scholarly journals The Introduction of Human Heme Oxygenase‐1 and Soluble Tumor Necrosis Factor‐α Receptor Type I With Human IgG1 Fc in Porcine Islets Prolongs Islet Xenograft Survival in Humanized Mice

2015 ◽  
Vol 16 (1) ◽  
pp. 44-57 ◽  
Author(s):  
H.‐S. Lee ◽  
J.‐G. Lee ◽  
H. J. Yeom ◽  
Y. S. Chung ◽  
B. Kang ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Heme Oxygenase ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Humanized Mice ◽  
Heme Oxygenase 1 ◽  
Type I ◽  
Human Igg1 ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor α acceleration of inflammatory responses by down-regulating heme oxygenase 1 in human peripheral monocytes

2007 ◽  
Vol 56 (2) ◽  
pp. 464-475 ◽  
Author(s):  
Yohei Kirino ◽  
Mitsuhiro Takeno ◽  
Shuji Murakami ◽  
Masayoshi Kobayashi ◽  
Hideo Kobayashi ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Heme Oxygenase ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Inflammatory Responses ◽  
Heme Oxygenase 1 ◽  
Factor Α ◽  
Necrosis Factor

Heme oxygenase-1 inhibits TNF-α-induced apoptosis in cultured fibroblasts

2000 ◽  
Vol 278 (2) ◽  
pp. L312-L319 ◽  
Author(s):  
Irina Petrache ◽  
Leo E. Otterbein ◽  
Jawed Alam ◽  
Gordon W. Wiegand ◽  
Augustine M. K. Choi
Keyword(s):  
Carbon Monoxide ◽  
Tumor Necrosis Factor ◽  
Heme Oxygenase ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Heme Oxygenase 1 ◽  
Cultured Fibroblasts ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

Heme oxygenase (HO)-1 catalyzes the oxidative cleavage of heme to yield equimolar amounts of biliverdin, iron, and carbon monoxide. HO-1 is a stress response protein, the induction of which is associated with protection against oxidative stress. The mechanism(s) of protection is not completely elucidated, although it is suggested that one or more of the catalytic by-products provide antioxidant functions either directly or indirectly. The involvement of reactive oxygen species in apoptosis raised the question of a possible role for HO-1 in programmed cell death. Using the tetracycline-regulated expression system, we show here that conditional overexpression of HO-1 prevents tumor necrosis factor-α-induced apoptosis in murine L929 fibroblasts. Inhibition of apoptosis was not observed in the presence of tin protoporphyrin, a specific inhibitor of HO activity, and in cells overexpressing antisense HO-1. Interestingly, exogenous administration of a low concentration of carbon monoxide also prevented tumor necrosis factor-α-induced apoptosis in L929 fibroblasts. Inhibition of tumor necrosis factor-α-induced apoptosis by HO-1 overexpression was reversed by 1 H-(1,2,4)oxadiazolo(4,3- a)quinoxalin-1-one, an inhibitor of guanylate cyclase, which is a target enzyme for carbon monoxide. Taken together, our data suggest that the antiapoptotic effect of HO-1 may be mediated via carbon monoxide.

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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