scholarly journals The Role of Cytokines Produced via the NLRP3 Inflammasome in Mouse Macrophages Stimulated with Dental Calculus in Osteoclastogenesis

2021 ◽  
Vol 22 (22) ◽  
pp. 12434
Author(s):  
Megumi Mae ◽  
Mohammad Ibtehaz Alam ◽  
Yasunori Yamashita ◽  
Yukio Ozaki ◽  
Kanako Higuchi ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Alveolar Bone ◽  
Mouse Bone Marrow ◽  
Dependent Manner ◽  
Deficient Mouse ◽  
Dental Calculus ◽  
Mouse Macrophages ◽  
D Cells ◽  
Culture Supernatants

Dental calculus (DC) is a common deposit in periodontitis patients. We have previously shown that DC contains both microbial components and calcium phosphate crystals that induce an osteoclastogenic cytokine IL-1β via the NLRP3 inflammasome in macrophages. In this study, we examined the effects of cytokines produced by mouse macrophages stimulated with DC on osteoclastogenesis. The culture supernatants from wild-type (WT) mouse macrophages stimulated with DC accelerated osteoclastogenesis in RANKL-primed mouse bone marrow macrophages (BMMs), but inhibited osteoclastogenesis in RANKL-primed RAW-D cells. WT, but not NLRP3-deficient, mouse macrophages stimulated with DC produced IL-1β and IL-18 in a dose-dependent manner, indicating the NLRP3 inflammasome-dependent production of IL-1β and IL-18. Both WT and NLRP3-deficient mouse macrophages stimulated with DC produced IL-10, indicating the NLRP3 inflammasome-independent production of IL-10. Recombinant IL-1β accelerated osteoclastogenesis in both RANKL-primed BMMs and RAW-D cells, whereas recombinant IL-18 and IL-10 inhibited osteoclastogenesis. These results indicate that DC induces osteoclastogenic IL-1β in an NLRP3 inflammasome-dependent manner and anti-osteogenic IL-18 and IL-10 dependently and independently of the NLRP3 inflammasome, respectively. DC may promote alveolar bone resorption via IL-1β induction in periodontitis patients, but suppress resorption via IL-18 and IL-10 induction in some circumstances.

scholarly journals Giardia duodenalis Induces Proinflammatory Cytokine Production in Mouse Macrophages via TLR9-Mediated p38 and ERK Signaling Pathways

2021 ◽  
Vol 9 ◽  
Author(s):  
Xudong Pu ◽  
Xin Li ◽  
Lili Cao ◽  
Kaiming Yue ◽  
Panpan Zhao ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathways ◽  
Proinflammatory Cytokines ◽  
Giardia Duodenalis ◽  
Erk Signaling ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Mouse Macrophages ◽  
Host Inflammatory Response

Giardia duodenalis, also known as Giardia lamblia or Giardia intestinalis, is an important opportunistic, pathogenic, zoonotic, protozoan parasite that infects the small intestines of humans and animals, causing giardiasis. Several studies have demonstrated that innate immunity-associated Toll-like receptors (TLRs) are critical for the elimination of G. duodenalis; however, whether TLR9 has a role in innate immune responses against Giardia infection remains unknown. In the present study, various methods, including reverse transcriptase–quantitative polymerase chain reaction, Western blot, enzyme-linked immunosorbent assay, immunofluorescence, inhibitor assays, and small-interfering RNA interference, were utilized to probe the role of TLR9 in mouse macrophage-mediated defenses against G. lamblia virus (GLV)–free or GLV-containing Giardia trophozoites. The results revealed that in G. duodenalis–stimulated mouse macrophages, the secretion of proinflammatory cytokines, including interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and IL-12 p40, was enhanced, concomitant with the significant activation of TLR9, whereas silencing TLR9 attenuated the host inflammatory response. Notably, the presence of GLV exacerbated the secretion of host proinflammatory cytokines. Moreover, G. duodenalis stimulation activated multiple signaling pathways, including the nuclear factor κB p65 (NF-κB p65), p38, ERK, and AKT pathways, the latter three in a TLR9-dependent manner. Additionally, inhibiting the p38 or ERK pathway downregulated the G. duodenalis–induced inflammatory response, whereas AKT inhibition aggravated this process. Taken together, these results indicated that G. duodenalis may induce the secretion of proinflammatory cytokines by activating the p38 and ERK signaling pathways in a TLR9-dependent manner in mouse macrophages. Our in vitro findings on the mechanism underlying the TLR9-mediated host inflammatory response may help establish the foundation for an in-depth investigation of the role of TLR9 in the pathogenicity of G. duodenalis.

