scholarly journals Dexamethasone Promotes Aspergillus fumigatus Growth in Macrophages by Triggering M2 Repolarization via Targeting PKM2

2021 ◽  
Vol 7 (2) ◽  
pp. 70
Author(s):  
Maureen K. Luvanda ◽  
Wilfried Posch ◽  
Jonathan Vosper ◽  
Viktoria Zaderer ◽  
Asma Noureen ◽  
...  
Keyword(s):  
Aspergillus Fumigatus ◽  
Immune Modulation ◽  
Fungal Infections ◽  
Macrophage Polarization ◽  
Corticosteroid Treatment ◽  
High Morbidity ◽  
Phenotypic Properties ◽  
Metabolic Switch ◽  
Anti Inflammatory ◽  
The Impact

Since long-term corticosteroid treatment is associated with emerging opportunistic fungal infections causing high morbidity and mortality in immune-suppressed individuals, here we characterized the impact of dexamethasone (Dex) treatment on Aspergillus fumigatus-related immune modulation. We found by high content screening and flow cytometric analyses that during monocyte-to-macrophage differentiation, as little as 0.1 µg/mL Dex resulted in a shift in macrophage polarization from M1 to M2-like macrophages. This macrophage repolarization mediated via Dex was characterized by significant upregulation of the M2 marker CD163 and downmodulation of M1 markers CD40 and CD86 as well as changes in phenotypic properties and adherence. These Dex-mediated phenotypic alterations were furthermore associated with a metabolic switch in macrophages orchestrated via PKM2. Such treated macrophages lost their ability to prevent Aspergillus fumigatus germination, which was correlated with accelerated fungal growth, destruction of macrophages, and induction of an anti-inflammatory cytokine profile. Taken together, repolarization of macrophages following corticosteroid treatment and concomitant switch to an anti-inflammatory phenotype might play a prominent role in triggering invasive aspergillosis (IA) due to suppression of innate immunological responses necessary to combat extensive fungal outgrowth.

scholarly journals Comparative Phenotypic and Functional Analyses of the Effects of IL-10 or TGF-β on Porcine Macrophages

Animals ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 1098
Author(s):  
Tania Carta ◽  
Elisabetta Razzuoli ◽  
Floriana Fruscione ◽  
Susanna Zinellu ◽  
Dionigia Meloni ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
Phagocytic Cells ◽  
Mhc Ii ◽  
Tnf Α ◽  
Regulated Expression ◽  
Inflammatory Phenotype ◽  
Anti Inflammatory ◽  
Functional Analyses ◽  
The Impact ◽  
Immunosuppressive Cytokines

Macrophages are phagocytic cells involved in maintaining tissue homeostasis and defense against pathogens. Macrophages may be polarized into different functionally specialized subsets. M2c macrophages arise following stimulation with IL-10 or TGF-β and mediate anti-inflammatory and tissue repair functions. M2c macrophages remain poorly characterized in the pig, thus we investigated the impact of these regulatory cytokines on porcine monocyte-derived macrophages (moMΦ). The phenotype and functionality of these cells was characterized though confocal microscopy, flow cytometry, ELISA, and RT-qPCR. Both cytokines induced CD14 and MHC II DR down-regulation and reduced IL-6, TNF-α, and CD14 expression, suggestive of an anti-inflammatory phenotype. Interestingly, neither IL-10 or TGF-β were able to trigger IL-10 induction or release by moMΦ. Differences between these cytokines were observed: stimulation with IL-10, but not TGF-β, induced up-regulation of both CD16 and CD163 on moMΦ. In addition, IL-10 down-regulated expression of IL-1β and IL-12p40 4h post-stimulation and induced a stronger impairment of moMΦ ability to respond to either TLR2 or TLR4 agonists. Overall, our results provide an overview of porcine macrophage polarization by two immunosuppressive cytokines, revealing differences between IL-10 and TGF-β, and reporting some peculiarity of swine, which should be considered in translational studies.

scholarly journals Mechanisms Involved in Type II Macrophage Activation and Effector Functions

2021 ◽  
Author(s):  
◽  
Marie Clare Lydia Kharkrang
Keyword(s):  
Immune Responses ◽  
Inflammatory Responses ◽  
Surface Marker ◽  
Alternative Activation ◽  
Type Ii ◽  
Activated Macrophages ◽  
Phenotypic Properties ◽  
Anti Inflammatory ◽  
The Impact

