Analysis of Pro-inflammatory Cytokine and Type II Interferon Induction by Nanoparticles

2017 ◽  
pp. 173-187 ◽  
Author(s):  
Timothy M. Potter ◽  
Barry W. Neun ◽  
Jamie C. Rodriguez ◽  
Anna N. Ilinskaya ◽  
Marina A. Dobrovolskaia
Keyword(s):  
Inflammatory Cytokine ◽  
Type Ii ◽  
Interferon Induction

scholarly journals Type II Activation of Monocytes in Multiple Sclerosis

2021 ◽  
Author(s):  
◽  
Delgertsetseg Chuluundorj
Keyword(s):  
Multiple Sclerosis ◽  
Immune Complexes ◽  
Inflammatory Cytokine ◽  
Inflammatory Marker ◽  
Type I ◽  
Type Ii ◽  
Blood Monocytes ◽  
Therapeutic Approaches ◽  
Human Red Blood Cells

<p><b>Multiple sclerosis (MS) is an incurable autoimmune disease of the CNS. Although its cause is not known, immune cells are involved in the disease progression. Among these cells, type I monocytes are first to arrive to the brain and initiate inflammation; however, if monocytes are type II activated, they can inhibit inflammation. Previous research has shown that immune responses can be modulated by treatments, such as glatiramer acetate (GA) and immune complexes (IC). Therefore, we aimed to determine whether GA and IC can induce type II activation of monocytes in MS.</b></p> <p>Human blood monocytes from healthy volunteers and MS patients were stimulated in vitro with bacterial lipopolysaccharide (classical activation) in the presence or absence of GA and immune complexes (IC) composed of IVIG and human red blood cells (type II activation). Flow cytometry, ELISA and cytometric bead array were used to assess levels of marker expression and cytokine production in order to define the activation of monocytes.</p> <p>Interestingly, while both GA and IC induced type II activation of monocytes, the characteristics of these type II monocytes were distinct. We have found that monocytes from both healthy people and MS patients have significantly lower levels of inflammatory marker CD40 and higher levels of the anti-inflammatory cytokine IL-10 after treatment with IC. In contrast, GA treatment reduced the levels of CD40, CD86 and the inflammatory cytokine IL- 12. Moreover, the combined addition of GA and IC appeared to be more effective in type II activating monocytes than either agent alone. We also found that both CD14++CD16- and CD14+CD16+ monocyte subsets can be type II activated by the treatments; however, an interaction between the subsets impaired their response to the treatments.</p> <p>Our study suggests that treatments with GA and IC, especially in combination, are effective in type II activation of human monocytes and can be beneficial therapeutic approaches for multiple sclerosis.</p>

scholarly journals Type II interferon induction and passive transfer depress the murine cytochrome P-450 drug metabolism system.

1980 ◽  
Vol 17 (6) ◽  
pp. 969-972 ◽  
Author(s):  
G Sonnenfeld ◽  
C L Harned ◽  
S Thaniyavarn ◽  
T Huff ◽  
A D Mandel ◽  
...  
Keyword(s):  
Drug Metabolism ◽  
Passive Transfer ◽  
Type Ii ◽  
Interferon Induction ◽  
Cytochrome P 450

scholarly journals Interleukin-1β is a potential therapeutic target for periodontitis: a narrative review

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Ran Cheng ◽  
Zhiwu Wu ◽  
Mingming Li ◽  
Meiying Shao ◽  
Tao Hu
Keyword(s):  
Therapeutic Target ◽  
Type Ii Diabetes ◽  
Inflammatory Cytokine ◽  
Clinical Evidence ◽  
Type Ii Diabetes Mellitus ◽  
Therapeutic Strategies ◽  
Type Ii ◽  
Potential Therapeutic Target ◽  
Inflammatory Reactions ◽  
Future Potential

AbstractInterleukin(IL)-1β, a pro-inflammatory cytokine, was elevated and participates in periodontitis. Not only the link between IL-1β and periodontitis was proved by clinical evidence, but also the increased IL-1β triggers a series of inflammatory reactions and promotes bone resorption. Currently, IL-1β blockage has been therapeutic strategies for autoimmune and autoinflammatory diseases such as rheumatoid arthritis, cryopyrin-associated periodic syndromes, gout and type II diabetes mellitus. It is speculated that IL-1β be a potential therapeutic target for periodontitis. The review focuses on the production, mechanism, present treatments and future potential strategies for IL-1β in periodontitis.