scholarly journals A Novel View of the Role of Prostaglandin E2 (PGE2) in Facilitating Engraftment of HSPCs By Activating the NOX2-ROS-Nlrp3 Inflammasome Axis to Incorporate the CXCR4 Receptor into Membrane Lipid Rafts

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 3-3
Author(s):  
Magdalena Kucia ◽  
Kamila Bujko ◽  
Arjun Thapa ◽  
Janina Ratajczak ◽  
Mariusz Z Ratajczak
Keyword(s):  
Lipid Rafts ◽  
Lipid Raft ◽  
Nlrp3 Inflammasome ◽  
Membrane Lipid ◽  
Inflammasome Activation ◽  
Dependent Manner ◽  
Hematopoietic Stem ◽  
Cxcr4 Receptor ◽  
Nlrp3 Inflammasomes

Background . It is known that prostaglandin E2 (PGE2) increases the homing and engraftment of hematopoietic stem/progenitor cells (HSPCs). However, aside from its role in upregulation of CXCR4 receptor expression on the surface of these cells, the exact mechanism has not been proposed. We have demonstrated in the past that an important step enabling the migration of HSPCs is the incorporation of CXCR4 into membrane lipid rafts on the leading surface (leading edge, in two dimensions) of migrating cells, which facilitates its interaction with cell migration signaling pathways (Wysoczynski M et al. Incorporation of CXCR4 into membrane lipid rafts primes homing-related responses of hematopoietic stem/progenitor cells to an SDF-1 gradient. Blood. 2005;105(1):40-48). Recently, we reported that Nlrp3 inflammasome-deficient HSPCs show a defect in lipid raft formation that results in defective migration of these cells in response to an SDF-1 gradient and their defective homing and engraftment after transplantation (Adamiak, M et al. Nlrp3 Inflammasome Signaling Regulates the Homing and Engraftment of Hematopoietic Stem Cells (HSPCs) by Enhancing Incorporation of CXCR4 Receptor into Membrane Lipid Rafts. Stem Cell Rev and Rep (2020). https://doi.org/10.1007/s12015-020-10005-w). An important activator of Nlrp3 inflammasomes is reactive oxygen species (ROS). Importantly, the enzyme that generates ROS, known as NADPH oxidase 2 (NOX2), is also associated with cell membrane lipid rafts. Hypothesis. Given the known roles of PGE2, membrane lipid rafts, and the Nlrp3 inflammasome in migration, homing, and engraftment of HSPCs, we hypothesized that PGE2 signaling promotes Nlrp3 inflammasome activation in a Nox2-ROS-dependent manner that results in incorporation of CXCR4 into membrane lipid rafts, which better explains the role of PGE2 in these phenomena.Materials and Methods. To test this hypothesis, murine SKL and human CD34+ cells enriched for HSPCs were stimulated with PGE2 to evaluate activation of genes of the Nlrp3 inflammasome complex at the mRNA and protein levels. Next, HSPCs from Nox2-KO mice were tested for membrane lipid raft formation in functional chemotaxis assays in response to SDF-1 gradients under conditions promoting membrane lipid raft formation. Formation of membrane lipid rafts in Nox2-KO cells was also evaluated by confocal analysis in the presence or absence of PGE2. Finally, the effect of the PGE2-Nox2-Nlrp3 inflammasome axis on the formation of membrane lipid rafts was evaluated in the presence of the ROS scavenger N-acethyl-cysteine (NAC). Results. We provide for the first time evidence that PGE2 activates Nlrp3 inflammasomes in HSPCs in a Nox2-ROS-dependent manner. This Nlrp3 inflammasome activation increases at the leading surface of migrating HSPCs with incorporation of the CXCR4 receptor into membrane lipid rafts. Formation of membrane lipid rafts was absent in Nox2-KO and Nlrp3-KO mouse HSPCs and in normal wild type cells after their exposure to NAC. Moreover, we also observed that Nox2-KO and Nlrp3-KO mice had a lower basal level of CXCR4 expression. Conclusions. Our results for the first time explain the role of PGE2 in promoting homing and migration of HSPCs, which occurs in response to PGE2 by activation of the Nox2-ROS-Nlrp3 inflammasome axis and thereby promotes incorporation of the CXCR4 receptor into membrane lipid rafts. Moreover, basal expression of the CXCR4 receptor was at a low level on the surface of HSPCs from Nlrp3-KO mice. Thus, our results provide evidence for the importance of the Nox2-ROS-Nlrp3 inflammasome axis in PGE2-mediated homing and engraftment of HSPCs and the role of PGE2-mediated lipid raft formation for optimal responsiveness of CXCR4 to SDF-1 in the BM microenvironment. Disclosures No relevant conflicts of interest to declare.

