneumoniae-induced apoptosis via stimulating proliferation and adhesion to porcine alveolar macrophages

- Cholesterol levels in porcine sera and lungs are positively correlated with Mycoplasma hyopneumoniae infection.
- Cholesterol exacerbates Mycoplasma hyopneumoniae-induced apoptosis of porcine alveolar macrophages.
- Cholesterol improves Mycoplasma hyopneumoniae proliferation and adherence to porcine alveolar macrophages.

Mycoplasma hyopneumoniae (M. hyo) is the agent of porcine enzootic pneumonia, a disease that causes considerable economic losses in the swine industry. Induction of apoptosis in porcine alveolar macrophages is an important pathogenic mechanism of M. hyo. Cholesterol has been reported to influence cell adherence and cell invasion of Mycoplasma gallisepticum and Mycoplasma fermentans leading to apoptosis, but the role of cholesterol on the apoptotic inducing activity of M. hyo remains unknown. In this study, we found a positive correlation between cholesterol level and M. hyo infection in porcine serum and lung tissue. Cholesterol exacerbated M. hyo-induced apoptosis in porcine alveolar macrophages (PAMs) in a dosage-dependent manner, which was associated with increased hydrogen peroxide (H2O2) and nitric oxide (NO) production, up-regulated TNF-α mRNA expression, and activated caspase-3. The pathogenicity-enhancing effect of cholesterol was related to increased M. hyo proliferation with an up-regulation of M. hyo genes responsible for DNA and protein synthesis, which led to improved M. hyo adherence to PAMs, presumably via increased mRNA expression of adhesin genes. In conclusion, cholesterol promotes the apoptotic effect of M. hyo through stimulating proliferation and enhancing its adherence to PAMs. Hence, the study gives new insights into the role of cholesterol on the PAM - M. hyo interations.