<p>Autoimmunities are extremely difficult to treat and involved in their pathogenesis are pro-inflammatory immune responses redirected against one's own tissues. Studies in our lab have shown macrophages that are induced to become type II macrophages protect against an animal model of MS, experimental autoimmune encephalomyelitis (EAE), with protection due to immune deviation. Another way to deviate immune responses away from inflammation is by infection with the parasitic helminth Schistosoma mansoni, which also protects against EAE. The contribution of type II macrophages in this protection is unknown, as are the mechanisms involved in promoting the phenotype induced by type II activation. This project investigates key mechanisms involved in type II activation, while also elucidating the possible effect of schistosome exposure on the induction of this activation state. Using a validated model of type II activation in vitro, we compared the effects of schistosome immune complexes on various macrophage properties such as cytokine, surface marker and enzymatic profiles. This thesis identified that exposure to schistosome complexes induces a macrophage state with characteristics of two distinct activation states (type II and alternative activation), as well as completely novel characteristics. This activation state shows many phenotypic properties associated with immune regulation, and may have important consequences for understanding mechanisms involved in protection against inflammatory illnesses. We also investigated key mechanisms involved in the anti-inflammatory responses induced by type II activation. Cytokine, chemokine and surface marker profiles of macrophages were assessed in response to type II activation in vitro, with the main emphasis on determining the effects of IL-10 and CD40 on the type II activation phenotype and function. This investigation found that type II activated macrophages depend on low levels of CD40/CD40L signalling to polarise Th2 development, as the expression of receptors for Th2-inducing cytokines are significantly impaired in the absence of this interaction. This suggests an important role for the low but maintained levels of CD40 on type II activated macrophages, in aiding the deviation of immune responses, while maintaining Th2 polarization. We also suggest a suppressive role of CD40/CD40L in IL-10 production, which is a novel find. The requirement of new treatments for MS is escalating as more people are affected each year. The impact of MS on the quality of life is severe and long lasting. Having a greater understanding of the mechanisms involved in deviating pro-inflammatory or anti-inflammatory responses will enable the development of much more effective treatments and therapies in the future.</p>

scholarly journals Corticosteroids Impair Granulocyte Transfusion Therapy By Targeting NET Formation and Neutrophil Antifungal Functions Via ROS/Dectin1 Pathways

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 2506-2506 ◽  
Author(s):  
Natarajaswamy Kalleda ◽  
Jorge Amich ◽  
Spoorthi Poreddy ◽  
Berkan Arslan ◽  
Mike Friedrich ◽  
...  
Keyword(s):  
Mouse Models ◽  
Defense Mechanisms ◽  
Fungal Infections ◽  
Corticosteroid Treatment ◽  
High Morbidity ◽  
Granulocyte Transfusion ◽  
Transfusion Therapy ◽  
Neutropenic Patients

Abstract Introduction: Invasive pulmonary Aspergillus fumigatus infections cause high morbidity and mortality in neutropenic patients. Granulocyte transfusions have been tested as an alternative therapy for the management of high-risk neutropenic patients with invasive A. fumigatus infections. To increase the granulocyte yield for transfusion, donors are treated with corticosteroids. Yet, the efficacy of granulocyte transfusion and functional defense mechanisms of granulocytes collected from corticosteroid treated donors remain largely elusive. Therefore, we investigated the efficacy of granulocyte transfusion and functional defense mechanisms of corticosteroid treated granulocytes using mouse models. Methods: To determine the effects of corticosteroids on granulocytes to control A. fumigatus infections, we performed granulocyte adoptive cell transfers using in vivo mouse models, in vitro human and mouse granulocyte and A. fumigatus functional co-culture experiments in combination with flow cytometry, cytokine analysis, fluorescence and electron microscopy. Results: Transfusion of granulocytes from corticosteroid treated mice did not protect cyclophosphamide immunosuppressed mice against lethal A. fumigatus infection in contrast to granulocytes from untreated mice. Upon infection increased levels of inflammatory cytokines helped to recruit granulocytes to the lungs without any recruitment defects in corticosteroid treated and infected mice or in cyclophosphamide immunosuppressed and infected mice that had received the granulocytes from corticosteroid treated mice. However, corticosteroid treated human or mouse neutrophils failed to form neutrophil extracellular traps (NETs) under in vitro and in vivo conditions. Furthermore, corticosteroid treated granulocytes exhibited impaired ROS production against A. fumigatus. Notably, corticosteroids impaired the β-glucan receptor Dectin-1 (CLEC7A) on mouse and human granulocytes to efficiently recognize and phagocytize A. fumigatus, which markedly impaired fungal killing. Conclusions: We conclude that corticosteroid treatment of granulocyte donors for increasing neutrophil yields or patients with ongoing corticosteroid treatment could result in deleterious effects on granulocyte antifungal functions, thereby limiting the benefit of granulocyte transfusion therapies against invasive fungal infections. Disclosures Einsele: Celgene: Consultancy, Honoraria, Speakers Bureau; Janssen: Consultancy, Honoraria, Speakers Bureau; Novartis: Consultancy, Honoraria; Amgen: Consultancy, Honoraria, Speakers Bureau.