Phytocystatin CsinCPI-2 Reduces Osteoclastogenesis and Alveolar Bone Loss

2021 ◽  
pp. 002203452110278
Author(s):  
N. Da Ponte Leguizamón ◽  
R.S. de Molon ◽  
G. Coletto-Nunes ◽  
A.V.B. Nogueira ◽  
S.V. Rocha ◽  
...  
Keyword(s):  
Bone Loss ◽  
Connective Tissue ◽  
Alveolar Bone ◽  
Osteoclast Differentiation ◽  
Alveolar Bone Loss ◽  
Inflammatory Cell Infiltrate ◽  
Mouse Bone Marrow ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Chronic Inflammatory Condition

Periodontal disease (PD) is a polymicrobial chronic inflammatory condition of the supporting tissues around the teeth, leading to the destruction of surrounding connective tissue. During the progression of PD, osteoclasts play a crucial role in the resorption of alveolar bone that eventually leads to the loss of teeth if the PD is left untreated. Therefore, the development of antiresorptive therapies targeting bone-resorbing cells will significantly benefit the treatment of PD. Here, we demonstrate the inhibitory effect of CsinCPI-2, a novel cysteine peptidase inhibitor from the orange tree, on periodontitis-induced inflammation, alveolar bone loss, and osteoclast differentiation. Using the ligature-induced periodontitis model in mice, we show that treatment with CsinCPI-2 (0.8 µg/g of body weight) significantly reduced inflammatory cell infiltrate in the connective tissue and prevented the loss of alveolar bone mass (BV/TV) caused by PD, effects associated with diminished numbers of TRAP-positive multinucleated cells. Furthermore, CsinCPI-2 significantly downregulated the numbers of inflammatory cells expressing CD3, CD45, MAC387, and IL-1β. In vitro, CsinCPI-2 inhibited RANKL-induced TRAP+ multinucleated osteoclast formation in mouse bone marrow macrophage cultures in a concentration-dependent manner. This effect was not due to cytotoxicity, as demonstrated by the MTT assay. CsinCPI-2 inhibited RANKL-induced mRNA expression of Acp5, Calcr, and Ctsk, as well as the RANKL-induced upregulation of Nfatc1, a crucial transcription factor for osteoclast differentiation. Based on our findings, CsinCPI-2 prevents bone loss induced by PD by controlling the inflammatory process and acting directly on osteoclastogenesis, suggesting an interesting potential for CsinCPI-2 in the strategy for PD treatment.

scholarly journals Important role of EP4, a subtype of prostaglandin (PG) E receptor, in osteoclast-like cell formation from mouse bone marrow cells induced by PGE2

1998 ◽  
Vol 158 (3) ◽  
pp. R1-R5 ◽  
Author(s):  
K Ono ◽  
T Akatsu ◽  
T Murakami ◽  
M Nishikawa ◽  
M Yamamoto ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Cells ◽  
Bone Marrow Cells ◽  
Therapeutic Potential ◽  
Cell Formation ◽  
Mouse Bone Marrow ◽  
Dependent Manner ◽  
Clinical Conditions

