Methylsulfonylmethane ameliorates inflammation via NF-κB and ERK/JNK-MAPK signaling pathway in chicken trachea and HD11 cells during Mycoplasma gallisepticum infection

Miao, Yusong; Dong, Na; Wang, Ze; Wang, Jian; Wu, Zhiyong; Bao, Jun; Jin, Xiaodi; Li, Rui; Ishfaq, Muhammad; Li, Jichang

doi:10.1016/j.psj.2022.101706

Cited by 11 publications

(13 citation statements)

References 54 publications

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“…This observation is in line with results of previous studies showing that supplementation of MSM (3 g/kg) decreased TBARS levels in serum of Cherry Valley male ducks ( Yan et al, 2020 ) and the works of Rasheed et al (2020a , b ) employing oxidized oil and Eimeria challenges in broilers, fed 0.5 and 4 g/kg MSM, respectively. On the mechanism, MSM has been shown to repress the transcriptional activity of NF-κB, which was confirmed in chickens by Miao et al (2022) , and the expression and activities of STAT, which altogether may lower the generation of ROS, plausibly explaining the lower levels of TBARS. Furthermore, several organosulfur compounds have shown to be electrophilic toward redox sensitive cysteine residues in proteins, and thereby take action in the redox regulation pathway.…”

Section: Discussionmentioning

confidence: 82%

“…More evidence is available in meat-type domestic birds ( Supplementary Table 1 ). In summary, MSM improved performance and lowered mortality ( Liu and Zhou, 2008 ; Hwang et al, 2017 ; Jiao et al, 2017 ; Yan et al, 2020 ), enhanced antioxidant defenses and reduced markers of oxidation ( Hwang et al, 2017 ; Rasheed et al, 2020a ; Yan et al, 2020 ; Miao et al, 2022 ), and showed immunosuppressive properties ( Yan et al, 2020 ; Miao et al, 2022 ). Finally, breast quality of MSM-fed poultry exhibited higher water-holding capacity ( WHC ) and lower drip loss, higher redness (a*), and lower concentrations of TBARS ( Hwang et al, 2017 ; Jiao et al, 2017 ; Yan et al, 2020 ).…”

Section: Introductionmentioning

confidence: 97%

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Effect of supplemental methyl sulfonyl methane on performance, carcass and meat quality and oxidative status in chronic cyclic heat-stressed finishing broilers

Zhang

Majdeddin²,

Degroote³

et al. 2023

Poultry Science

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Section: Discussionmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 97%

Effect of supplemental methyl sulfonyl methane on performance, carcass and meat quality and oxidative status in chronic cyclic heat-stressed finishing broilers

Zhang

Majdeddin²,

Degroote³

et al. 2023

Poultry Science

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“…MG infection mainly causes CRD in chicken, inducing serious inflammatory reactions and immune responses through colonization of the respiratory mucosa ( 36 , 37 ). Inflammatory damage and apoptosis are MG-infected important pathogenic mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Lnc90386 Sponges miR-33-5p to Mediate Mycoplasma gallisepticum-Induced Inflammation and Apoptosis in Chickens via the JNK Pathway

et al. 2022

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Mycoplasma gallisepticum (MG) is one of the most important pathogens, that causes chronic respiratory disease (CRD) in chickens. Long non-coding RNAs (lncRNAs) are emerging as new regulators for many diseases and some lncRNAs can function as competing endogenous RNAs (ceRNAs) to regulate mRNAs by competitively binding to miRNAs. Here, we found that miR-33-5p was significantly up-regulated both in MG-infected chicken embryonic lungs and chicken embryo fibroblast cells (DF-1), and Lnc90386 negatively correlated with miR-33-5p. miR-33-5p, as a new regulator for MG infection, repressed apoptosis, inflammatory factors in DF-1 cells by targeting JNK1. Further analyses showed that Lnc90386 sponged miR-33-5p to weaken its inhibitory effect on JNK1, forming the ceRNA regulatory network. Furthermore, knockdown of Lnc90386 significantly inhibited apoptosis and inflammatory factors, and promoted DF-1 cells proliferation. However, co-treatment with miR-33-5p inhibitor and Lnc90386 siRNA showed that knockdown of Lnc90386 could partially eliminate the inhibiting effect of miR-33-5p inhibitor on inflammation, cell apoptosis and proliferation. In conclusion, Lnc90386 sponges miR-33-5p to defend against MG infection by inhibiting the JNK signaling pathway.

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“…To determine the extent of MG infection, a standard curve was established using a cloned MG gene recombinant plasmid to detect the absolute abundance of MG by quantitative real time PCR [ 22 ]. Briefly, DNA from cells or spleens were extracted under aseptic conditions and the 16Sribosomal RNA gene of MG was subsequently amplified as part of the MG genomic DNA using qPCR and sequenced.…”

Section: Methodsmentioning

confidence: 99%

Extracellular HMGB1 as Inflammatory Mediator in the Progression of Mycoplasma Gallisepticum Infection

Wang

et al. 2022

Cells

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High-mobility group box 1 (HMGB1), a member of damage-associated molecular patterns (DAMPs), is involved in the immune regulation of several infectious diseases. Mycoplasma gallisepticum (MG) infection is proved to cause an abnormal immune response, but the role of HMGB1 in MG-induced chronic respiratory disease (CRD) is unclear. In this study, we found that HMGB1 was released from the nucleus to the extracellular in macrophages upon infection with MG. Extracellular HMGB1 bound to TLR2 activating the NF-κB pathway triggering a severe inflammatory storm and promoting the progression of MG infection. More importantly, TLR4 could be activated by HMGB1 to trigger immune disorders after TLR2 was silenced. This disease process could be interrupted by ethyl pyruvate (EP) inhibition of HMGB1 release or glycyrrhizic acid (GA). Furthermore, treatment of MG-infected chickens with GA significantly alleviated immune organ damage. In conclusion, we demonstrate that HMGB1 is secreted extracellularly to form an inflammatory environment upon MG infection, triggering a further cellular inflammatory storm in a positive feedback approach. Blocking MG-induced HMGB1 release or suppression downstream of the HMGB1-TLR2/TLR4 axis may be a promising novel strategy for the treatment of CRD. Furthermore, this study may provide a theoretical reference for understanding non-LPS-activated TLR4 events.

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Methylsulfonylmethane ameliorates inflammation via NF-κB and ERK/JNK-MAPK signaling pathway in chicken trachea and HD11 cells during Mycoplasma gallisepticum infection

Cited by 11 publications

References 54 publications

Effect of supplemental methyl sulfonyl methane on performance, carcass and meat quality and oxidative status in chronic cyclic heat-stressed finishing broilers

Effect of supplemental methyl sulfonyl methane on performance, carcass and meat quality and oxidative status in chronic cyclic heat-stressed finishing broilers

Lnc90386 Sponges miR-33-5p to Mediate Mycoplasma gallisepticum-Induced Inflammation and Apoptosis in Chickens via the JNK Pathway

Extracellular HMGB1 as Inflammatory Mediator in the Progression of Mycoplasma Gallisepticum Infection

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