Responses to ozone are increased in obese mice

Area of Science:

• Environmental Health
• Immunology
• Pulmonary Medicine

Background:

• Asthma incidence is rising in overweight populations.
• Ozone (O3) is a known asthma trigger.
• Obesity may worsen asthma responses to environmental triggers.

Purpose of the Study:

• Compare ozone-induced airway hyperresponsiveness and inflammation in lean versus obese mice.
• Investigate the role of leptin in ozone-induced airway responses.
• Determine if obesity influences the severity of ozone-induced asthma.

Main Methods:

• Used lean wild-type (C57BL/6J) and genetically obese (ob/ob) mice.
• Measured airway responsiveness via forced oscillation following methacholine challenge.
• Exposed mice to ozone (2 parts/million for 3 h) and assessed airway inflammation.

Main Results:

• Obese ob/ob mice exhibited greater baseline airway resistance and hyperresponsiveness compared to wild-type mice.
• Ozone exposure significantly enhanced airway hyperresponsiveness and inflammation in ob/ob mice relative to wild-type mice.
• Exogenous leptin administration did not ameliorate, but rather increased, airway inflammation in wild-type mice.

Conclusions:

• Ozone-induced airway responses are amplified in obese mice.
• Increased inhaled ozone dose per lung tissue in obese mice may contribute to enhanced responses.
• Obesity, independent of inhaled ozone dose, likely exacerbates asthma severity.
• The hormone leptin, elevated in obesity, can increase airway inflammation.