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.

Veterinary Research
|December 5, 2022
PubMed

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.