Galectin-3 Regulates Indoleamine-2,3-dioxygenase-Dependent Cross-Talk between Colon-Infiltrating Dendritic Cells and T Regulatory Cells and May Represent a Valuable Biomarker for Monitoring the Progression of Ulcerative Colitis

Volarević, Vladislav; Zdravković, Nataša; Harrell, Carl Randall; Arsenijević, Nebojša; Fellabaum, Crissy; Djonov, Valentin; Lukić, Miodrag L.; Marković, Bojana Simović

doi:10.3390/cells8070709

Cited by 23 publications

(21 citation statements)

References 64 publications

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“…For instance, Simovic Markovic et al (2016) showed an important pro-inflammatory role that Gal3 plays in events that accompany UC, while other authors found that Gal3 reduces the colon inflammation in animal models of experimental colitis (Tsai et al, 2016); (Lippert et al, 2015). More recently, it has been shown that the effects of Gal3 deletion vary as colon inflammation progresses since Gal3 may direct the polarization of colonic macrophages towards inflammatory or anti-inflammatory phenotype (Volarevic et al, 2019). Moreover, Gal3 seems to be involved in processes that maintain the barrier in the colon.…”

Section: Discussionmentioning

confidence: 99%

Galectin-3 Deletion Reduces LPS and Acute Colitis-Induced Pro-Inflammatory Microglial Activation in the Ventral Mesencephalon

et al. 2021

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Parkinson’s disease is a highly prevalent neurological disorder for which there is currently no cure. Therefore, the knowledge of risk factors as well as the development of new putative molecular targets is mandatory. In this sense, peripheral inflammation, especially the originated in the colon, is emerging as a predisposing factor for suffering this disease. We have largely studied the pleiotropic roles of galectin-3 in driving microglia-associated immune responses. However, studies aimed at elucidating the role of galectin-3 in peripheral inflammation in terms of microglia polarization are lacking. To achieve this, we have evaluated the effect of galectin-3 deletion in two different models of acute peripheral inflammation: intraperitoneal injection of lipopolysaccharide or gut inflammation induced by oral administration of dextran sodium sulfate. We found that under peripheral inflammation the number of microglial cells and the expression levels of pro-inflammatory mediators take place specifically in the dopaminergic system, thus supporting causative links between Parkinson’s disease and peripheral inflammation. Absence of galectin-3 highly reduced neuroinflammation in both models, suggesting an important central regulatory role of galectin-3 in driving microglial activation provoked by the peripheral inflammation. Thus, modulation of galectin-3 function emerges as a promising strategy to minimize undesired microglia polarization states.

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Section: Discussionmentioning

confidence: 99%

Galectin-3 Deletion Reduces LPS and Acute Colitis-Induced Pro-Inflammatory Microglial Activation in the Ventral Mesencephalon

et al. 2021

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“…Immune cell infiltration is an important biomarker of inflammation. DSS feeding resulted in an increased production of macrophage-derived cytokines in BALB/c mice [ 26 ]. We also found macrophages accounted for the highest proportion of immune infiltrating cells in the DSS-induced UC model (Figures 5(a) and 5(b) ).…”

Section: Discussionmentioning

confidence: 99%

Ursolic Acid Regulates Intestinal Microbiota and Inflammatory Cell Infiltration to Prevent Ulcerative Colitis

