Christopher L Reading
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Christopher L Reading has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Angela Wang
VA San Diego Healthcare System, 3350 La Jolla Village Dr., San Diego, CA 92161, USA
1 shared publication - Anna M van Heeckeren
Case Western Reserve University, School of Medicine, Pediatric Pulmonology, 10900 Euclid Avenue, Cleveland, OH 44106-4948, USA
1 shared publication - Dominick L. Auci
Harbor Biosciences, San Diego, California, USA
1 shared publication - Douglas J. Conrad
Medicine, Univ of California At San Diego Med Ctr, La Jolla, CA, United States
1 shared publication - Dwight Stickney
Harbor Biosciences, 9171 Towne Centre Drive, Suite 180, San Diego, CA 92122, USA
1 shared publication - Ferdinando Nicoletti
IRCCS Neuromed, 86077 Pozzilli, Italy
1 shared publication
Latest Publications
- Open Access
- 30 October 2010
- Published by Springer Nature in Journal of Inflammation
- Vol. 7 (1) , 52
HE3286, an oral synthetic steroid, treats lung inflammation in mice without immune suppression
Background: 17α-Ethynyl-5-androsten-3β, 7β, 17β-triol (HE3286) is a synthetic derivative of an endogenous steroid androstenetriol (β-AET), a metabolite of the abundant adrenal steroid deyhdroepiandrosterone (DHEA), with broad anti-inflammatory activities. We tested the ability of this novel synthetic steroid with improved pharmacological properties to limit non-productive lung inflammation in rodents and attempted to gauge its immunological impact.Methods and Results: In mice, oral treatment with HE3286 (40 mg/kg) significantly (p< 0.05) decreased neutrophil counts and exudate volumes (~50%) in carrageenan-induced pleurisy, and myeloperoxidase in lipopolysaccharide-induced lung injury. HE3286 (40 mg/kg) was not found to be profoundly immune suppressive in any of the classical animal models of immune function, including those used to evaluate antigen specific immune responsesin vivo(ovalbumin immunization). When mice treated for two weeks with HE3286 were challenged withK. pneumoniae, nearly identical survival kinetics were observed in vehicle-treated, HE3286-treated and untreated groups.Conclusions: HE3286 represents a novel, first-in-class anti-inflammatory agent that may translate certain benefits of β-AET observed in rodents into treatments for chronic inflammatory pulmonary disease.
- 30 October 2010
- Published by Springer Nature in Journal of Inflammation
- Vol. 7 (1) , 52
Open AccessHE3286, an oral synthetic steroid, treats lung inflammation in mice without immune suppression
Background: 17α-Ethynyl-5-androsten-3β, 7β, 17β-triol (HE3286) is a synthetic derivative of an endogenous steroid androstenetriol (β-AET), a metabolite of the abundant adrenal steroid deyhdroepiandrosterone (DHEA), with broad anti-inflammatory activities. We tested the ability of this novel synthetic steroid with improved pharmacological properties to limit non-productive lung inflammation in rodents and attempted to gauge its immunological impact.Methods and Results: In mice, oral treatment with HE3286 (40 mg/kg) significantly (p< 0.05) decreased neutrophil counts and exudate volumes (~50%) in carrageenan-induced pleurisy, and myeloperoxidase in lipopolysaccharide-induced lung injury. HE3286 (40 mg/kg) was not found to be profoundly immune suppressive in any of the classical animal models of immune function, including those used to evaluate antigen specific immune responsesin vivo(ovalbumin immunization). When mice treated for two weeks with HE3286 were challenged withK. pneumoniae, nearly identical survival kinetics were observed in vehicle-treated, HE3286-treated and untreated groups.Conclusions: HE3286 represents a novel, first-in-class anti-inflammatory agent that may translate certain benefits of β-AET observed in rodents into treatments for chronic inflammatory pulmonary disease.