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At least 109 records · Page 6Linked to original sources
PubMed1993

[Cytokine and inflammation: role of IL-5 and its receptor system in inflammation].

The inflammatory response is mediated by various cytokines. IL-5 is one of the inflammatory cytokines. The study of IL-5 has its origins in the search for one of the B-cell differentiation factors, named T-cell-replacing factor (TRF), that induces antigen-stimulated B cells to differentiate into antibody-forming cells. Eosinophil-differentiation factor, EDF, is a factor produced by thoracic duct lymphocytes of parasite-infected rats. cDNA cloning and mAb against IL-5 enable us to identify this molecule as a cytokine (TRF/EDF) that has pleiotropic activity on various target cells besides B cells and eosinophils. The pleiotropic activity of IL-5 is directly dependent on the initial binding to the IL-5 receptor (IL-5R) on the target cell surface. IL-5 transduces its signals through high affinity IL-5R which is constructed by two distinct polypeptides, alpha and beta. IL-5R alpha binds IL-5 with low affinity and associates with the beta chain which can convert low affinity IL-5R to high affinity IL-5R. IL-5R beta that does not bind IL-5 by itself is essential for the IL-5 signaling and is shared among IL-5R, IL-3R, and GM-CSFR. These results imply why IL-5, IL-3, and GM-CSF are eosinophylopoietin. The truncated IL-5R alpha and IL-5R beta complexes can not transduce IL-5 signals, although they bound IL-5 with high affinity, suggesting that IL-5-specific signaling may be transduced through IL-5R alpha.

Animals↗
PubMed2003

The radioprotective activities of turpentine-induced inflammation and alpha2-macroglobulin: the effect of dexamethasone on the radioprotective efficacy of the inflammation.

This work was aimed at the radioprotective efficacy of turpentine oil (TO), alpha2-Macroglobulin (alpha2-M), Amifostine (Ami) and/or dexamethasone (Dex). These agents were administrated, alone or in combination, prior to irradiation of rats with 6.7 Gy (LD(50/30)). The survival was recorded daily for 4 weeks after irradiation and body weight, peripheral leukocytes and thrombocytes were measured. The plasma concentration of alpha2-M and other acute phase proteins were determined by crossed immunoelectrophoresis. All rats receiving alpha2-M and Ami alone or in combination survived the radiation injury, whereas the rate of survival of TO-treated rats was 90%. Radiation and therapy-induced changes in the expression of acute phase protein genes were atypical for the acute phase reaction. Dex alone was lethal for 45% and 55% of control and irradiated rats, respectively. Pretreatment with 1mg Dex reduced radioprotective efficacy of TO and Ami to 30% and 40%, respectively. Given together TO and Ami provided 70% protection to rats receiving Dex. The TO and alpha2-M enhanced the rate of survival from 50% to 90% and 100%, respectively. In the presence of 1mg Dex the TO-induced radioprotectors and Ami exhibited radiosensitizing rather than radioprotecting activities.

Amifostine↗
PubMed2003

STAT4 signal pathways regulate inflammation and airway physiology changes in allergic airway inflammation locally via alteration of chemokines.

Mice homozygous for the STAT4-null mutation were sensitized to cockroach Ag, challenged intratracheally 21 days later, and compared with STAT4-competent allergic mice. The STAT4(-/-) mice showed significant decreases in airway hyperreactivity (AHR) and peribronchial eosinophils compared with wild-type controls. In addition, pulmonary levels of chemokines were decreased in the STAT4(-/-) mice, including CC chemokine ligand (CCL)5, CCL6, CCL11, and CCL17. However, levels of Th2-type cytokines, such as IL-4 and IL-13, as well as serum IgE levels were similar in the two groups. Transfer of splenic lymphocytes from sensitized wild-type mice into sensitized STAT4(-/-) mice did not restore AHR in the mutant mice. Furthermore, chemokine production and peribronchial eosinophilia were not restored during the cellular transfer experiments. Thus, it appears that STAT4 expression contributes to a type 2 process such as allergen-induced chemokine production and AHR. In additional studies, competent allergic mice were treated with anti-IL-12 locally in the airways at the time of allergen rechallenge. These latter studies also demonstrated a decrease in AHR. Altogether, these data suggest that STAT4-mediated pathways play a role locally within the airway for the exacerbation of the allergen-induced responses.

Administration, Intranasal↗