Sheng

Chen

et al. 2021

Journal of Immunology Research

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Ulcerative colitis (UC) is a chronic and relapsing inflammatory bowel disorder in the colon and rectum leading to low life-quality and high societal costs. Ursolic acid (UA) is a natural product with pharmacological and biological activities. The studies are aimed at investigating the protective and treatment effects of UA against the dextran sulfate sodium- (DSS-) induced UC mouse model and its underlying mechanism. UA was orally administered at different time points before and after the DSS-induced model. Mice body weight, colon length, and histological analysis were used to evaluate colon tissue damage and therapeutic evaluation. Intestinal transcriptome and microbe 16 s sequencing was used to analyze the mechanisms of UA in the prevention and treatment of UC. The early prevention effect of UA could effectively delay mouse weight loss and colon length shorten. UA alleviated UC inflammation and lowered serum and colon IL-6 levels. Three classical inflammatory pathways: MAPKs, IL-6/STAT3, and PI3K were downregulated by UA treatment. The proportion of macrophages and neutrophils in inflammatory cell infiltration was reduced in UA treatment groups. UA could significantly reduce the richness of intestinal flora to avoid the inflammatory response due to the destruction of the intestinal epithelial barrier. The function of UA against UC was through reducing intestinal flora abundance and regulating inflammatory and fatty acid metabolism signaling pathways to affect immune cell infiltration and cytokine expression.

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“…Our data revealed that both total absence (Lgals3 −/− BALB/c mice) or reduction of galectin-3 in the gut-liver axis induced by milk supplementation increased atypical behaviors. The role of galectin-3 as immunomodulatory factor in the gut and liver has been attracted the attention of specialists 15,20 .…”

Section: Discussionmentioning

confidence: 99%

Galectin-3 in the Gut-liver axis Regulates Autistic-like Behaviors by Mechanism Associated with Cerebral Shank-3+ cell Niches in BALB/c Mice

Lemos¹,

Prins²,

Carpi-Santos³

et al. 2021

Preprint

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Galectin-3 stabilizes cell-cell junctions and regulates inflammatory pathways in the gut-liver axis. Galectin-3 knockout (Lgals3−/−) mice have atypical behaviors by obscure mechanisms. Given that BALB/c mice naturally develop low-sociability, stereotypies and restrict interest, they have been included as autism experimental model. Our major aims were to investigate whether galectin-3 in the gut-liver axis interferes with autistic-like behaviors analyzing BALB/c Lgals3−/− mice or under partial inhibition of galectin-3 oral intake of cow’s milk for 7 days. Behavioral patterns were assessed using a three-chambers test, open field, and self-grooming. Histological analysis and immunohistochemistry (Galectin-3, NOS-2, Iba-1, Ki-67, Dll-4, Shank-3, Synaptophysin and Drebrin) were performed in gut, liver, and/or brain. Lgals3−/− mice amplified stereotypies, social retraction and restrict interest associated with reduction of cerebral Shank-3+ cells. In Lgals3+/+ mice, cow’s milk intake also amplified atypical behaviors, reduced galectin-3 in enterocytes and Kupffer cells, and disturbed niches of intestinal KI67+ and Dll-4+ cells and hepatic NOS2+ cells. In the brain of milk-treated mice, Iba-1+ microglial cells and NOS2+ Purkinje cells were increased whereas Shank-3+ and Drebrin+Synaptophysin+ cells were reduced suggesting, for the first time, that galectin-3 interferes with autistic behavior. Perhaps, a perspective to new therapies in genetically predisposed individuals to atypical behaviors.

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Galectin-3 Regulates Indoleamine-2,3-dioxygenase-Dependent Cross-Talk between Colon-Infiltrating Dendritic Cells and T Regulatory Cells and May Represent a Valuable Biomarker for Monitoring the Progression of Ulcerative Colitis

Cited by 23 publications

References 64 publications

Galectin-3 Deletion Reduces LPS and Acute Colitis-Induced Pro-Inflammatory Microglial Activation in the Ventral Mesencephalon

Galectin-3 Deletion Reduces LPS and Acute Colitis-Induced Pro-Inflammatory Microglial Activation in the Ventral Mesencephalon

Ursolic Acid Regulates Intestinal Microbiota and Inflammatory Cell Infiltration to Prevent Ulcerative Colitis

Galectin-3 in the Gut-liver axis Regulates Autistic-like Behaviors by Mechanism Associated with Cerebral Shank-3+ cell Niches in BALB/c Mice

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