Biochemical and Biophysical Research Communications
Regular ArticleAdrenomedullin Inhibits the Secretion of Cytokine-Induced Neutrophil Chemoattractant, a Member of the Interleukin-8 Family, from Rat Alveolar Macrophages
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Endogenous inhibitory mechanisms in asthma
2023, Journal of Allergy and Clinical Immunology: GlobalSystems Biology in Immunotoxicology
2018, Comprehensive Toxicology: Third EditionBench-to-bedside pharmacology of adrenomedullin
2015, European Journal of PharmacologyCitation Excerpt :Similarly, according to a report by Isumi et al. (1999), AM suppressed interleukin-1β-induced tumor necrosis factor-α production in the Swiss T3T fibroblast cell line. These effects were reportedly mimicked by 8-bromo-cAMP or attenuated by H-89, a protein kinase A inhibitor, suggesting a cAMP-dependent intracellular mechanism of action (Isumi et al., 1999; Kamoi et al., 1995). On the basis of these findings from patients or immune cells, a number of experimental therapeutic studies were carried out with various animal models of systematic inflammatory response syndrome or sepsis (Ertmer et al., 2007; Hyvelin et al., 2002; Müller-Redetzky et al., 2014; Yang et al., 2002).
Stable-state midrange-proadrenomedullin level is a strong predictor of mortality in patients with COPD
2014, ChestCitation Excerpt :The higher mortality rate in patients with higher serum MR-proADM levels may reflect an increased severity of inflammatory lung disease, which is not directly reflected by the ADO score or BODE index. A variety of cells may augment ADM secretion in response to various cytokines.38,39 The increased MR-proADM may also reflect the more systemic effects of COPD, including COPD-induced cardiopulmonary stress or cardiovascular comorbidity.
Shared and separate functions of the RAMP-based adrenomedullin receptors
2011, PeptidesCitation Excerpt :Alveolar macrophages are likely the main source of increased AM expression in the lungs, as their expression of AM mRNA is substantially elevated in rats and humans with severe heart failure [98]. The elevated AM levels may limit pulmonary infiltration of neutrophils because AM inhibits the cytokine-induced secretion of neutrophil chemoattractant from rat alveolar macrophages in vitro [62]. Hemodynamic stress and angiotensin II are both key mediators of cardiac hypertrophy induced by pressure overload (POL; by aortic banding) or volume overload (VOL; by aortocaval shunt).
Adrenomedullin level in the nasal discharge from allergic rhinitis cohort
2011, PeptidesCitation Excerpt :Therefore, decrease of AM release also contributes to attenuation of the prolonged inflammatory cycle in allergic inflammation through regulating histamine release and CC-chemokine production. In a study of pulmonary inflammation, it was shown that AM may play a role in the inhibitory regulation of inflammatory processes by several pathways, such as inhibition of binding of neutrophils to vascular endothelial cells and subsequent neutrophil emigration [17,38] and inhibition of cytokine secretion from macrophages, such as TNF-α, IL-6 and cytokine-induced neutrophil chemoattractant [17,23]. Although we have no direct evidence, the immunostaining pattern observed in the present study suggests that mast cells may compensate for the decreased content of AM.