gga-miR-142-3p negatively regulates Mycoplasma gallisepticum (HS strain)-induced inflammatory cytokine production via the NF-κB and MAPK signaling by targeting TAB2

Luo

et al. 2022

J. Agric. Food Chem.

Self Cite

Mycoplasma gallisepticum (MG) is the primary pathogen of chronic respiratory diseases (CRDs) in chickens. In poultry production, antibiotics are mostly used to prevent and control MG infection, but the drug resistance and residue problems caused by them cannot be ignored. Glycyrrhizic acid (GA) is derived from licorice, a herb traditionally used to treat various respiratory diseases. Our study results showed that GA significantly inhibited the mRNA and protein expression of pMGA1.2 and GapA in vitro and in vivo. Furthermore, the network pharmacology study revealed that GA most probably resisted MG infection through the MAPK signaling pathway. Our results demonstrated that GA inhibited MG-induced expression of MMP2/MMP9 and inflammatory factors through the p38 and JUN signaling pathways, but not the ERK pathway in vitro. Besides, histopathological sections showed that GA treatment obviously attenuated tracheal and lung damage caused by MG invasion. In conclusion, GA can inhibit MG-triggered inflammation and apoptosis by suppressing the expression of MMP2/MMP9 through the JNK and p38 pathways and inhibit the expression of virulence genes to resist MG. Our results suggest that GA might serve as one of the antibiotic alternatives to prevent MG infection.

Section: ■ Discussionmentioning

confidence: 82%

Glycyrrhizic Acid against Mycoplasma gallisepticum-Induced Inflammation and Apoptosis Through Suppressing the MAPK Pathway in Chickens

Luo

et al. 2022

J. Agric. Food Chem.

Self Cite

“…Host miRNAs affect the replication of pathogenic microorganisms and these microorganisms develop highly complex mechanisms to evade the host immune response. Gga-miR-142-3p, which mainly suppresses the expression of pro-inflammatory cytokines (such as TNF-α, IL-1 and IL-6), influences the cell cycle and activates signaling pathways, thereby influencing M. gallisepticum infection [ 99 ]. FOXO3 belongs to the O subclass of the forkhead family of transcription factors and plays a crucial role in cell proliferation and apoptosis [ 100 ].…”

Section: Escape From Innate Immune Responsementioning

confidence: 99%

Immune Evasion of Mycoplasma gallisepticum: An Overview

Liu,

Wang,

Zheng

2024

IJMS

Mycoplasma gallisepticum is one of the smallest self-replicating organisms. It causes chronic respiratory disease, leading to significant economic losses in poultry industry. Following M. gallisepticum invasion, the pathogen can persist in the host owing to its immune evasion, resulting in long-term chronic infection. The strategies of immune evasion by mycoplasmas are very complex and recent research has unraveled these sophisticated mechanisms. The antigens of M. gallisepticum exhibit high-frequency changes in size and expression cycle, allowing them to evade the activation of the host humoral immune response. M. gallisepticum can invade non-phagocytic chicken cells and also regulate microRNAs to modulate cell proliferation, inflammation, and apoptosis in tracheal epithelial cells during the disease process. M. gallisepticum has been shown to transiently activate the inflammatory response and then inhibit it by suppressing key inflammatory mediators, avoiding being cleared. The regulation and activation of immune cells are important for host response against mycoplasma infection. However, M. gallisepticum has been shown to interfere with the functions of macrophages and lymphocytes, compromising their defense capabilities. In addition, the pathogen can cause immunological damage to organs by inducing an inflammatory response, cell apoptosis, and oxidative stress, leading to immunosuppression in the host. This review comprehensively summarizes these evasion tactics employed by M. gallisepticum, providing valuable insights into better prevention and control of mycoplasma infection.

“…Mycoplasma gallisepticum (MG), an avian pathogen, is known to induce chronic respiratory disease in chickens, causing considerable economic losses to the poultry industry [ 1 – 3 ]. Current studies have demonstrated that MG adheres to the host respiratory mucosa through its membrane proteins (mainly GapA, PvpA, CrmA, pMGA1.2 and MGC2/3), while attenuated strains lacking adhesion proteins are unable to bind to host cell receptors to establish infection [ 4 – 8 ].…”

Section: Introductionmentioning

confidence: 99%

Mycoplasma gallisepticum escapes the host immune response via gga-miR-365-3p/SOCS5/STATs axis

Han

et al. 2022

Vet Res

Self Cite

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. Graphic Abstract