scholarly journals HLA-DRB1 allelic epitopes that associate with autoimmune disease risk or protection activate reciprocal macrophage polarization

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Vincent van Drongelen ◽  
Bruna Miglioranza Scavuzzi ◽  
Sarah Veloso Nogueira ◽  
Frederick W. Miller ◽  
Amr H. Sawalha ◽  
...  
Keyword(s):  
Autoimmune Disease ◽  
Immune Modulation ◽  
Disease Risk ◽  
Macrophage Polarization ◽  
Specific Antigen ◽  
Human Leukocyte ◽  
Allele Specific ◽  
Anti Inflammatory ◽  
Mechanistic Basis

AbstractAssociations between particular human leukocyte antigen (HLA) alleles and susceptibility to—or protection from—autoimmune diseases have been long observed. Allele-specific antigen presentation (AP) has been widely proposed as a culprit, but it is unclear whether HLA molecules might also have non-AP, disease-modulating effects. Here we demonstrate differential macrophage activation by HLA-DRB1 alleles known to associate with autoimmune disease risk or protection with resultant polarization of pro-inflammatory (“M1”) versus anti-inflammatory (“M2”) macrophages, respectively. RNA-sequencing analyses of in vitro-polarized macrophages in the presence of AP-incompetent short synthetic peptides corresponding to the third allelic hypervariable regions coded by those two HLA-DRB1 alleles showed reciprocal activation of pro- versus anti-inflammatory transcriptomes, with implication of corresponding gene ontologies and upstream regulators. These results identify a previously unrecognized mechanism of differential immune modulation by short HLA-DRB1-coded allelic epitopes independent of AP, and could shed new light on the mechanistic basis of HLA-disease association.

scholarly journals Mechanisms Involved in Type II Macrophage Activation and Effector Functions

2021 ◽  
Author(s):  
◽  
Marie Clare Lydia Kharkrang
Keyword(s):  
Immune Responses ◽  
Inflammatory Responses ◽  
Surface Marker ◽  
Alternative Activation ◽  
Type Ii ◽  
Activated Macrophages ◽  
Phenotypic Properties ◽  
Anti Inflammatory ◽  
The Impact

