Innate immune mechanisms of chronic inflammatory diseases of mucosal tissues

The focus of this PhD thesis was chronic inflammation of the gut and lungs in the context of 1) comorbid gut and lung disease and 2) neonatal origins of lung inflammation. In brief, four key findings were made: 1) Gut inflammation in SHIP-1-deficient mice is dependent on environment and associated with altered lung inflammation; 2) G-CSF-deficiency is protective against gut inflammation in SHIP-1-deficient mice; 3) DSS-induced colitis in TCRδ-deficient mice is associated with lung inflammation and enlargement of air spaces; and 4) SHIP-1-deficiency in eosinophils leads to eosinophilia in the developing lung, leading to lung inflammation and altered lung development.