scholarly journals The influence of surface modified poly(l-lactic acid) films on the differentiation of human monocytes into macrophages

2017 ◽  
Vol 5 (3) ◽  
pp. 551-560 ◽  
Author(s):  
Clara R. Correia ◽  
Joana Gaifem ◽  
Mariana B. Oliveira ◽  
Ricardo Silvestre ◽  
João F. Mano

The interaction of human monocytes with different surface modified poly(l-lactic acid) films was evaluated. All surface modified films disrupted the balance of macrophage polarization towards a favorable anti-inflammatory profile, particularly after an LPS stimulus.

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Caroline M vanStijn ◽  
Jason Kim ◽  
Rajendra K Tangirala

Adiponectin, an adipocytokine produced by the adipose tissue, exerts metabolic, anti-inflammatory and anti-atherogenic effects to ameliorate diabetes and cardiovascular disease and is a potentially important therapeutic target. However, mechanisms of adiponectin vascular actions and the regulation of macrophage adiponectin receptor expression under inflammatory/atherogenic activation remain unclear. Our studies with human monocytes/macrophages revealed differential adiponectin receptor regulation in subjects with insulin-resistance. Here, we investigated adiponectin regulation of macrophage gene expression under pro- and anti-inflammatory conditions. We addressed the hypothesis that differential activation of macrophages into the classical (M1) or alternative (M2) program alters their adiponectin receptor (AdipoR1 and AdipoR2) expression. The microarray gene expression analyses in human monocytes exposed to TNF-α showed that adiponectin inhibited several inflammatory/atherogenic genes. Our studies revealed that adiponectin itself induces AdipoR1 and AdipoR2 expression in macrophages. We further investigated the effects of macrophage polarization (M1 or M2) on adiponectin receptor expression in bone marrow-derived and peritoneal macrophages. These studies demonstrated that M1 activation (IFN-γ and LPS) significantly reduced AdipoR1 and AdipoR2 expression. In contrast, M2 activation of (IL-4 or IL-10) maintains a significantly higher level of AdipoR1 and AdipoR2. In M2 activation, adiponectin receptor expression was more substantial in IL-10 than IL-4-polarized macrophages. These results provide important evidence that macrophage polarization profoundly alters their adiponectin receptor expression and thus functional responses to adiponectin. Thus, adiponectin-mediated macrophage functions are regulated by adiponectin receptor expression which is modulated by the macrophage polarization which controls their inflammatory and atherogenic properties.


Biomedicines ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 24
Author(s):  
David Rivera ◽  
Yanet Ocampo ◽  
Luis A. Franco

As part of the search for new bioactive plants from the Colombian Caribbean, the dichloromethane fraction of the calyces of Physalis angulata L. (PADF) was selected for its anti-inflammatory activity. In this work, we investigated the immunomodulatory effect of PADF in activated macrophages and during dextran sulfate sodium (DSS)-induced colitis. PADF displayed a low content of withanolides or phenolic compounds, and a higher content of sucrose esters, representative anti-inflammatory metabolites of the Physalis genus. The PADF fraction at 12.5 μg/mL prevented the induction of interleukin (IL)-1β, tumor necrosis factor (TNF-α), IL-6, IL-12, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) by lipopolysaccharide (LPS), while increased the levels of arginase (ARG1), IL-10, and mannose receptor C (MRC1). The polarization towards an anti-inflammatory profile was also observed in resting macrophages, without promoting the typical gene profile induced by IL-4, suggesting that PADF promotes a shift to a regulatory status rather than to an alternative one. In vivo, the administration of PADF to mice with chronic DSS-colitis reduced disease signs (i.e., body weight loss and colon shortening), and improved the histology score by diminishing the levels of pro-inflammatory cytokines and increasing the production of IL-10. Overall, results suggest that the regulatory effect on PADF towards macrophages might contribute to the therapeutic activity observed in the murine model of inflammatory bowel disease.


Pneumologie ◽  
2015 ◽  
Vol 69 (07) ◽  
Author(s):  
A Zakrzewicz ◽  
S Wilker ◽  
S Janciauskiene ◽  
R Tikkanen ◽  
W Padberg ◽  
...  

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Jiaqi Wang ◽  
Shanshan Lu ◽  
Fuming Yang ◽  
Yi Guo ◽  
Zelin Chen ◽  
...  

