Mycoplasma gallisepticum escapes the host immune response via gga-miR-365-3p/SOCS5/STATs axis
Yingjie Wang1, Yun Han1, Lulu Wang1
1Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction, Ministry of Education, Huazhong Agricultural University, Hubei, 430070, Wuhan, China.
Abstract:
A disruption in the expression of gga-miR-365-3p was confirmed in the Mycoplasma gallisepticum (MG)-infected Chicken primary alveolar type II epithelial (CP-II) cells based on previous sequencing results, but the role it plays in the infection was unclear. In the present study, we demonstrate that MG evaded cellular host immunity via a gga-miR-365-3p/SOCS5-JAK/STATs negative feedback loop. Specifically, we found that at the initial stage of MG infection in cells, gga-miR-365-3p was rapidly increased and activated the JAK/STAT signaling pathway by inhibiting SOCS5, which induced the secretion of inflammatory factors and triggered immune response against MG infection. Over time, though, the infection progressed, MG gradually destroyed the immune defences of CP-II cells. In late stages of infection, MG escaped host immunity by reducing intracellular gga-miR-365-3p and inhibiting the JAK/STAT pathway to suppress the secretion of inflammatory factors and promote MG adhesion or invasion. These results revealed the game between MG and host cell interactions, providing a new perspective to gain insight into the pathogenic mechanisms of MG or other pathogens. Meanwhile, they also contributed to novel thoughts on the prevention and control of MG and other pathogenic infections, shedding light on the immune modulating response triggered by pathogen invasion and their molecular targeting.
Insights
Mycoplasma gallisepticum (MG) infection in chickens involves a gga-miR-365-3p/SOCS5-JAK/STATs feedback loop. MG initially triggers immunity but later suppresses it by reducing gga-miR-365-3p to evade host defenses.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Mycoplasma gallisepticum (MG) infection disrupts gga-miR-365-3p expression in chicken cells.
- The precise role of gga-miR-365-3p in MG pathogenesis remained unclear.
Purpose of the Study:
- To elucidate the function of gga-miR-365-3p during MG infection.
- To investigate the molecular mechanisms by which MG evades host immunity.
Main Methods:
- Analysis of gga-miR-365-3p expression levels in chicken primary alveolar type II epithelial (CP-II) cells at different stages of MG infection.
- Investigation of the gga-miR-365-3p/SOCS5-JAK/STATs signaling pathway.
- Assessment of inflammatory factor secretion and immune response activation.
Main Results:
- Early MG infection rapidly increases gga-miR-365-3p, inhibiting SOCS5 and activating the JAK/STAT pathway, leading to inflammation.
- Late MG infection reduces gga-miR-365-3p, suppressing the JAK/STAT pathway and inflammatory response.
- MG utilizes this feedback loop to evade host immunity, promoting its adhesion and invasion.
Conclusions:
- MG employs a gga-miR-365-3p/SOCS5-JAK/STATs negative feedback loop to manipulate host immunity.
- Understanding this interaction provides insights into MG pathogenesis and potential therapeutic targets.
- This study offers novel strategies for controlling MG and other pathogen infections.


