Activation of the porcine alveolar macrophages via toll-like receptor 4/NF-κB mediated pathway provides a mechanism of resistin leading to inflammation

Bi, Li; Fang, Jing; Zuo, Zhicai; Yin, Sirui; He, Tingting; Yang, Mingxian; Deng, Junliang; Shen, Liuhong; Ma, Xiaoping; Yu, Shumin; Ya, Wang; Ren, Zhihua; Cui, Hengmin

doi:10.1016/j.cyto.2018.04.002

Cited by 19 publications

(13 citation statements)

References 48 publications

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“…In a neuronal cell study, resistin was found to inhibit neuronal autophagy by binding to TLR4 in wild-type mice but not in TLR4 gene knockout mice [64]. The resistin-induced activation of porcine alveolar macrophages via TLR4 promotes the production of proinflammatory cytokines [65]. These studies indicate that TLR4 as a cell surface receptor plays an important role in resistin-induced inflammation.…”

Section: Possible Pathogenetic Mechanisms Underlying Resistin-indumentioning

confidence: 99%

An Update on the Emerging Role of Resistin on the Pathogenesis of Osteoarthritis

Zhao

Gao

Song

et al. 2019

Mediators of Inflammation

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Background. Resistin may be involved in the pathogenesis of osteoarthritis (OA), but a systematic understanding of the role of resistin in OA is lacking. Methods. We reviewed studies that evaluated the role of resistin in OA. The expression levels of resistin in vitro experiments and OA/rheumatoid arthritis (RA) patients were analyzed. We also studied potential resistin receptors and the signaling pathways that these receptors activate, ultimately leading to cartilage degeneration. Results. Resistin levels in both the serum and synovial fluid were higher in OA and RA patients than in healthy subjects. Overall, resistin levels are much higher in serum than in synovial fluid. In human cartilage, resistin induces the expression of proinflammatory factors such as degradative enzymes, leading to the inhibition of cartilage matrix synthesis, perhaps by binding to Toll-like receptor 4 and the adenylyl cyclase-associated protein 1 receptor, which then activates the p38-mitogen-activated phosphate kinase, protein kinase A–cyclic AMP, nuclear factor-κB, and C/enhancer-binding protein β signaling pathways. Conclusion. Resistin levels are higher in OA patients than in healthy controls; however, the precise role of resistin in the pathogenesis of OA needs to be studied further. Resistin may be a novel therapeutic target in OA in the future.

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Section: Possible Pathogenetic Mechanisms Underlying Resistin-indumentioning

confidence: 99%

An Update on the Emerging Role of Resistin on the Pathogenesis of Osteoarthritis

Zhao

Gao

Song

et al. 2019

Mediators of Inflammation

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“…Accumulating evidence has indicated that resistin is closely related to the expression of proinflammation indicators, such as interleukin-1β, IL-6, TNF-α, C-reactive protein and soluble vascular adhesion molecule [37][38][39][40][41][42]. Resistin activates nuclear factor κB (NF-κB) by binding to its receptors and exerting proinflammatory effects [43], while the resistin receptor and its roles in proinflammation and inflammation mechanisms remain unclear. In this study, we demonstrated that resistin upregulated IL-1β and IL-6 in both HFD mice (▶Fig.…”

Section: Discussionmentioning

confidence: 99%

Acute Elevated Resistin Exacerbates Mitochondrial Damage and Aggravates Liver Steatosis Through AMPK/PGC-1α Signaling Pathway in Male NAFLD Mice

et al. 2020

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Resistin was identified as a link between obesity and insulin resistance and is associated with many diseases in mice. Deciphering the related development and molecular mechanism is necessary for the treatment of these diseases. Previous studies have revealed that increased resistin levels are correlated with lipid accumulation and play a role in non-alcoholic fatty liver disease (NAFLD) development. However, the exact mechanisms underlying these processes remain unclear. To further clarify whether acute elevated resistin level exacerbated liver steatosis, a high-fat diet-induced NAFLD animal model was used and treated with or without resistin for 6 days. We discovered that resistin altered mitochondrial morphology, decreased mitochondrial content, and increased lipid accumulation in HFD mice. qRT-PCR and western blot analysis showed that acute elevated resistin significantly altered the gene expression of mitochondrial biogenesis and liver lipid metabolism molecules in HFD mice. Consequently, in vitro experiments verified that resistin reduced the mitochondrial content, impaired the mitochondrial function and increased the lipid accumulation of palmitate-treated HepG2 cells. Additionally, we demonstrated that resistin upregulated proinflammatory factors, which confirmed that resistin promoted the development of inflammation in NAFLD mice and palmitate-treated HepG2 cells. Signaling-transduction analysis demonstrated that acute elevated resistin aggravated liver steatosis through AMPK/PGC-1α pathway in male mice. This reveals a novel pathway through which lipogenesis is induced by resistin and suggests that maintaining mitochondrial homeostasis may be key to treatments for preventing resistin-induced NAFLD aggravation.

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“…In the porcine model of pulmonary infection with Actinobacillus pleuropneumoniae, the expression of resistin was significantly up-regulated in the porcine lung and hilar lymph nodes, indicating that resistin may play a role in the antiinfection immune response of lung (69,70). At present, studies only show that resistin(in humans and pigs but not in mice) have the ability to modulate lung cellular responses, including promoting immune cells recruitment, proinflammatory cytokines expression, and the NETs formation, which may indirectly resist pathogen invasion (17,23,71). However, whether resistin can play a direct bactericidal role as a bactericidal protein in the lung is still unclear, and further research is needed to confirm.…”

Section: Antibacterial Function In Vivomentioning

confidence: 95%

Resistin, a Novel Host Defense Peptide of Innate Immunity

Yang

Cai

et al. 2021

Front. Immunol.

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Resistin, a cysteine-rich protein, expressed in adipocytes, was initially proposed as a link between obesity and diabetes in mice. In humans, resistin is considered to be a pro-inflammatory molecule expressed in immune cells, which plays a regulatory role in many chronic inflammatory diseases, metabolic diseases, infectious diseases, and cancers. However, increasing evidence shows that resistin functions as a host defense peptide of innate immunity, in terms of its wide-spectrum anti-microbial activity, modulation of immunity, and limitation of microbial product-induced inflammation. To date, the understanding of resistin participating in host defense mechanism is still limited. The review aims to summarize current knowledge about the biological properties, functions, and related mechanisms of resistin in host defense, which provides new insights into the pleiotropic biological function of resistin and yields promising strategies for developing new antimicrobial therapeutic agents.

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Activation of the porcine alveolar macrophages via toll-like receptor 4/NF-κB mediated pathway provides a mechanism of resistin leading to inflammation

Cited by 19 publications

References 48 publications

An Update on the Emerging Role of Resistin on the Pathogenesis of Osteoarthritis

An Update on the Emerging Role of Resistin on the Pathogenesis of Osteoarthritis

Acute Elevated Resistin Exacerbates Mitochondrial Damage and Aggravates Liver Steatosis Through AMPK/PGC-1α Signaling Pathway in Male NAFLD Mice

Resistin, a Novel Host Defense Peptide of Innate Immunity

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