<p>Autoimmunities are extremely difficult to treat and involved in their pathogenesis are pro-inflammatory immune responses redirected against one's own tissues. Studies in our lab have shown macrophages that are induced to become type II macrophages protect against an animal model of MS, experimental autoimmune encephalomyelitis (EAE), with protection due to immune deviation. Another way to deviate immune responses away from inflammation is by infection with the parasitic helminth Schistosoma mansoni, which also protects against EAE. The contribution of type II macrophages in this protection is unknown, as are the mechanisms involved in promoting the phenotype induced by type II activation. This project investigates key mechanisms involved in type II activation, while also elucidating the possible effect of schistosome exposure on the induction of this activation state. Using a validated model of type II activation in vitro, we compared the effects of schistosome immune complexes on various macrophage properties such as cytokine, surface marker and enzymatic profiles. This thesis identified that exposure to schistosome complexes induces a macrophage state with characteristics of two distinct activation states (type II and alternative activation), as well as completely novel characteristics. This activation state shows many phenotypic properties associated with immune regulation, and may have important consequences for understanding mechanisms involved in protection against inflammatory illnesses. We also investigated key mechanisms involved in the anti-inflammatory responses induced by type II activation. Cytokine, chemokine and surface marker profiles of macrophages were assessed in response to type II activation in vitro, with the main emphasis on determining the effects of IL-10 and CD40 on the type II activation phenotype and function. This investigation found that type II activated macrophages depend on low levels of CD40/CD40L signalling to polarise Th2 development, as the expression of receptors for Th2-inducing cytokines are significantly impaired in the absence of this interaction. This suggests an important role for the low but maintained levels of CD40 on type II activated macrophages, in aiding the deviation of immune responses, while maintaining Th2 polarization. We also suggest a suppressive role of CD40/CD40L in IL-10 production, which is a novel find. The requirement of new treatments for MS is escalating as more people are affected each year. The impact of MS on the quality of life is severe and long lasting. Having a greater understanding of the mechanisms involved in deviating pro-inflammatory or anti-inflammatory responses will enable the development of much more effective treatments and therapies in the future.</p>

scholarly journals C1q/TNF-Related Protein 3 (CTRP-3) Deficiency of Adipocytes Affects White Adipose Tissue Mass but Not Systemic CTRP-3 Concentrations

2021 ◽  
Vol 22 (4) ◽  
pp. 1670
Author(s):  
Andreas Schmid ◽  
Martin Roderfeld ◽  
Jonas Gehl ◽  
Elke Roeb ◽  
Andrea Nist ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Peroxisome Proliferator ◽  
Related Protein ◽  
Tissue Mass ◽  
Inflammatory Phenotype ◽  
Anti Inflammatory ◽  
The Impact

CTRP-3 (C1q/TNF-related protein-3) is an adipokine with endocrine and immunological function. The impact of adipocyte CTRP-3 production on systemic CTRP-3 concentrations and on adipocyte biology is unknown. A murine model of adipocyte CTRP-3 knockout (KO) was established (via the Cre/loxP system). Serum adipokine levels were quantified by ELISA and adipose tissue (AT) gene expression by real-time PCR. Preadipocytes were isolated from AT and differentiated into adipocytes. Comparative transcriptome analysis was applied in adipocytes and liver tissue. Body weight and AT mass were reduced in CTRP-3 KO mice together with decreased serum leptin. In primary cells from visceral AT of KO mice, expression of adiponectin, progranulin, and resistin was induced, while peroxisome proliferator activated receptor γ (PPARγ) was decreased. M1/M2 macrophage polarization markers were shifted to a more anti-inflammatory phenotype. CTRP-3 expression in AT did not contribute to serum concentrations. AT and liver morphology remained unaffected by CTRP-3 KO. Myelin transcription factor 1-like (Myt1l) was identified as a highly upregulated gene. In conclusion, adipocyte CTRP-3 has a role in adipogenesis and AT weight gain whereas adipocyte differentiation is not impaired by CTRP-3 deficiency. Since no effects on circulating CTRP-3 levels were observed, the impact of adipocyte CTRP-3 KO is limited to adipose tissue. Modified AT gene expression indicates a rather anti-inflammatory phenotype.

scholarly journals Karakteristik penyakit kulit pada anak di poliklinik kulit dan kelamin RSUP. Dr. M. Djamil Padang periode 2016-2018

2020 ◽  
Vol 20 (3) ◽  
Author(s):  
Rina Gustia ◽  
Satya Wydya Yenny ◽  
Sigya Octari
Keyword(s):  
Fungal Infection ◽  
Skin Disease ◽  
Medical Records ◽  
Skin Diseases ◽  
Fungal Infections ◽  
Common Disease ◽  
High Morbidity ◽  
Common Skin ◽  
The Impact