Of various PGs, PGE1 and PGE2 are shown to be the most potent stimulators of osteoclastogenesis in vitro. PGE receptors have been classified into four subtypes, EP1-EP4. Little is known about PGE receptors functioning in bone cells. In this study, using mouse marrow culture, we investigated which PGE receptors are important in osteoclast-like cell (OCL) formation induced by PGE. 11-deoxy-PGE1 (EP2, EP3 and EP4 agonist) stimulated OCL formation potently. Butaprost (EP2 agonist) stimulated it slightly, while sulprostone (EP1 and EP3 agonist) and ONO-AP-324-01 (EP3 agonist) did not. AH23848B (EP4 antagonist) inhibited PGE2-induced OCL formation in a dose-dependent manner. The expression of EP4 mRNA in mouse bone marrow was confirmed by RT-PCR. The results indicate an important role of EP4 in PGE2-induced OCL formation in marrow cultures and suggest therapeutic potential of EP4 antagonists in some clinical conditions with accelerated bone resorption.

Effects of Sulfonylureas on Periodontopathic Bacteria-Induced Inflammation

2020 ◽  
Vol 99 (7) ◽  
pp. 830-838 ◽  
Author(s):  
Y. Kawahara ◽  
T. Kaneko ◽  
Y. Yoshinaga ◽  
Y. Arita ◽  
K. Nakamura ◽  
...  
Keyword(s):  
Cell Death ◽  
Nlrp3 Inflammasome ◽  
Alveolar Bone ◽  
Periodontal Diseases ◽  
Human Monocyte ◽  
Periodontal Pathogen ◽  
Enzyme Linked Immunosorbent Assay ◽  
Periodontopathic Bacteria ◽  
Caspase 1 ◽  
Culture Supernatants

Interleukin-1β (IL-1β) is an inflammatory cytokine produced by monocytes/macrophages and is closely associated with periodontal diseases. The NLRP3 inflammasome is involved in IL-1β activation through pro–IL-1β processing and pyroptotic cell death in bacterial infection. Recently, glyburide, a hypoglycemic sulfonylurea, has been reported to reduce IL-1β activation by suppressing activation of the NLRP3 inflammasome. Therefore, we evaluated the possibility of targeting the NLRP3 inflammasome pathway by glyburide to suppress periodontal pathogen-induced inflammation. THP-1 cells (a human monocyte cell line) were differentiated to macrophage-like cells by treatment with phorbol 12-myristate 13-acetate and stimulated by periodontopathic bacteria, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, or Fusobacterium nucleatum, in the presence of glyburide. IL-1β and caspase-1 expression in the cells and culture supernatants were analyzed by Western blotting and enzyme-linked immunosorbent assay, and cell death was analyzed by lactate dehydrogenase assay. Stimulation of THP-1 macrophage-like cells with every periodontopathic bacteria induced IL-1β secretion without cell death, which was suppressed by the NLRP3 inhibitor, MCC950, and caspase-1 inhibitor, z-YVAD-FMK. Glyburide treatment suppressed IL-1β expression in culture supernatants and enhanced intracellular IL-1β expression, suggesting that glyburide may have inhibited IL-1β secretion. Subsequently, a periodontitis rat model was generated by injecting periodontal bacteria into the gingiva, which was analyzed histologically. Oral administration of glyburide significantly suppressed the infiltration of inflammatory cells and the number of osteoclasts in the alveolar bone compared with the control. In addition to glyburide, glimepiride was shown to suppress the release of IL-1β from THP-1 macrophage-like cells, whereas other sulfonylureas (tolbutamide and gliclazide) or other hypoglycemic drugs belonging to the biguanide family, such as metformin, failed to suppress IL-1β release. Our results suggest that pharmacological targeting of the NLRP3 pathway may be a strategy for suppressing periodontal diseases.

scholarly journals Role of the DinB Homologs Rv1537 and Rv3056 in Mycobacterium tuberculosis

2010 ◽  
Vol 192 (8) ◽  
pp. 2220-2227 ◽  
Author(s):  
Bavesh D. Kana ◽  
Garth L. Abrahams ◽  
Nackmoon Sung ◽  
Digby F. Warner ◽  
Bhavna G. Gordhan ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Alkylating Agents ◽  
Spontaneous Mutation ◽  
Dna Polymerases ◽  
Binding Motif ◽  
Dependent Manner ◽  
Mouse Macrophages ◽  
Y Family

