Alison S. Williams
Research Subjects
Research Interests
Alison S. Williams has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
- Allison P. Wurmbrand
Department of Environmental Health and
1 shared publication - Bruce David Levy
Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts
1 shared publication - David I. Kasahara
Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard T.H. Chan School of Public Health, 665 Huntington Av Bld1 room 319, Boston, MA, 02115, USA
1 shared publication - Frank Cuttitta
Center for Cancer Research, National Cancer Institute, Bethesda, Maryland; and
1 shared publication - Jeffrey D. Brand
Department of Environmental Health and
1 shared publication - Joel Andrew Mathews
Ionis Pharmaceuticals, Carlsbad, CA
1 shared publication
Latest Publications
- 1 March 2018
- Published by Oxford University Press (OUP) in American Journal of Respiratory Cell and Molecular Biology
- Vol. 58 (3) , 341-351
Augmented Responses to Ozone in Obese Mice Require IL-17A and Gastrin-Releasing Peptide
Ozone and obesity both increase IL-17A in the lungs. In mice, obesity augments the airway hyperresponsiveness and neutrophil recruitment induced by acute ozone exposure. Therefore, we examined the role of IL-17A in obesity-related increases in the response to ozone observed in obese mice. Lean wild-type and obese db/db mice were pretreated with IL-17A–blocking or isotype antibodies, exposed to air or ozone (2 ppm for 3 h), and evaluated 24 hours later. Microarray analysis of lung tissue gene expression was used to examine the mechanistic basis for effects of anti–IL-17A. Compared with lean mice, ozone-exposed obese mice had greater concentrations of BAL IL-17A and greater numbers of pulmonary IL-17A+ cells. Ozone-induced increases in BAL IL-23 and CCL20, cytokines important for IL-17A+ cell recruitment and activation, were also greater in obese mice. Anti–IL-17A treatment reduced ozone-induced airway hyperresponsiveness toward levels observed in lean mice. Anti–IL-17A treatment also reduced BAL neutrophils in both lean and obese mice, possibly because of reductions in CXCL1. Microarray analysis identified gastrin-releasing peptide (GRP) receptor (Grpr) among those genes that were both elevated in the lungs of obese mice after ozone exposure and reduced after anti–IL-17A treatment. Furthermore, ozone exposure increased BAL GRP to a greater extent in obese than in lean mice, and GRP-neutralizing antibody treatment reduced obesity-related increases in ozone-induced airway hyperresponsiveness and neutrophil recruitment. Our data indicate that IL-17A contributes to augmented responses to ozone in db/db mice. Furthermore, IL-17A appears to act at least in part by inducing expression of Grpr.
- 1 March 2018
- Published by Oxford University Press (OUP) in American Journal of Respiratory Cell and Molecular Biology
- Vol. 58 (3) , 341-351
Augmented Responses to Ozone in Obese Mice Require IL-17A and Gastrin-Releasing Peptide
Ozone and obesity both increase IL-17A in the lungs. In mice, obesity augments the airway hyperresponsiveness and neutrophil recruitment induced by acute ozone exposure. Therefore, we examined the role of IL-17A in obesity-related increases in the response to ozone observed in obese mice. Lean wild-type and obese db/db mice were pretreated with IL-17A–blocking or isotype antibodies, exposed to air or ozone (2 ppm for 3 h), and evaluated 24 hours later. Microarray analysis of lung tissue gene expression was used to examine the mechanistic basis for effects of anti–IL-17A. Compared with lean mice, ozone-exposed obese mice had greater concentrations of BAL IL-17A and greater numbers of pulmonary IL-17A+ cells. Ozone-induced increases in BAL IL-23 and CCL20, cytokines important for IL-17A+ cell recruitment and activation, were also greater in obese mice. Anti–IL-17A treatment reduced ozone-induced airway hyperresponsiveness toward levels observed in lean mice. Anti–IL-17A treatment also reduced BAL neutrophils in both lean and obese mice, possibly because of reductions in CXCL1. Microarray analysis identified gastrin-releasing peptide (GRP) receptor (Grpr) among those genes that were both elevated in the lungs of obese mice after ozone exposure and reduced after anti–IL-17A treatment. Furthermore, ozone exposure increased BAL GRP to a greater extent in obese than in lean mice, and GRP-neutralizing antibody treatment reduced obesity-related increases in ozone-induced airway hyperresponsiveness and neutrophil recruitment. Our data indicate that IL-17A contributes to augmented responses to ozone in db/db mice. Furthermore, IL-17A appears to act at least in part by inducing expression of Grpr.