Abstrak. Latar belakang : Penyakit kulit menyebabkan morbiditas yang tinggi, termasuk pada anak. Prevalensi dermatosis pada anak berkisar 34-87,7% dengan pola yang sangat bervariasi dan dipengaruhi oleh banyak faktor. Dampak penyakit kulit ini dapat mempengaruhi kualitas hidup anak.Metode : Penelitian retrospektif deskriptif  dengan  mengambil data dari rekam medis pasien anak dengan umur 1-18 tahun yang berobat ke Poliklinik Kulit dan Kelamin RSUP.Dr. M. Djamil Padang pada periode Januari 2016– Desember 2018. Hasil : Selama 3 tahun didapatkan 277 pasien baru, perempuan 123 (44,4%) dan laki - laki 154 (55,6%). Berdasarkan kelompok  penyakit yang terbanyak adalah dermatitis  (29, 9%), diikuti oleh infeksi jamur (16,9%), infestasi parasit (13, 4%),  infeksi virus (13, 3%), dan infeksi bakteri (6,9%).Kesimpulan:  Penyakit kulit terbanyak terjadi pada anak laki – laki. Infeksi jamur merupakan penyakit kulit paling sering, diikuti oleh infestasi parasit. Infeksi jamur yang sering terjadi adalah pitiriasis versikolor, sedangkan infestasi parasit yang paling sering adalah skabies.              Kata kunci: karakteristik penyakit kulit, anak, penelitian retrospektif Abstrack. Background: Skin disease causes high morbidity, including in children. The prevalence of dermatosis in children ranges from 34 to 87.7% with a pattern that is varied and influenced by many factors. The impact of this skin disease can affect the quality of life of childrenMethod : A descriptive retrospective, which is taking data from the medical records of patients aged 1 - 18 years who seek treatment at Dermatology and Venereology outpatient clinic at RSUP. M. Djamil Padang in the period January 2016 - December 2018.Result : During 3 years,there were 277 new patient which consist of 123 boy  (44.4%) and 154 girl (55.6%). Based on the group of diseases, dermatitis were the most common  disease (29,9%), followed by fungal infection (16.9%), parasit infestations (13,4%), viral infection (13,3%) and bacterial infection (6,9%). Conclusion : Most skin diseases occur in boys. Fungal infections were the most common skin diseases, followed by parasit infestations. The most common fungal infection is pityriasis versicolor, while the most frequent parasit infestation is scabies.Keywords:characterization of skin diseases, children, retrospective study

scholarly journals The Impact of the PCSK-9 / VLDL-Receptor Axis on Inflammatory Cell Polarization

2021 ◽  
Author(s):  
Maria Luisa Barcena ◽  
Misael Estepa ◽  
Louis Marx ◽  
Anne Breiter ◽  
Natalie Haritonow ◽  
...  
Keyword(s):  
Inflammatory Cell ◽  
Macrophage Polarization ◽  
Inflammatory Cells ◽  
Cell Polarization ◽  
Pcsk9 Inhibitors ◽  
Tnf Α ◽  
Inflammatory Phenotype ◽  
Ifn Γ ◽  
Anti Inflammatory ◽  
The Impact

Abstract Background: Studies have shown that lipoproteins, including LDL, VLDL, and ApoE2 have an impact on macrophage polarization, important to atherosclerosis progression. PCSK9 is a key mediator regulating the expression of lipoprotein receptors. The present study investigates the effect of the VLDL/VLDL-R axis on mononuclear cell polarization, as well as the role of PCSK9 and PCSK9 inhibitors (PCSK9i) within this network.Methods: Human monocytic THP-1 cells and human monocyte-derived macrophages isolated from PBMC were treated with LPS/IFN-γ to induce a pro-inflammatory phenotype or with IL-4 /IL-13 to induce an anti-inflammatory phenotype. Cells were then subjected to further treatments including VLDL, LDL, PCSK9, PCSK9i, anti-LDL-R; PMA and TSP-1.Results: LPS/IFN-γ treatment promoted a pro-inflammatory state with an increased expression of pro-inflammatory mediators e.g., TNF-α, CD80, and IL-1β. VLDL co-treatment induced a switch of this pro-inflammatory phenotype to an anti-inflammatory phenotype. In pro-inflammatory cells, VLDL significantly decreased the expression of the M1-markers e.g., TNF-α, CD80, and IL-1β. These effects were eliminated by PCSK9 and restored by co-incubation with a PCSK9i. Migration assays demonstrated that pro-inflammatory cells displayed a significantly higher invasive capacity compared to untreated cells or anti-inflammatory cells. Moreover, pro-inflammatory cell chemotaxis was significantly decreased by VLDL-mediated acquisition of the anti-inflammatory phenotype. PCSK9 significantly lessened this VLDL-mediated migration inhibition, which was reversed by the PCSK9i.Conclusion: VLDL promotes macrophage differentiation towards the anti-inflammatory phenotype. PCSK9, via its capacity to inhibit VLDL-R expression, reverses the VLDL-mediated anti-inflammatory switch, thereby promoting a pro-inflammatory phenotype. Thus, anti-PCSK9 therapies may exert pro-inflammatory suppression within the vessel wall.

