LncRNA MEG3 Regulates Glaesserella parasuis-Induced Apoptosis of Porcine Alveolar Macrophages via Regulating...

Area of Science:

• Veterinary Microbiology
• Immunology
• Molecular Biology

Background:

• Glaesserella parasuis (G. parasuis) causes significant disease in pigs, including respiratory illness and systemic infections.
• Alveolar macrophages are crucial for pulmonary innate immunity, and their dysregulated apoptosis contributes to G. parasuis pathogenesis.
• The role of long non-coding RNA maternally expressed gene 3 (MEG3) in G. parasuis infection is not fully understood.

Purpose of the Study:

• To investigate the role of MEG3 in G. parasuis-induced apoptosis of porcine alveolar macrophages (3D4/21 cell line).
• To elucidate the molecular mechanism by which MEG3 influences G. parasuis pathogenesis.

Main Methods:

• Overexpression of MEG3 in 3D4/21 cells infected with G. parasuis.
• Analysis of apoptosis-related proteins, including caspase-8 (CASP8) and caspase-3 (CASP3).
• Investigation of the interaction between MEG3, ssc-miR-135, and CASP8 using competing endogenous RNA (ceRNA) mechanisms.
• Functional rescue experiments with ssc-miR-135 mimics and CASP8 siRNA.

Main Results:

• MEG3 overexpression enhanced G. parasuis-induced apoptosis in 3D4/21 cells.
• MEG3 upregulated the expression of key extrinsic pathway proteins, CASP8 and CASP3.
• MEG3 acted as a ceRNA by sponging ssc-miR-135, thereby relieving its inhibition on CASP8.
• Rescue experiments confirmed that MEG3's pro-apoptotic effect was mediated by the ssc-miR-135/CASP8 axis.

Conclusions:

• MEG3 promotes G. parasuis-induced apoptosis in porcine alveolar macrophages by competitively binding ssc-miR-135 and upregulating CASP8.
• This study elucidates a novel molecular mechanism contributing to G. parasuis pathogenicity.
• Findings provide new insights into the host-pathogen interactions during G. parasuis infection.