scholarly journals Evaluation of the inflammatory response in experimentally induced synovitis in the horse: a comparison of recombinant equine interleukin 1 beta and lipopolysaccharide

2012 ◽  
Vol 20 (12) ◽  
pp. 1583-1590 ◽  
Author(s):  
T.N. Ross ◽  
J.D. Kisiday ◽  
T. Hess ◽  
C.W. McIlwraith
Keyword(s):  
Inflammatory Response ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Experimentally Induced

scholarly journals Transient inflammatory response mediated by interleukin-1β is required for proper regeneration in zebrafish fin fold

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Tomoya Hasegawa ◽  
Christopher J Hall ◽  
Philip S Crosier ◽  
Gembu Abe ◽  
Koichi Kawakami ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Tissue Regeneration ◽  
Essential Role ◽  
Tissue Injury ◽  
Interleukin 1 ◽  
Cellular Responses ◽  
Interleukin 1 Beta ◽  
Principal Source ◽  
Regenerative Cells ◽  
Underlying Processes

Cellular responses to injury are crucial for complete tissue regeneration, but their underlying processes remain incompletely elucidated. We have previously reported that myeloid-defective zebrafish mutants display apoptosis of regenerative cells during fin fold regeneration. Here, we found that the apoptosis phenotype is induced by prolonged expression of interleukin 1 beta (il1b). Myeloid cells are considered to be the principal source of Il1b, but we show that epithelial cells express il1b in response to tissue injury and initiate the inflammatory response, and that its resolution by macrophages is necessary for survival of regenerative cells. We further show that Il1b plays an essential role in normal fin fold regeneration by regulating expression of regeneration-induced genes. Our study reveals that proper levels of Il1b signaling and tissue inflammation, which are tuned by macrophages, play a crucial role in tissue regeneration.

scholarly journals Tumor necrosis factor alpha/cachectin and interleukin 1 beta initiate meningeal inflammation.

1990 ◽  
Vol 172 (2) ◽  
pp. 497-507 ◽  
Author(s):  
O Ramilo ◽  
X Sáez-Llorens ◽  
J Mertsola ◽  
H Jafari ◽  
K D Olsen ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Tnf Alpha ◽  
Interleukin 1 Beta ◽  
Necrosis Factor Alpha ◽  
Meningeal Inflammation ◽  
Factor Alpha ◽  
Necrosis Factor

Although previous studies using human cytokines in rabbits and rats have provided evidence of the participation of tumor necrosis factor alpha (TNF-alpha) and interleukin 1 beta (IL-1 beta) in the meningeal inflammatory cascade, the results obtained by several groups of investigators have been discordant or, at times, contradictory. In the present study, homologous cytokines were applied to the rabbit meningitis model. Intracisternal administration of 10(2)-10(5) IU of purified rabbit TNF-alpha (RaTNF-alpha) produced significant cerebrospinal fluid (CSF) inflammation. A similar response was observed after intracisternal inoculation of 5-200 ng of rabbit recombinant IL-1 beta (rrIL-1 beta). Preincubation of these two mediators with their specific antibodies resulted in an almost complete suppression of the CSF inflammatory response. In animals with Haemophilus influenzae type b lipooligosaccharide-induced meningitis, intracisternal administration of anti-rrIL-1 beta, anti-RaTNF-alpha, or both resulted in a significant modulation of meningeal inflammation. Simultaneous administration of 10(3) IU of RaTNF-alpha and 5 ng of rrIL-1 beta resulted in a synergistic inflammatory response manifested by a more rapid and significantly increased influx of white blood cells into the CSF compared with results after each cytokine given alone. These data provide evidence for a seminal role of TNF-alpha and IL-1 beta in the initial events of meningeal inflammation.

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