401. Pulmonary retention of PMN attracts primed intestinal lymphocytes in a mouse model of inflammatory bowel disease
- Author
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Steven Maltby, Sean W. Mateer, Bridie J. Goggins, Jay C. Horvat, Ellen Marks, Simon Keely, and Philip M. Hansbro
- Subjects
Pathology ,medicine.medical_specialty ,Lung ,business.industry ,Lymphocyte ,Inflammation ,CCL2 ,medicine.disease ,Biochemistry ,Inflammatory bowel disease ,digestive system diseases ,Neutrophilia ,Extravasation ,medicine.anatomical_structure ,Immunology ,Genetics ,medicine ,Colitis ,medicine.symptom ,business ,Molecular Biology ,Biotechnology - Abstract
Inflammatory bowel disease (IBD) is a group of chronic inflammatory conditions of the gastrointestinal (GI) tract. IBD is also associated with a number of co-morbidities that can include inflammation in the lung (Black et al. Chest 2007). IBD-induced pulmonary inflammation is characterized by polymorphonuclear neutrophil (PMN) and lymphocyte inflammation. We have demonstrated neutrophilia and an increase in PMN in the pulmonary system in the DSS model of colitis. We hypothesized that colitis induces PMN-mediated inflammation in the lung, which attracts GI-primed lymphocytes. Employing the DSS model of colitis, we observed a significant correlation between PMN in the circulatory and pulmonary system (R2=0.845, N=12). Extravasation of PMN into lung tissue was observed and was associated with a 2-fold increase in integrin β2 expression and an increase in IL-1β and CCL2 protein levels. To examine whether DSS pulmonary inflammation resulted in lymphocyte recruitment to the lungs, an adoptive transfer experimen...
- Published
- 2015