Levels of low-molecular-weight hyaluronan in periodontitis-treated patients and its immunostimulatory effects on CD4+ T lymphocytes

Castillo, Francisca; Monasterio, Gustavo; Ibarra, Juan Pablo; Guevara, José Ramón Vielma; Cafferata, Emilio A.; Vicencio, Emiliano; Cortéz, Cristian; Carvajal, Paola; Vernal, Rolando

doi:10.1007/s00784-021-03808-9

Cited by 9 publications

(9 citation statements)

References 52 publications

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“…Similarly, it has been reported that the therapeutic function of HA is dependent on its molecular weight and concentration [ 14 , 15 ]. Unfortunately, this dependency leads to problems if the exogenous HA undergoes fragmentation in the inflammation site, which can stimulate a pro-inflammatory cellular response [ 17 , 30 , 31 ]. We previously showed that a low molecular weight HA (AHA) can increase the expression levels of IL-1β in human macrophages [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

N-Butyrylated Hyaluronic Acid Achieves Anti-Inflammatory Effects In Vitro and in Adjuvant-Induced Immune Activation in Rats

et al. 2022

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Previously synthesized N-butyrylated hyaluronic acid (BHA) provides anti-inflammatory effects in rat models of acute gouty arthritis and hyperuricemia. However, the mechanism of action remains to be elucidated. Herein, the anti-inflammatory and antioxidative activities of BHA and the targeted signaling pathways were explored with LPS-induced RAW264.7 and an adjuvant-induced inflammation in a rat model. Results indicated that BHA inhibited the generation of pro-inflammatory cytokines TNFα, IL-1β and IL-6, reduced ROS production and down-regulated JAK1-STAT1/3 signaling pathways in LPS-induced RAW264.7. In vivo, BHA alleviated paw and joint swelling, decreased inflammatory cell infiltration in paw tissues, suppressed gene expressions of p38 and p65, down-regulated the NF-κB and MAPK signaling pathways and reduced protein levels of TNFα, IL-1β and IL-6 in joint tissues of arthritis rats. This study demonstrated the pivotal role of BHA in anti-inflammation and anti-oxidation, suggesting the potential clinical value of BHA in the prevention of inflammatory arthritis and is worthy for development as a new pharmacological treatment.

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Section: Discussionmentioning

confidence: 99%

N-Butyrylated Hyaluronic Acid Achieves Anti-Inflammatory Effects In Vitro and in Adjuvant-Induced Immune Activation in Rats

et al. 2022

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“…Alharbi et al 81 found that high molecular weight (1.5 MDa) HA effectively inhibited the adhesion of P. gingivalis by down-regulating the adhesion-related genes (f imA, mfa1, hagA, rgpA, and kgp). Moreover, Castillo et al 82 reported that HA is degraded into low molecular weight (MW-HA) inflammatory environment and can potentially promote osteogenesis. Dong et al 83 reported that PTX3, found in the ECM of mouse preosteoblast cells and thrives on HA, enhanced the synthesis of HA and augmented the manifestation of CD44 (the primary receptor for HA), which resulted in an enhancement of the interactions between HA and CD44.…”

Section: Hamentioning

confidence: 99%

“…Hydrogel delivers local oxygen to suppress subgingival biofilms and to restore tissue homeostasis. 82…”

Section: Hemoglobinmentioning

confidence: 99%

Advances in Hydrogels for Periodontitis Treatment

Li,

Wang,

Xiao

et al. 2024

ACS Biomater. Sci. Eng.

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Periodontitis is a common condition characterized by a bacterial infection and the disruption of the body's immune-inflammatory response, which causes damage to the teeth and supporting tissues and eventually results in tooth loss. Current therapy involves the systemic and local administration of antibiotics. However, the existing treatments cannot exert effective, sustained release and maintain an effective therapeutic concentration of the drug at the lesion site. Hydrogels are used to treat periodontitis due to their low cytotoxicity, exceptional water retention capability, and controlled drug release profile. Hydrogels can imitate the extracellular matrix of periodontal cells while offering suitable sites to load antibiotics. This article reviews the utilization of hydrogels for periodontitis therapy based on the pathogenesis and clinical manifestations of the disease. Additionally, the latest therapeutic strategies for smart hydrogels and the main techniques for hydrogel preparation have been discussed. The information will aid in designing and preparing future hydrogels for periodontitis treatment.

