Inhibition of Proinflammatory Cytokines in Cutibacterium acnes-Induced Inflammation in HaCaT Cells by Using Buddleja davidii Aqueous Extract

Acne is an inflammatory skin disorder; although some anti-inflammatory medicines for treating acne are available in a market, they have considerable side effects; therefore, new treatment options are needed. In the present study, among the 16 aqueous extracts of plants collected from Jeju Island in Korea which are used to test anti-inflammatory activity, B. davidii showed the strong decline of the proinflammatory cytokine expression against the inflammatory process caused by C. acnes in Human HaCaT keratinocyte cells. B. davidii downregulated the expression of 57% of COX-2, 41% of iNOS, and proinflammatory cytokines 29% of TNF-α, 32% of IL-1β, 21% of IL-6, and 35% of IL-8. Furthermore, B. davidii inhibited NF-κB and MAPK signaling cascades in keratinocytes that activated by toll-like receptor 2 (TLR-2) in response to C. acnes. Given those results, B. davidii is a potential agent to reduce the proinflammatory cytokine expression against C. acnes-induced inflammation and might provide an alternative to the current medications.

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Differential Regulation of Proinflammatory Cytokine Expression by Mitogen-Activated Protein Kinases in Macrophages in Response to Intestinal Parasite Infection

Infection and Immunity ◽

10.1128/iai.02279-14 ◽

2014 ◽

Vol 82 (11) ◽

pp. 4789-4801 ◽

Cited By ~ 26

Author(s):

Mei Xing Lim ◽

Chin Wen Png ◽

Crispina Yan Bing Tay ◽

Joshua Ding Wei Teo ◽

Huipeng Jiao ◽

...

Keyword(s):

Protein Expression ◽

Proinflammatory Cytokines ◽

Proinflammatory Cytokine ◽

Map Kinases ◽

Cytokine Expression ◽

Content Type ◽

Erk Activation ◽

Proinflammatory Cytokine Expression ◽

Tnf Α ◽

Mitogen Activated Protein

ABSTRACTBlastocystisis a common enteric protistan parasite that can cause acute, as well as chronic, infection and is associated with irritable bowel syndrome (IBS). However, the pathogenic status ofBlastocystisinfection remains unclear. In this study, we found thatBlastocystisantigens induced abundant expression of proinflammatory cytokines, including interleukin 1β (IL-1β), IL-6, and tumor necrosis factor alpha (TNF-α), in mouse intestinal explants, in mouse colitis colon, and in macrophages. Further investigation utilizing RAW264.7 murine macrophages showed thatBlastocystistreatment in RAW264.7 macrophages induced the activation of ERK, JNK, and p38, the three major groups of mammalian mitogen-activated protein (MAP) kinases that play essential roles in the expression of proinflammatory cytokines. ERK inhibition in macrophages significantly suppressed both mRNA and protein expression of IL-6 and TNF-α and mRNA expression of IL-1β. On the other hand, JNK inhibition resulted in reductions in both c-Jun and ERK activation and significant suppression of all three proinflammatory cytokines at both the mRNA and protein levels. Inhibition of p38 suppressed only IL-6 protein expression with no effect on the expression of IL-1β and TNF-α. Furthermore, we found that serine proteases produced byBlastocystisplay an important role in the induction of ERK activation and proinflammatory cytokine expression by macrophages. Our study thus demonstrated for the first time thatBlastocystiscould induce the expression of various proinflammatory cytokines via the activation of MAP kinases and that infection withBlastocystismay contribute to the pathogenesis of inflammatory intestinal diseases through the activation of inflammatory pathways in host immune cells, such as macrophages.

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Activated cholangiocytes release macrophage-polarizing extracellular vesicles bearing the DAMP S100A11

AJP Cell Physiology ◽

10.1152/ajpcell.00250.2019 ◽

2019 ◽

Vol 317 (4) ◽

pp. C788-C799 ◽

Cited By ~ 7

Author(s):

Tomohiro Katsumi ◽

Maria Eugenia Guicciardi ◽

Adiba Azad ◽

Steven F. Bronk ◽

Anuradha Krishnan ◽

...

