Tumor necrosis factor-α, interleukin-8 and eosinophil cationic protein as serum markers of glucocorticoid efficacy in the treatment of bronchial asthma.

BACKGROUND: Bronchial asthma (BA) is a common chronic respiratory disease that has exhibited a rising global incidence in recent years. Glucocorticoids are used for the treatment of BA. Emerging evidence has demonstrated the roles of tumor necrosis factor (TNF-α), interleukin-8 (IL-8) and eosinophil cationic protein (ECP) in BA. The present study investigated whether TNF-α, IL-8 and ECP were associated with the clinical stages and severity of BA and the efficacy of glucocorticoids in the treatment of BA. METHODS: A total of 199 patients with BA and 174 healthy individuals were included in this study. Patients with BA underwent glucocorticoid treatment, and the TNF-α, IL-8 and ECP levels and lung functions of the subjects were measured. The correlations of the TNF-α, IL-8 and ECP levels with BA severity, clinical staging and lung functions were assessed. We investigated whether the TNF-α, IL-8 and ECP levels aided in evaluating the efficacy of using glucocorticoids for the treatment of BA. RESULTS: TNF-α, IL-8 and ECP exhibited high levels in patients with BA, and glucocorticoid treatment notably decreased these levels. The TNF-α, IL-8 and ECP levels were positively correlated with the clinical stages and severity of BA and negatively correlated with lung function. TNF-α, IL-8 and ECP can be used as serum markers to predict the efficacy of glucocorticoids in the treatment of BA. CONCLUSION: The key findings of this study collectively support a role for TNF-α, IL-8 and ECP in BA development, and TNF-α, IL-8 and ECP can be used as serum markers of glucocorticoid efficacy in BA.

Prenatal maternal stress induces visceral hypersensitivity of adult rat offspring through activation of cystathionine-ß-synthase signaling in primary sensory neurons.

Irritable bowel syndrome is a disorder of unknown etiology characterized by widespread, chronic abdominal pain associated with altered bowel movements. Increasing amounts of evidence indicate that stressors presented during gestational periods could have long-term effects on the offspring's tissue structure and function, which may predispose to gastrointestinal diseases. The aim of the present study is to determine whether prenatal maternal stressis a adverse factor affecting gastrointestinal sensitivity and to investigate possible mechanisms underlying prenatal maternal stress-induced visceral hypersensitivity in adult offspring. Prenatal maternal stress was induced in pregnant Sprague-Dawley rats by exposure to heterotypic intermitent stress from gestational day 7 to delivery. Prenatal maternal stress significantly increased visceromotor response to colorectal distention in adult offspring from the age of 6 weeks to 10 weeks. Prenatal maternal stress also enhanced neuronal excitability including depolarization of resting membrane potentials, reduction in rheobase, and an increase in the number of action potentials evoked by 2× and 3× rheobase current stimultion of colon-specific dorsal root ganglion neurons. Prenatal maternal stress remarkably enhanced expression of cystathionine-ß-synthase and Nav1.7 in T13-L2 thoracolumbar dorsal root ganglions both at protein and mRNA levels. Intraperitoneal injection of aminooxyacetic acid, an inhibitor of cystathionine-ß-synthase, attenuated prenatal maternal stress-induced visceral hypersensitivity in a dose-dependent manner. A consecutive seven-day administration of aminooxyacetic acid reversed the hyperexcitability of colon-specific dorsal root ganglion neurons and markedly reduced Nav1.7 expression. These results indicate that the presence of multiple psychophysical stressors during pregnancy is associated with visceral hypersensitivity in offspring, which is likely mediated by an upregualtion of cystathionine-ß-synthase and Nav1.7 expression. Prenatal maternal stress might be a significant contributor to irritable bowel syndrome, and cystathionine-ß-synthase might be a potential target for treatment for chronic visceral hypersensitivity in patients with irritable bowel syndrome.