A associação da obesidade e asma atópica está bem descrita. Embora reconhecidamente uma patologia mediada por eosinófilos, à asma apresenta fenótipos distintos onde os neutrófilos exercem relevante papel na inflamação pulmonar e manutenção da inflamação. Existem dados de que mulheres obesas asmáticas são mais propensas a desenvolver a asma mediada por neutrófilos, cuja característica é ser de difícil controle, e ainda refrataria a corticoterapia. Ainda não existem modelos experimentais de asma neutrofílica, que visem a ligar os mecanismos associados à resistência aos corticoides em mulheres com asma neutrofílica. Neste estudo caracterizamos um modelo experimental de asma neutrofilica em camundongos fêmeas e apresentamos dados do papel da obesidade na inflamação pulmonar. Nossos dados permitem sugerir que o modelo de asma neutrofílica está, sob ponto de vista inflamatório caracterizado, e que o recrutamento de neutrófilos independe da obesidade. Nosso estudo pode contribuir para a compreensão dos mecanismos que regulam a asma de neutrofilica em mulheres obesas. / The association of obesity and atopic asthma is well described. Although admittedly an eosinophil-mediated pathology, asthma presents distinct phenotypes where neutrophils exert a relevant role in lung inflammation and maintenance of inflammation. There are data that obese asthmatic women are more likely to develop neutrophil-mediated asthma, which is difficult to control and still refractory to corticosteroids. There are as yet no experimental models of neutrophilic asthma to link mechanisms associated with resistance to corticosteroids in women with neutrophilic asthma. In this study we characterized an experimental model of neutrophilic asthma in female mice and presented data on the role of obesity in pulmonary inflammation. Our data allow us to suggest that the neutrophilic asthma model is, under a characterized inflammatory point of view, and that neutrophil recruitment is independent of obesity. Our study may contribute to understanding the mechanisms that regulate neutrophilic asthma in obese women.

Air and saline P-V curves were run on the excised lungs of rats starved 1-4 days. Stability estimates based on % of maximum volume retained on deflation tended toward decreases, but atelectasis was not increased according to buoyancy measurements. Compliance was not significantly affected, with whatever trend existed being toward increases. Average air P-V curves for day 3 and 4 of starvation were essentially superimposable on control curves. Surface tension of lung lavage fluid was measured (Surfactometer) during cyclic compression and expansion of the film. Min and max γ were elevated, and the activity index (s) depressed, but the area of the hysteresis loop was relatively unchanged. It is concluded that despite increases in γ of lung washings, pulmonary mechanics was little affected by 1-4 days of food deprivation. The effects on surface tension may be due to a decrease in quantity of surfactant extractable, without any change in composition.