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IL-1bInterleukin-1 Beta
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Some pro-inflammatory cytokines, particularly IL-1b, can access and ultimately influence the brain by several special pathways before stimulating the release of corticotropin-releasing hormone (CRH) or arginine vasopressin (AVP) from para-ventricular nucleus of the hypothalamus, which activates the release of adrenocorticotropic hormone (ACTH) from the pituitary, which, in turn, travels to the adrenals, stimulating the release of cortisol.22 It is known that corticosteroid secreting rhythm disturbance plays a critical role in the mechanism of depression.23 Thus, T2S with comorbid depression occurs possibly through such a mechanism.
Association of IL-1A and IL-1B polymorphisms with ankylosing spondylitis among the Chinese Han population: a case-control study.
Analysis of inflammatory markers in the blood after 8 months on treatment showed that methotrexate had no effect on levels of IL-1B, IL-6, and hsCRP.
[23,24] Platelets produce endogenous danger signals, i.e., CD40L and IL-1b that affect the dendritic cells activation in tissue injury.
IL-1B drives inflammatory responses to Propionibacterium acnes in vitro and in vivo.
Eradication rate of Helicobacter pylori according to genotypes of CYP2C19, IL-1B, and TNF-A.
Emerging evidence suggests they constitutively produce cytokines (e.g., IL-1b, IL-2, IL-8, IL-10, IL-4, IL-17, IFN-g, TGF-b, and TNF-[alpha]) (54,55).
At the time of ENL reaction there were also increases in serum TGF-[beta], interferon gamma (INF-I3), interleukin-10 (IL-10), IL-6, IL-8 and IL-1B, while IL-4 and IL-5 remained unchanged.5 In this study of 22 patients, who experienced recurrent ENL reaction, the highest levels of TGF-[beta] at a level of 50-100 pg/ml were seen in 10 (45.5%) patients, with a mean of 62.6 +- 30.4 pg/ml, in contrast to the control group, with nonrecurring reaction, the highest level of < 50 pg/ml was seen in 12 (54.6%) patients with a mean of 47 +- 21.6 pg/ml.
IL-1b, TNF-a and IL-6 release from monocytes in haemodialysis patients in relation to dialytic age.
In the present study, we have endeavored to show that only serum IL-1B, among several proinflammatory cytokines and other traditional measures of inflammation, acted as a promising disease biomarker in predicting the activity of CPA, by exploring its association with the patients' clinical manifestations, microbiological manifestations, laboratory test results, and imaging findings.
The amount of IL-1b, IL-6, CXCL8, TNF alpha, CCL2, and PTX3 was determined using commercially available ELISA kits (R&D Systems Inc., Minneapolis, MN, USA), according to the manufacturer's protocols.
According to Wilson et al.'s experiment, IL-1b could induce cell apoptosis in the corneal stroma, altering the normal architecture of the tissue in keratoconus patients [28].