scholarly journals Proteoglycan-4 is an Essential Regulator of Synovial Macrophage Polarization and Inflammatory Macrophage Joint Infiltration

2021 ◽  
Author(s):  
Marwa Qadri ◽  
Gregory D. Jay ◽  
Ling X. Zhang ◽  
Tannin A. Schmidt ◽  
Jennifer Totonchy ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
Polarization Spectrum ◽  
Membrane Thickness ◽  
Type I ◽  
Synovial Hyperplasia ◽  
Arginase 1 ◽  
Liposomal Clodronate ◽  
Inflammatory Phenotype ◽  
Anti Inflammatory ◽  
The Impact

Abstract Background: Synovial macrophages (SMs) perform a multitude of functions that include clearance of cell debris and foreign bodies, tissue immune surveillance, and resolution of inflammation. At one end of the macrophage polarization spectrum is the inflammatory phenotype (M1), which secretes IL-1β, IL-6 and expresses iNOS. On the opposite end of the spectrum is the anti-inflammatory phenotype (M2) which is characterized by the secretion of IL-10 and TGF-β. PRG4 is an important regulator of synovial hyperplasia and fibrotic remodeling and the involvement of SM activation in PRG4’s homeostatic role is yet to be defined. Our objectives were to study PRG4’s importance to SM homeostasis, M1 and M2 polarization and joint infiltration of bone marrow-derived macrophages (BMDMs) and investigate the role of SMs in mediating synovial fibrosis in Prg4 gene-trap (Prg4GT/GT) murine knee joints.Methods: SM phenotyping in Prg4GT/GT and Prg4+/+ joints was performed using flow cytometry and the balance between CD86+/CD206- (M1) and CD86-/CD206+ (M2) SMs was studied as animals aged. Expression of iNOS and IL-6 in CD86+ SMs, arginase-1 in CD206+ SMs and the impact of Prg4 recombination on SM polarization and BMDM infiltration following a TLR2 agonist challenge were determined. Inflammatory SMs were depleted using liposomal clodronate and synovial membrane thickness and expression of fibrotic markers: α-SMA, PLOD2 and collagen type I (COL-I) were assessed using immunohistochemistry.Results: Total macrophages in Prg4GT/GT joints were higher than corresponding age-matched Prg4+/+ joints (p<0.0001) and the percentages of CD86+/CD206- and CD86+/CD206+ SMs increased in Prg4GT/GT joints as animals aged (p<0.0001), whereas the percentage of CD86-/CD206+ SMs decreased (p<0.001). CD86+ SMs expressed iNOS and IL-6 compared to CD86- SMs (p<0.0001) while CD206+ SMs also expressed arginase-1. Prg4 re-expression limited the accumulation of CD86+ SMs, increased CD86-/CD206+ SMs and attenuated BMDM recruitment (p<0.001). Liposomal clodronate reduced inflammatory SMs and in turn reduced synovial hyperplasia, α-SMA, PLOD2 and COL-I expression in the synovium (p<0.0001).Conclusions: SM accumulation in the joint and the balance between inflammatory and anti-inflammatory SM subsets are regulated by PRG4. In the absence of PRG4’s role, the synovium is populated with inflammatory macrophages that drive synovial fibrosis.

The anti-inflammatory effect of external use and the impact on scalded mice model of Arisaema

2014 ◽  
Author(s):  
Mingsan Miao ◽  
Dandan Liu ◽  
Jiaojiao Jia ◽  
Xiaofang Guo ◽  
Kai Xiao
Keyword(s):  
Mice Model ◽  
Anti Inflammatory ◽  
The Impact ◽  
Inflammatory Effect
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