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“…It was previously reported that osmotic challenge of the inner ear activated the periaqueductal bone marrow and induced chemotactic attraction of monocytes, neutrophils and eosinophilic leukocytes to the ES 38 . The detailed mechanism of NET formation remains unclear but it may be caused by chromosomal DNA release following histone depolym- www.nature.com/scientificreports/ erization involving myeloperoxidase, neutrophil elastase, and peptidylarginine deiminase 4 39 . Interestingly, one of the MD patients in the current study carried multiple genetic variants associated with both autoimmune and autoinflammatory reactions and demonstrated vascular congestion over the ES, indicating vasculitis 15 .…”

Section: Existence Of Molecular Machinery In the Inner Ear And Es To ...mentioning

confidence: 99%

Elevated G-CSF, IL8, and HGF in patients with definite Meniere’s disease may indicate the role of NET formation in triggering autoimmunity and autoinflammation

Zou

Zhao

Song

et al. 2022

Sci Rep

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The etiology and mechanism causing Meniere’s disease (MD) are not understood. The present study investigated the possible molecular mechanism of autoimmunity and autoinflammation associated with MD. Thirty-eight patients with definite MD and 39 normal volunteers were recruited, and 48 human cytokines/chemokines were quantified. In patients with MD pure tone audiograms, tympanograms and standard blood tests were performed. The mean hearing loss in the worse ear was 44.1 dB nHL. Compared to the referents, the concentrations of TNFα, IL1α, IL8, CTACK, MIP1α, MIP1β, G-CSF, and HGF in the sera of patients with MD were significantly elevated, while those of TRAIL and PDGFBB were significantly decreased. The area under the receiver operating characteristic curve (AUC) showed that G-CSF, MIP1α, and IL8 were above 0.8 and could be used to diagnose MD (p < 0.01), and the AUCs of CTACK and HGF were above 0.7 and acceptable to discriminate the MD group from the control group (p < 0.01). The revised AUCs (1 − AUC) of TRAIL and PDGFBB were above 0.7 and could also be used in the diagnosis of MD (p < 0.01). The linear regression showed significant correlations between MIP1α and GCSF, between IL2Rα and GCSF, between IL8 and HGF, between MIP1α and IL8, and between SCF and CTACK; there was a marginal linear association between IP10 and MIP1α. Linear regression also showed that there were significant age-related correlations of CTACK and MIG expression in the MD group (p < 0.01, ANOVA) but not in the control group. We hypothesize that G-CSF, IL8, and HGF, which are involved in the development of neutrophil extracellular traps (NETs) and through various mechanisms influence the functions of macrophages, lymphocytes, and dendritic cells, among others, are key players in the development of EH and MD and could be useful in elucidating the pathophysiological mechanisms leading to MD. Biomarkers identified in the present study may suggest that both autoimmune and autoinflammatory mechanisms are involved in MD. In the future, it will be valuable to develop a cost-effective method to detect G-CSF, IL8, HGF, CTACK, MIP1α, TRAIL, and PDGFBB in the serum of patient that have diagnostic relevance.

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Levels of low-molecular-weight hyaluronan in periodontitis-treated patients and its immunostimulatory effects on CD4+ T lymphocytes

Cited by 9 publications

References 52 publications

N-Butyrylated Hyaluronic Acid Achieves Anti-Inflammatory Effects In Vitro and in Adjuvant-Induced Immune Activation in Rats

N-Butyrylated Hyaluronic Acid Achieves Anti-Inflammatory Effects In Vitro and in Adjuvant-Induced Immune Activation in Rats

Advances in Hydrogels for Periodontitis Treatment

Elevated G-CSF, IL8, and HGF in patients with definite Meniere’s disease may indicate the role of NET formation in triggering autoimmunity and autoinflammation

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