CD30L is involved in the regulation of the inflammatory response through inducing homing and differentiation of monocytes via CCL2/CCR2 axis and NF-κB pathway in mice with colitis

Mei, Chenxue; Meng, Fanxiang; Wang, Xiao; Yan, Siqi; Zheng, Qianqian; Zhang, Xiaoqing; Fu, Wenda; Xue, Junxiu; Wang, Shengyi; He, Ya‐Ling; Sun, Xun; Jiang, Xuefeng; Wang, Yuanyuan

doi:10.1016/j.intimp.2022.108934

Cited by 9 publications

(6 citation statements)

References 45 publications

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“…The elevation of p65 in the cell has been linked to neurodegenerative diseases, rheumatoid arthritis, and inflammatory bowel disease [ 73 , 75 ]. Interestingly, it was very recently demonstrated in a pre-clinical experimental model, that the CCL2/NF-κB signaling pathway is implicated in the pathogenesis of colitis and suggested as a therapeutic target [ 76 ].…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effects of β-FNA are sex-dependent in a pre-clinical model of LPS-induced inflammation

et al. 2023

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Background Inflammation is present in neurological and peripheral disorders. Thus, targeting inflammation has emerged as a viable option for treating these disorders. Previous work indicated pretreatment with beta-funaltrexamine (β-FNA), a selective mu-opioid receptor (MOR) antagonist, inhibited inflammatory signaling in vitro in human astroglial cells, as well as lipopolysaccharide (LPS)-induced neuroinflammation and sickness-like-behavior in mice. This study explores the protective effects of β-FNA when treatment occurs 10 h after LPS administration and is the first-ever investigation of the sex-dependent effects of β-FNA on LPS-induced inflammation in the brain and peripheral tissues, including the intestines. Results Male and female C57BL/6J mice were administered LPS followed by treatment with β-FNA-immediately or 10 h post-LPS. Sickness- and anxiety-like behavior were assessed using an open-field test and an elevated-plus-maze test, followed by the collection of whole brain, hippocampus, prefrontal cortex, cerebellum/brain stem, plasma, spleen, liver, large intestine (colon), proximal small intestine, and distal small intestine. Levels of inflammatory chemokines/cytokines (interferon γ-induced-protein, IP-10 (CXCL10); monocyte-chemotactic-protein 1, MCP-1 (CCL2); interleukin-6, IL-6; interleukin-1β, IL-1β; and tumor necrosis factor-alpha, TNF-α) in tissues were measured using an enzyme-linked immunosorbent assay. Western blot analysis was used to assess nuclear factor-kappa B (NF-κB) expression. There were sex-dependent differences in LPS-induced inflammation across brain regions and peripheral tissues. Overall, LPS-induced CXCL10, CCL2, TNF-α, and NF-κB were most effectively downregulated by β-FNA; and β-FNA effects differed across brain regions, peripheral tissues, timing of the dose, and in some instances, in a sex-dependent manner. β-FNA reduced LPS-induced anxiety-like behavior most effectively in female mice. Conclusion These findings provide novel insights into the sex-dependent anti-inflammatory effects of β-FNA and advance this agent as a potential therapeutic option for reducing both neuroinflammation an intestinal inflammation.

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Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effects of β-FNA are sex-dependent in a pre-clinical model of LPS-induced inflammation

et al. 2023

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“…And TNFSF8, known as CD30 ligand (CD30L), is a membrane-associated glycoprotein belonging to the TNF superfamily. Previous studies have shown that CD30/CD30L signaling system has been implicated in the pathogenesis of several autoimmune and inflammatory conditions including rheumatoid arthritis and ulcerative colitis patients (30)(31)(32). However, there are very few studies exploring these genes in CAEBV in children.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis to screen the key genes in pediatric Chronic Active Epstein-Barr Virus infection

Yi Zhang,

Wenli Liu,

Yue Li

et al. 2023

Cell Mol Biol (Noisy-le-grand)

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“…This, in turn, induces monocytes homing in a colitis mouse model via the CCL2/CCR2 axis. 55,56 Importantly, researches have indicated that the chemotactic cytokine PSMP is upregulated earlier than CCL2 in experimental colitis and promotes the expression of CCL2. This suggests that PSMP may initiate the early recruitment of circulating Ly6C hi CCR2 + monocytes to the tissue, working in concert with CCL2 and CCL7 to drive colitis.…”

Section: Migration and Recruitment Of Monocytes During Ibd Important ...mentioning

confidence: 99%

“…Classical monocytes, when activated by CD30L, tend towards inflammatory monocytes through the CCL2/CCR2 and NF-κB signaling pathways. 56 Schridde et al demonstrated that TGF-β is pivotal for intestinal monocytes differentiation into macrophages. 98 Furthermore, during IBD inflammation, moMφs' TGF-β activation ability via integrin αvβ8 diminishes.…”

Section: The Relationship Between Cytokines and Monocytes Differentia...mentioning

confidence: 99%

Origin and Function of Monocytes in Inflammatory Bowel Disease

Liao,

Liu,

Guo

et al. 2024

JIR

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Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), is a chronic disease resulting from the interaction of various factors such as social elements, autoimmunity, genetics, and gut microbiota. Alarmingly, recent epidemiological data points to a surging incidence of IBD, underscoring an urgent imperative: to delineate the intricate mechanisms driving its onset. Such insights are paramount, not only for enhancing our comprehension of IBD pathogenesis but also for refining diagnostic and therapeutic paradigms. Monocytes, significant immune cells derived from the bone marrow, serve as precursors to macrophages (Mφs) and dendritic cells (DCs) in the inflammatory response of IBD. Within the IBD milieu, their role is twofold. On the one hand, monocytes are instrumental in precipitating the disease's progression. On the other hand, their differentiated offsprings, namely moMφs and moDCs, are conspicuously mobilized at inflammatory foci, manifesting either pro-inflammatory or anti-inflammatory actions. The phenotypic spectrum of these effector cells, intriguingly, is modulated by variables such as host genetics and the subtleties of the prevailing inflammatory microenvironment. Notwithstanding their significance, a palpable dearth exists in the literature concerning the roles and mechanisms of monocytes in IBD pathogenesis. This review endeavors to bridge this knowledge gap. It offers an exhaustive exploration of monocytes' origin, their developmental trajectory, and their differentiation dynamics during IBD. Furthermore, it delves into the functional ramifications of monocytes and their differentiated progenies throughout IBD's course. Through this lens, we aspire to furnish novel perspectives into IBD's etiology and potential therapeutic strategies.

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CD30L is involved in the regulation of the inflammatory response through inducing homing and differentiation of monocytes via CCL2/CCR2 axis and NF-κB pathway in mice with colitis

Cited by 9 publications

References 45 publications

Anti-inflammatory effects of β-FNA are sex-dependent in a pre-clinical model of LPS-induced inflammation

Anti-inflammatory effects of β-FNA are sex-dependent in a pre-clinical model of LPS-induced inflammation

Bioinformatics analysis to screen the key genes in pediatric Chronic Active Epstein-Barr Virus infection

Origin and Function of Monocytes in Inflammatory Bowel Disease

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