RSV Infection in the Setting of STAT1 Deficiency

RSV Infection in the Setting of STAT1 Deficiency

Aberrant Type 2 Responses to RSV

Aberrant Type 2 Responses to RSV

GLP-1R signaling inhibits innate allergic immune response

GLP-1R signaling inhibits innate allergic immune response

ILC

ILC

PGE2 regulation of aspirin-exacerbated respiratory disease

PGE2 regulation of aspirin-exacerbated respiratory disease

RSV A2 infection induces gob5 expression in Stat1-/- mice

RSV A2 infection induces gob5 expression in Stat1-/- mice

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The Laboratory of Dr. Stokes Peebles, M.D.

The Peebles Lab investigates mechanisms regulating lung inflammation, with specific emphasis on allergen-induced and virus-mediated disease.  Allergic airway inflammation is one of the most common diseases in both children and adults, and is a strong predisposing factor for the development of asthma.  Viral infections are causative in approximately 80% of children and 50% of adults.  Our lab has a particular interest in the interaction of allergic disease and respiratory syncytial virus in causing airways responsiveness.  While we are interested in study host immune responses to both allergens and viruses, we are particularly interested in the contribution of group 2 innate lymphoid cells (ILC2) as an initiator of lung inflammatory responses.  Additionally, our lab has a long-standing interest in how prostaglandins, particularly PGI2, regulate lung inflammatory responses.  We have developed a variety of tools to understand how both endogenous and exogenous prostaglandin signaling modulates both allergen-induced and virus-induced pulmonary inflammation.  Lastly, we are now investigating how glucagon-like peptide-1 signaling regulates lung inflammation, as a possible treatment for asthma in the setting of obesity.

IL-33 expression in the lung as shown by citrine reporter

IL-33_exp-in-lung_by-citrine-reporter.jpg