ABSTRACT The environment encountered by Mycobacterium tuberculosis during infection is genotoxic. Most bacteria tolerate DNA damage by engaging specialized DNA polymerases that catalyze translesion synthesis (TLS) across sites of damage. M. tuberculosis possesses two putative members of the DinB class of Y-family DNA polymerases, DinB1 (Rv1537) and DinB2 (Rv3056); however, their role in damage tolerance, mutagenesis, and survival is unknown. Here, both dinB1 and dinB2 are shown to be expressed in vitro in a growth phase-dependent manner, with dinB2 levels 12- to 40-fold higher than those of dinB1. Yeast two-hybrid analyses revealed that DinB1, but not DinB2, interacts with the β-clamp, consistent with its canonical C-terminal β-binding motif. However, knockout of dinB1, dinB2, or both had no effect on the susceptibility of M. tuberculosis to compounds that form N 2-dG adducts and alkylating agents. Similarly, deletion of these genes individually or in combination did not affect the rate of spontaneous mutation to rifampin resistance or the spectrum of resistance-conferring rpoB mutations and had no impact on growth or survival in human or mouse macrophages or in mice. Moreover, neither gene conferred a mutator phenotype when expressed ectopically in Mycobacterium smegmatis. The lack of the effect of altering the complements or expression levels of dinB1 and/or dinB2 under conditions predicted to be phenotypically revealing suggests that the DinB homologs from M. tuberculosis do not behave like their counterparts from other organisms.

scholarly journals Sphingosine Kinases are Involved in Macrophage NLRP3 Inflammasome Transcriptional Induction

2020 ◽  
Vol 21 (13) ◽  
pp. 4733
Author(s):  
Shahzad Nawaz Syed ◽  
Andreas Weigert ◽  
Bernhard Brüne
Keyword(s):  
Nlrp3 Inflammasome ◽  
De Novo ◽  
Inflammasome Activation ◽  
Relative Contribution ◽  
Mouse Macrophages ◽  
Sphingosine Kinases ◽  
Transcriptional Induction ◽  
Human And Mouse ◽  
Inflammasome Activity

Recent studies suggested an important contribution of sphingosine-1-phospate (S1P) signaling via its specific receptors (S1PRs) in the production of pro-inflammatory mediators such as Interleukin (IL)-1β in cancer and inflammation. In an inflammation-driven cancer setting, we previously reported that myeloid S1PR1 signaling induces IL-1β production by enhancing NLRP3 (NOD-, LRR- and Pyrin Domain-Containing Protein 3) inflammasome activity. However, the autocrine role of S1P and enzymes acting on the S1P rheostat in myeloid cells are unknown. Using human and mouse macrophages with pharmacological or genetic intervention we explored the relative contribution of sphingosine kinases (SPHKs) in NLRP3 inflammasome activity regulation. We noticed redundancy in SPHK1 and SPHK2 activities towards macrophage NLRP3 inflammasome transcriptional induction and IL-1β secretion. However, pharmacological blockade of both kinases in unison completely abrogated NLRP3 inflammasome induction and IL-1β secretion. Interestingly, human and mouse macrophages demonstrate varied responses towards SPHKs inhibition and IL-1β secretion. Clinical datasets of renal cell carcinoma and psoriasis patients showed a positive correlation between enzymes affecting the S1P rheostat with NLRP3 inflammasome components expression, which corroborates our finding. Our data provide a better understanding on the role of SPHKs and de novo synthesized S1P in macrophage NLRP3 inflammasome activation.

scholarly journals NLRP3 Inflammasome Promotes the Progression of Acute Myeloid Leukemia via IL-1β Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Chaoqing Zhong ◽  
Ruiqing Wang ◽  
Mingqiang Hua ◽  
Chen Zhang ◽  
Fengjiao Han ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Myeloid Leukemia ◽  
Nlrp3 Inflammasome ◽  
Myeloid Leukemia ◽  
Therapeutic Option ◽  
Leukemia Cells ◽  
Dependent Manner ◽  
Networks Analysis ◽  
Acute Myeloid

