Biochemical and Biophysical Research Communications
Regular ArticleEstablishment of Radioimmunoassay for Human Neutrophil Peptides and Their Increases in Plasma and Neutrophil in Infection
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Exercise, Immunity, and Illness
2018, Muscle and Exercise PhysiologyValidation of a quantitative assay for human neutrophil peptide-1, -2, and -3 in human plasma and serum by liquid chromatography coupled to tandem mass spectrometry
2010, Journal of Chromatography B: Analytical Technologies in the Biomedical and Life SciencesAlarmins link neutrophils and dendritic cells
2009, Trends in ImmunologyCitation Excerpt :Numerous studies have shown the participation of alarmins in the development of inflammation and immune responses. The levels of neutrophil-derived alarmins are high under many inflammatory conditions, whereas blockade of some of these mediators has been shown to ameliorate the manifestation of acute inflammatory reactions [3,23,24,29,51,55,98]. In addition, administration of exogenous α-defensin(s), cathelicidin, lactoferrin or HMGB1 together with an antigen promotes antigen-specific immune responses [10,12–15,25,70,83].
Human α-defensins inhibit BK virus infection by aggregating virions and blocking binding to host cells
2008, Journal of Biological ChemistryCitation Excerpt :Our findings show that the IC50 of HNP1 and HD5 on BKV infection was 23.2 and 9.1 μg/ml, respectively. HNP1 levels in the human plasma range from 400 ng/ml in healthy individuals to 13 μg/ml in individuals with bacteria infections and may be found in concentrations as high as 6 mg/ml within neutrophils (63-66). Less is known about the concentration of HD5 in the small intestines, however, analysis of urethral lavages from men with gonorrhea infections show HD5 concentrations in inflamed genital tracts at 0.6 ± 0.68 μg/ml (17).
Suppression of hepatic glucose production by human neutrophil α-defensins through a signaling pathway distinct from insulin
2008, Journal of Biological ChemistryCitation Excerpt :HNPs are released into the blood by granulocytes in response to bacterial infections (8). Normally, plasma levels of HNPs vary between 13.2 and 42 ng/ml (3.8–12 nm) (16, 17), which is well below the effective level (100–300 nm) of HNPs in suppression of hepatic gluconeogenesis. Therefore, under normal physiological conditions, it is unlikely that HNPs or other defensins play a significant role in the regulation of hepatic gluconeogenesis.