Type I and Type II Interferons Inhibit Both Basal and Tumor Necrosis Factor-α-Induced CXCL8 Secretion in Primary Cultures of Human Thyrocytes

2013 ◽  
Vol 33 (9) ◽  
pp. 508-513 ◽  
Author(s):  
Mario Rotondi ◽  
Francesca Coperchini ◽  
Riccardo Sideri ◽  
Gloria Groppelli ◽  
Luca de Martinis ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Primary Cultures ◽  
Type I ◽  
Type Ii ◽  
Cxcl8 Secretion ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Cannabinoid Reduces Inflammatory Cytokines, Tumor Necrosis Factor-α, and Type I Interferons in Dermatomyositis In Vitro

2017 ◽  
Vol 137 (11) ◽  
pp. 2445-2447 ◽  
Author(s):  
Elizabeth S. Robinson ◽  
Paul Alves ◽  
Muhammad M. Bashir ◽  
Majid Zeidi ◽  
Rui Feng ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Cytokines ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Type I Interferons ◽  
Type I ◽  
Factor Α ◽  
Necrosis Factor

Anti-inflammatory Effects of Clostridial Collagenase

2015 ◽  
Vol 105 (6) ◽  
pp. 509-519 ◽  
Author(s):  
Richard C. Galperin ◽  
Darrell L. Lange ◽  
Sarah J. Ramsay ◽  
Lei Shi ◽  
Kathy A. Weedon ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Diabetic Patients ◽  
Type I ◽  
Resolution Of Inflammation ◽  
Markers Of Inflammation ◽  
Factor Α ◽  
Necrosis Factor

Background Digestion of collagen with clostridial collagenase (CC) produces peptides that can induce cellular responses consistent with wound healing in vivo. However, nonhealing human wounds are typically in a state of chronic inflammation. We evaluated the effects of CC on markers of inflammation in cell culture and wound fluid from diabetic patients. Methods Lipopolysaccharide-induced release of tumor necrosis factor-α and interleukin-6 from interferon-γ–activated THP-1 monocytes was measured in the presence or absence of CC or CC collagen digests. In the clinical study, 17 individuals with mildly inflamed diabetic foot ulcers were randomized to receive CC ointment (CCO) or hydrogel. Weekly assessments included wound appearance and measurements. Wound exudate was collected at baseline and at 2 and 4 weeks of treatment. A multiplex assay was used to measure levels of analytes, including those associated with inflammation and with inflammation resolution. Results Lower levels of tumor necrosis factor-α and interleukin-6 were found in media of cells cultured with CC or CC digests of collagen type I or III than for untreated lipopolysaccharide controls (P < .05). Clinically, CCO and hydrogel resulted in improvement in wound appearance and a decrease in mean wound area. The CCO, but not the hydrogel, was found to increase the level of analytes associated with resolution of inflammation while decreasing those associated with inflammation. There was a general correlation between resolution of inflammation and healing. Conclusions These results support a hypothesis that debridement with CCO is associated with decreased inflammation and greater progress toward healing.

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