scholarly journals Type II Activation of Monocytes in Multiple Sclerosis

2021 ◽  
Author(s):  
◽  
Delgertsetseg Chuluundorj
Keyword(s):  
Multiple Sclerosis ◽  
Immune Complexes ◽  
Inflammatory Cytokine ◽  
Inflammatory Marker ◽  
Type I ◽  
Type Ii ◽  
Blood Monocytes ◽  
Therapeutic Approaches ◽  
Human Red Blood Cells

<p><b>Multiple sclerosis (MS) is an incurable autoimmune disease of the CNS. Although its cause is not known, immune cells are involved in the disease progression. Among these cells, type I monocytes are first to arrive to the brain and initiate inflammation; however, if monocytes are type II activated, they can inhibit inflammation. Previous research has shown that immune responses can be modulated by treatments, such as glatiramer acetate (GA) and immune complexes (IC). Therefore, we aimed to determine whether GA and IC can induce type II activation of monocytes in MS.</b></p> <p>Human blood monocytes from healthy volunteers and MS patients were stimulated in vitro with bacterial lipopolysaccharide (classical activation) in the presence or absence of GA and immune complexes (IC) composed of IVIG and human red blood cells (type II activation). Flow cytometry, ELISA and cytometric bead array were used to assess levels of marker expression and cytokine production in order to define the activation of monocytes.</p> <p>Interestingly, while both GA and IC induced type II activation of monocytes, the characteristics of these type II monocytes were distinct. We have found that monocytes from both healthy people and MS patients have significantly lower levels of inflammatory marker CD40 and higher levels of the anti-inflammatory cytokine IL-10 after treatment with IC. In contrast, GA treatment reduced the levels of CD40, CD86 and the inflammatory cytokine IL- 12. Moreover, the combined addition of GA and IC appeared to be more effective in type II activating monocytes than either agent alone. We also found that both CD14++CD16- and CD14+CD16+ monocyte subsets can be type II activated by the treatments; however, an interaction between the subsets impaired their response to the treatments.</p> <p>Our study suggests that treatments with GA and IC, especially in combination, are effective in type II activation of human monocytes and can be beneficial therapeutic approaches for multiple sclerosis.</p>

Comparison of inflammatory cytokine levels among type I/type II and manic/hypomanic/euthymic/depressive states of bipolar disorder

2014 ◽  
Vol 166 ◽  
pp. 187-192 ◽  
Author(s):  
Ya-Mei Bai ◽  
Tung-Ping Su ◽  
Shih-Jen Tsai ◽  
Chiou Wen-Fei ◽  
Cheng-Ta Li ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Inflammatory Cytokine ◽  
Type I ◽  
Type Ii ◽  
Cytokine Levels ◽  
Depressive States

Type II Solar Radio Bursts over Solar Cycle 21

1994 ◽  
Vol 144 ◽  
pp. 283-284
Author(s):  
G. Maris ◽  
E. Tifrea
Keyword(s):  
Solar Radio ◽  
Interplanetary Space ◽  
Impulsive Phase ◽  
Radio Bursts ◽  
Type Ii ◽  
Solar Radio Bursts ◽  
Strong Energy ◽  
Mass Ejection ◽  
Geophysical Effect ◽  
Radio Event

The type II solar radio bursts produced by a shock wave passing through the solar corona are one of the most frequently studied solar activity phenomena. The scientific interest in this type of phenomenon is due to the fact that the presence of this radio event in a solar flare is an almost certain indicator of a future geophysical effect. The origin of the shock waves which produce these bursts is not at all simple; besides the shocks which are generated as a result of a strong energy release during the impulsive phase of a flare, there are also the shocks generated by a coronal mass ejection or the shocks which appear in the interplanetary space due to the supplementary acceleration of the solar particles.

Heat-Etching with a Bullivant Type II Simple Freeze-Cleave Device

1970 ◽  
Vol 28 ◽  
pp. 106-107 ◽  
Author(s):  
Ronald S. Weinstein ◽  
N. Scott McNutt
Keyword(s):  
New Zealand ◽  
General Hospital ◽  
Massachusetts General Hospital ◽  
Type I ◽  
Type Ii ◽  
Collaborative Effort ◽  
Temperature And Pressure ◽  
The University

The Type I simple cold block device was described by Bullivant and Ames in 1966 and represented the product of the first successful effort to simplify the equipment required to do sophisticated freeze-cleave techniques. Bullivant, Weinstein and Someda described the Type II device which is a modification of the Type I device and was developed as a collaborative effort at the Massachusetts General Hospital and the University of Auckland, New Zealand. The modifications reduced specimen contamination and provided controlled specimen warming for heat-etching of fracture faces. We have now tested the Mass. General Hospital version of the Type II device (called the “Type II-MGH device”) on a wide variety of biological specimens and have established temperature and pressure curves for routine heat-etching with the device.

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