Keyword(s):

Mrna Expression ◽

Cell Lines ◽

Extracellular Vesicles ◽

Proinflammatory Cytokines ◽

Proinflammatory Cytokine ◽

Inflammatory Diseases ◽

Cell Communication ◽

Cytokine Expression ◽

Proinflammatory Cytokine Expression ◽

Primary Mouse

In mouse models of biliary tract diseases, macrophages are recruited to the periductal milieu and promote injury and cholestasis. Although cell necrosis with release of biomolecules termed damage-associated molecular patterns (DAMPs) promotes recruitment and activation of macrophages, necrosis was not observed in these studies. Because extracellular vesicles (EVs) are important in cell-to-cell communication, we postulated that activated cholangiocytes may release EVs containing DAMPs as cargo. Both the human (NHC) and mouse cholangiocyte (603B) cell lines display constitutive activation with mRNA expression of chemokines. Proteomic analysis revealed that EVs from both cell lines contained the DAMP S100A11, a ligand for the receptor for advanced glycation end products (RAGE). Bone marrow-derived macrophages (BMDM) incubated with EVs derived from the mouse 603B cell line increased mRNA expression of proinflammatory cytokines. Genetic or pharmacologic inhibition of RAGE reduced BMDM expression of proinflammatory cytokines treated with EVs. RAGE signaling resulted in activation of the canonical NF-κB pathway, and consistently, proinflammatory cytokine expression was blunted by the IKKα/β inhibitor TPCA-1 in BMDM incubated with EVs. We also demonstrated that primary mouse cholangiocyte-derived organoids express chemokines indicating cholangiocyte activation, release EVs containing S100A11, and stimulate proinflammatory cytokine expression in BMDM by a RAGE-dependent pathway. In conclusion, these observations identify a non-cell death mechanism for cellular release of DAMPs by activated cholangiocytes, namely by releasing DAMPs as EV cargo. These data also suggest RAGE inhibitors may be salutary in macrophage-associated inflammatory diseases of the bile ducts.

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Pancreatitis-Associated Ascitic Fluid Induces Proinflammatory Cytokine Expression in THP-1 Cells by Inhibiting Anti-inflammatory Signaling

Pancreas ◽

10.1097/mpa.0b013e318279fe5c ◽

2013 ◽

Vol 42 (5) ◽

pp. 855-860 ◽

Cited By ~ 12

Author(s):

Jing Wang ◽

Ping Xu ◽

Yan-Qiang Hou ◽

Kai Xu ◽

Qing-Hua Li ◽

...

Keyword(s):

Ascitic Fluid ◽

Proinflammatory Cytokine ◽

Cytokine Expression ◽

Inflammatory Signaling ◽

Proinflammatory Cytokine Expression ◽

Anti Inflammatory

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Biomimetic nanotherapy: core–shell structured nanocomplexes based on the neutrophil membrane for targeted therapy of lymphoma

Journal of Nanobiotechnology ◽

10.1186/s12951-021-00922-4 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Qiangqiang Zhao ◽

Duanfeng Jiang ◽

Xiaoying Sun ◽

Qiuyu Mo ◽

Shaobin Chen ◽

...

Keyword(s):

Mesoporous Silica Nanoparticles ◽

Treatment Options ◽

Inflammatory Factors ◽

Main Method ◽

Tnf Α ◽

Good Biocompatibility ◽

Inflammatory Drugs ◽

Anti Inflammatory ◽

New Treatment ◽

Lymphoma Therapy

Abstract Background Non-Hodgkin’s lymphoma (NHL) is a malignant disease of lymphoid tissue. At present, chemotherapy is still the main method for the treatment of NHL. R-CHOP can significantly improve the survival rate of patients. Unfortunately, DOX is the main cytotoxic drug in R-CHOP and it can lead to adverse reactions. Therefore, it is particularly important to uncover new treatment options for NHL. Results In this study, a novel anti-tumor nanoparticle complex Nm@MSNs-DOX/SM was designed and constructed in this study. Mesoporous silica nanoparticles (MSNs) loaded with Doxorubicin (DOX) and anti-inflammatory drugs Shanzhiside methylester (SM) were used as the core of nanoparticles. Neutrophil membrane (Nm) can be coated with multiple nanonuclei as a shell. DOX combined with SM can enhance the anti-tumor effect, and induce apoptosis of lymphoma cells and inhibit the expression of inflammatory factors related to tumorigenesis depending on the regulation of Bcl-2 family-mediated mitochondrial pathways, such as TNF-α and IL-1β. Consequently, the tumor microenvironment (TME) was reshaped, and the anti-tumor effect of DOX was amplified. Besides, Nm has good biocompatibility and can enhance the EPR effect of Nm@MSNs-DOX/SM and increase the effect of active targeting tumors. Conclusions This suggests that the Nm-modified drug delivery system Nm@MSNs-DOX/SM is a promising targeted chemotherapy and anti-inflammatory therapy nanocomplex, and may be employed as a specific and efficient anti-Lymphoma therapy.

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