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Simple Summary: Mycoplasma gallisepticum causes respiratory disease in chickens. This study used RNA-seq to investigate the immune response of chicken embryos and chicks to infection. Weight loss and immune damage were observed in infected chickens of both ages. Transcriptome analysis revealed differentially expressed genes related to innate immunity and inflammation, with toll-like receptors and cytokine pathways playing a dominant role in the immune response. The immune response was stronger in embryos than in chicks. These findings provide valuable insights for developing disease control strategies. Mycoplasma gallisepticum (MG) is a major cause of chronic respiratory diseases in chickens, with both horizontal and vertical transmission modes and varying degrees of impact on different ages. The innate immune response is crucial in resisting MG infection. Therefore, this study aimed to investigate the innate immune response of chicken embryos and newly hatched chicks to MG infection using comparative RNA-seq analysis. We found that MG infection caused weight loss and immune damage in both chicken embryos and chicks. Transcriptome sequencing analysis revealed that infected chicken embryos had a stronger immune response than chicks, as evidenced by the higher number of differentially expressed genes associated with innate immunity and inflammation. Toll-like receptor and cytokine-mediated pathways were the primary immune response pathways in both embryos and chicks. Furthermore, TLR7 signaling may play an essential role in the innate immune response to MG infection. Overall, this study sheds light on the development of innate immunity to MG infection in chickens and can help in devising disease control strategies. [ABSTRACT FROM AUTHOR]

Mycoplasma gallisepticum (MG) can cause chronic respiratory disease (CRD) in chickens. While several studies have reported the inflammatory functions of microRNAs during MG infection, the mechanism by which exosomal miRNAs regulate MG‐induced inflammation remains to be elucidated. The expression of exosome‐microRNA derived from MG‐infected chicken type II pneumocytes (CP‐II) was screened, and the target genes and function of differentially expressed miRNAs (DEGs) were predicted. To verify the role of exosomal gga‐miR‐451, Western blot, ELISA and RT‐qPCR were used in this study. The results showed that a total of 722 miRNAs were identified from the two exosomal small RNA (sRNA) libraries, and 30 miRNAs (9 up‐regulated and 21 down‐regulated) were significantly differentially expressed. The target miRNAs were significantly enriched in the treatment group, such as cell cycle, Toll‐like receptor signalling pathway and MAPK signalling pathway. The results have also confirmed that gga‐miR‐451‐absent exosomes derived from MG‐infected CP‐II cells increased inflammatory cytokine production in chicken fibroblast cells (DF‐1), and wild‐type CP‐II cell–derived exosomes displayed protective effects. Collectively, our work suggests that exosomes from MG‐infected CP‐II cells alter the dynamics of the DF‐1 cells, and may contribute to pathology of the MG infection via exosomal gga‐miR‐451 targeting YWHAZ involving in inflammation. [ABSTRACT FROM AUTHOR]

Mycoplasma gallisepticum (MG) is the pathogen of chronic respiratory disease (CRD), hallmarked by vigorous inflammation in chickens, causing the poultry industry enormous losses. miRNAs have emerged as important regulators of animal diseases. Previous miRNA sequencing data has demonstrated that miR-130b-3p is up-regulated in MG-infected chicken embryo lungs. Therefore, we aimed to investigate the function of miR-130b-3p in MG infection of chickens. RT-qPCR results confirmed that miR-130b-3p was up-regulated both in MG-infected chicken embryo lungs and chicken embryonic fibroblast cells (DF-1 cells). Furthermore, functional studies showed that overexpression of miR-130b-3p promoted MG-infected DF-1 cell proliferation and cell cycle, whereas inhibition of miR-130b-3p weakened these cellular processes. Luciferase reporter assay combined with gene expression data supported that phosphatase and tensin homolog deleted on chromosome ten (PTEN) was a direct target of miR-130b-3p. Additionally, overexpression of miR-130b-3p resulted in up-regulations of phosphatidylinositol-3 kinase (PI3K), serine/threonine kinase (AKT), and nuclear factor-κB (NF-κB), whereas inhibition of miR-130b-3p led to the opposite results. Altogether, upon MG infection, up-regulation of miR-130b-3p activates the PI3K/AKT/NF-κB pathway, facilitates cell proliferation and cell cycle via down-regulating PTEN. This study helps to understand the mechanism of host response to MG infection. [ABSTRACT FROM AUTHOR]