NLRP3 inflammasome has been reported to be associated with the pathogenesis of multiple solid tumors. However, the role of NLRP3 inflammasome in acute myeloid leukemia (AML) remains unclear. We showed that NLRP3 inflammasome is over-expressed and highly activated in AML bone marrow leukemia cells, which is correlated with poor prognosis. The activation of NLRP3 inflammasome in AML cells promotes leukemia cells proliferation, inhibits apoptosis and increases resistance to chemotherapy, while inactivation of NLRP3 by caspase-1 or NF-κB inhibitor shows leukemia-suppressing effects. Bayesian networks analysis and cell co-culture tests further suggest that NLRP3 inflammasome acts through IL-1β but not IL-18 in AML. Knocking down endogenous IL-1β or anti-IL-1β antibody inhibits leukemia cells whereas IL-1β cytokine enhances leukemia proliferation. In AML murine model, up-regulation of NLRP3 increases the leukemia burden in bone marrow, spleen and liver, and shortens the survival time; furthermore, knocking out NLRP3 inhibits leukemia progression. Collectively, all these evidences demonstrate that NLRP3 inflammasome promotes AML progression in an IL-1β dependent manner, and targeting NLRP3 inflammasome may provide a novel therapeutic option for AML.

Activation of local innate immune signal induces periodontitis in microbiota-dependent manner

2019 ◽  
Vol 366 (12) ◽  
Author(s):  
Nan Wang ◽  
Dengsheng Xia
Keyword(s):  
Alveolar Bone ◽  
Chronic Inflammatory Disease ◽  
Systemic Administration ◽  
Innate Immune ◽  
Dependent Manner ◽  
Local Inflammation ◽  
Tlr2 Activation ◽  
The Difference ◽  
The Relationship

ABSTRACT Periodontitis is a chronic inflammatory disease. Both inflammation and dysbiosis have been implicated in periodontitis development. However, the relationship between local inflammation and dysbiosis, and the precise roles of local inflammation in periodontitis are not well-elucidated. In present study, we explored the role of local inflammation in periodontitis. We established a periodontitis model by administration of Pam3CSK4 to local oral area and compared the difference of outcome between local and systemic administration. We monitored the pro-inflammatory cytokine expression, local inflammation and alveolar bone loss. We also evaluated the dysbiosis, NF-κB activation. Local but not systemic administration of Pam3CSK4-induced pro-inflammatory cytokines productions and finally resulted in periodontitis. Pam3CSK4 caused dysbiosis and promoted Porphyromonas gingivalis growth. The bacterial growth and NF-κB activation were required for Pam3CSK4-induced periodontitis. We evaluated the effect of local inflammation by inducing TLR2 activation on dysbiosis and periodontitis. Activation of local innate immune signal induces periodontitis in microbiota-dependent manner.

scholarly journals TNFRSF21 participates in Streptococcus agalactiae-induced inflammatory necrosis through the NLRP3 inflammasome pathway

2021 ◽  
Author(s):  
Lu Yuan ◽  
Jian Ruan ◽  
Mangling Zhang ◽  
Xiaojun Jiang ◽  
Jun Li ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Streptococcus Agalactiae ◽  
Nlrp3 Inflammasome ◽  
Bovine Mastitis ◽  
Animal Husbandry ◽  
Economic Loss ◽  
Dependent Manner ◽  
Isolation And Identification ◽  
Inflammatory Cytokine Production

Abstract Bovine mastitis caused by Streptococcus agalactiae (S. agalactiae) has resulted in substantial economic loss to the animal husbandry industry; however, the associated molecular mechanism remains unclear and the role of TNFRSF21 in the inflammatory response caused by S. agalactiae is unknown. In this study, we focused on bacterial isolation and identification, histological observations, and provide the first report of the association between TNFRSF21 and pyroptosis. The results showed that S. agalactiae-induced inflammation can cause increasing damage of the tissue and pyroptosis ratio, significantly increased the level of inflammatory cytokine production (e.g., NLRP3, caspase-1, and IL-1β), and upregulate TNFRSF21 following S. agalactiae infection in a time-dependent manner. In conclusion, these findings indicated that it may fight against the inflammatory response induced by S. agalactiae by inhibiting TNFRSF21 expression and reducing NLRP3 inflammasome pathway-mediated inflammatory necrosis.

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