AbstractAcupuncture is used in the treatment of a variety of inflammatory conditions and diseases. However, the mechanisms of its anti-inflammatory action are complex and have not been systematically investigated. Macrophages are key components of the innate immune system, thus, balancing the M1/M2 macrophage ratio and modulating cytokine levels in the inflammatory environment may be desirable therapeutic goals. Evidence has shown that acupuncture has anti-inflammatory actions that affect multiple body systems, including the immune, locomotory, endocrine, nervous, digestive, and respiratory systems, by downregulating pro-inflammatory M1 and upregulating anti-inflammatory M2 macrophages, as well as by modulating associated cytokine secretion. Macrophage polarization is controlled by the interlocking pathways of extrinsic factors, the local tissue microenvironment, and the neural-endocrine-immune systems. It has been suggested that polarization of T lymphocytes and cytokine secretions resulting in modulation of the autonomic nervous system and the hypothalamic–pituitary–adrenal axis, may be upstream mechanisms of acupuncture-induced macrophage polarization. We further propose that macrophage polarization could be the principal pathway involved in acupuncture immune regulation and provide the scientific basis for the clinical application of acupuncture in inflammatory conditions.


Author(s):  
Aureli Luquero ◽  
Gemma Vilahur ◽  
Javier Crespo ◽  
Lina Badimon ◽  
Maria Borrell‐Pages

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Keizo Kohno ◽  
Satomi Koya-Miyata ◽  
Akira Harashima ◽  
Takahiko Tsukuda ◽  
Masataka Katakami ◽  
...  

Abstract Background NK-4 has been used to promote wound healing since the early-1950s; however, the mechanism of action of NK-4 is unknown. In this study, we examined whether NK-4 exerts a regulatory effect on macrophages, which play multiple roles during wound healing from the initial inflammatory phase until the tissue regeneration phase. Results NK-4 treatment of THP-1 macrophages induced morphological features characteristic of classically-activated M1 macrophages, an inflammatory cytokine profile, and increased expression of the M1 macrophage-associated molecules CD38 and CD86. Interestingly, NK-4 augmented TNF-α production by THP-1 macrophages in combination with LPS, Pam3CSK4, or poly(I:C). Furthermore, NK-4 treatment enhanced THP-1 macrophage phagocytosis of latex beads. These results indicate that NK-4 drives macrophage polarization toward an inflammatory M1-like phenotype with increased phagocytic activity. Efferocytosis is a crucial event for resolution of the inflammatory phase in wound healing. NK-4-treated THP-1 macrophages co-cultured with apoptotic Jurkat E6.1 (Apo-J) cells switched from an M1-like phenotype to an M2-like phenotype, as seen in the inverted ratio of TNF-α to IL-10 produced in response to LPS. We identified two separate mechanisms that are involved in this phenotypic switch. First, recognition of phosphatidylserine molecules on Apo-J cells by THP-1 macrophages downregulates TNF-α production. Second, phagocytosis of Apo-J cells by THP-1 macrophages and activation of PI3K/Akt signaling pathway upregulates IL-10 production. Conclusion It is postulated that the phenotypic switch from a proinflammatory M1-like phenotype to an anti-inflammatory M2-like phenotype is dysregulated due to impaired efferocytosis of apoptotic neutrophils at the wound site. Our results demonstrate that NK-4 improves phagocytosis of apoptotic cells, suggesting its potential as a therapeutic strategy to resolve sustained inflammation in chronic wounds.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wuyang Huang ◽  
Ky Young Cho ◽  
Di Meng ◽  
W. Allan Walker

AbstractAn excessive intestinal inflammatory response may have a role in the pathogenesis of necrotizing enterocolitis (NEC) in very preterm infants. Indole-3-lactic acid (ILA) of breastmilk tryptophan was identified as the anti-inflammatory metabolite involved in probiotic conditioned media from Bifidobacteria longum subsp infantis. This study aimed to explore the molecular endocytic pathways involved in the protective ILA effect against inflammation. H4 cells, Caco-2 cells, C57BL/6 pup and adult mice were used to compare the anti-inflammatory mechanisms between immature and mature enterocytes in vitro and in vivo. The results show that ILA has pleiotropic protective effects on immature enterocytes including anti-inflammatory, anti-viral, and developmental regulatory potentials in a region-dependent and an age-dependent manner. Quantitative transcriptomic analysis revealed a new mechanistic model in which STAT1 pathways play an important role in IL-1β-induced inflammation and ILA has a regulatory effect on STAT1 pathways. These studies were validated by real-time RT-qPCR and STAT1 inhibitor experiments. Different protective reactions of ILA between immature and mature enterocytes indicated that ILA’s effects are developmentally regulated. These findings may be helpful in preventing NEC for premature infants.


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