• gga-miR-21 was significantly up-regulated in MG-HS infection, while target gene MAP3K1 was significantly down-regulated. • gga-miR-21 activates MAPKs and NF-κB signaling pathways via targeting MAP3K1. • gga-miR-21 increases the production of inflammatory cytokines, including TNF-α, IL-1β, IL-6, IL-8 after MG infection. • gga-miR-21 promotes cell proliferation by increasing the cell cycle progression and suppressing cell apoptosis. Mycoplasma gallisepticum (MG) can target host cells and cause chronic respiratory disease (CRD) in chickens that is characterized by pMGA and concomitant. Although microRNAs (miRNAs) have been manifested are crucial regulatory noncoding RNAs with important effects on microbial pathogenesis and inflammatory response, how miRNAs regulate MG-induced inflammation remains to be discovered. The results showed that gga-miR-21 was up-regulated in MG-infected chicken embryonic lungs and MG infection of chicken embryo fibroblast cells (DF-1) compared with the control group. Overexpression of gga-miR-21 increased the inflammatory cytokines production, including tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-8 (IL-8) after MG infection, knockdown of gga-miR-21 had thoroughly inverse effects. Gene expression data combined with bioinformatics analysis and luciferase reporter assays demonstrated that mitogen-activated protein kinase kinase kinase 1(MAP3K1) was a novel target of gga-miR-21. The inhibition of MAP3K1 by gga-miR-21 resulted in the accumulation of NF-κB in the nucleus, which in turn generate higher inflammatory cytokines. Furthermore, upregulation of gga-miR-21 significantly inhibited MG propagation and promoted MG-infected DF-1 cells proliferation by increasing the cell cycle progression and suppressing cell apoptosis. Our study provides evidence for proinflammatory effects of gga-miR-21 which is mediated at least in part by targeting MAP3K1 in the MG-infected DF-1 cells. gga-miR-21 activates MAPKs and NF-κB signaling pathways via targeting MAP3K1 , and then promotes the production of inflammatory cytokines and cell proliferation by increasing the cell cycle progression and suppressing cell apoptosis to defend against MG infection. [ABSTRACT FROM AUTHOR]

• Puerarin, like Try, has a significant effect in the treatment of MG infection in chicken. • Puerarin can effectively inhibit inflammation and apoptosis via suppressing the TLR6/MyD88/NF- κ B signal pathway. • Puerarin can effectively inhibit the expression of MG adhesion protein pMGA1.2. • Puerarin at appropriate concentrations is not cytotoxic. Mycoplasma gallisepticum (MG) is the primary etiological agent of chicken chronic respiratory disease (CRD), which mainly causes inflammatory damage of the host respiratory system. Previous studies suggest that puerarin (PUE) plays a pivotal regulatory role in inflammatory diseases, whereas the impacts of PUE on MG -induced inflammation remain unclear. This study investigated the effects of PUE on MG -HS infection in vitro and in vivo and indicated its potential therapeutic and preventive value. Experimental results showed that PUE significantly suppressed pMGA1.2 expression, promoted MG -infected cell proliferation and cell cycle process by reducing apoptosis. Histopathological examination of lung tissue showed severe histopathological lesions including thickened alveolar walls, narrowed alveolar cavity, and inflammatory cell infiltration in the MG -infected chicken group. However, PUE treatment significantly ameliorated MG -induced pathological damage in lung. Compared to the MG -infected group, PUE effectively inhibited the expression of MG -induced inflammatory genes, including tumor necrosis factor-α (TNF- α), interleukin-1β (IL-1 β), cytokines interleukin-6 (IL-6), toll-like receptor 6 (TLR6), myeloid differentiation primary response gene 88 (MyD88) and nuclear factor κ B (NF- κ B). Moreover, PUE dose-dependently inhibited MG -induced NF- κ B p65 to enter the cell nucleus. In conclusion, our findings indicate that PUE treatment can efficiently inhibit MG -induced inflammatory response and apoptosis, and protect the lung from MG infection-induced damage by inhibiting the TLR6/MyD88/NF- κ B signaling pathway activation. The study suggests that PUE may be a potential anti-inflammatory agent defense against MG infection in chicken. [ABSTRACT FROM AUTHOR]