While this research did culminate in strong evidence regarding weight loss and its effects on lung airway responses, the precise mechanism for this phenomenon remains unknown.
Bariatric surgery-induced weight loss among asthmatic individuals with obesity positively impacts the circulating factors enhancing proinflammatory responses of human airway epithelial and bronchial smooth muscle cells, according to new findings.1
These findings on asthmatic individuals with obesity were conducted to assess the effect of bariatric surgery, a procedure designed to alter patients’ digestive systems or to reduce the size of the stomach.2 The research was authored by Paola E. Peña-García, from the Vermont Lung Center at the University of Vermont, Burlington.
Peña-García and colleagues noted that asthma development as an obesity response, as well as symptom resolution for weight loss, were generally less well-covered by existing research.
“The objective of this study was to elucidate the impact of circulating and adipocyte-derived factors on airway epithelial and bronchial smooth muscle cells in the context of obesity and weight loss after bariatric surgery,” Peña-García and colleagues wrote.
The investigators recruited those undergoing evaluation for bariatric surgery who had been seen at the University of Vermont Medical Center. Criteria for inclusion comprised the following: obese individuals that had allergic asthma, elevated total Immunoglobulin E levels, a history of asthma, house dust mite allergies, a positive response to methacholine or bronchodilator, and reported allergies which impact asthma; obese controls without history of asthma; obese patients that had nonallergic asthma.
The lean controls were shown to have a body mass index (BMI) of 18.5–24.9 kg/m2, as well as no asthma or malignancy instances and undergoing elective abdominal surgery. The research team’s criteria for participant exclusion comprised patients with a smoking history exceeding 20 pack-years, recent smokers, those who were pregnant, or those that had chronic lung diseases other than asthma, pulmonary arterial hypertension (PAH), lung cancer, or sarcoidosis.
The team’s assessment of participants given bariatric surgery took place preoperatively, and visceral (omental) adipose tissue samples were drawn during surgery. Study subjects were followed for a total of 12 months, with plasma and other types of measures taken at selected time points to determine the acute effects of the surgery and longitudinal follow-up over the course of the year.
The controls of normal weight had adipose tissue samples drawn only at the time of their surgery. The investigators conducted anthropomorphism questionnaires and lung function evaluations, with visceral adipose tissue (VAT) samples being taken during bariatric surgery and from normal weight controls without asthma given elective abdominal surgery.
The participants’ human bronchial epithelial (HBEC3-KT) cells were exposed by the investigators to plasma or to conditioned media from cultured VAT adipocytes that were with or without agonists. The cells of human bronchial smooth muscle (HBSM) were also exposed to adipocyte-conditioned media.
Overall, in the team’s initial subject cohort, allergic obese asthmatic subjects were found to have substantially reduced FEV1 values as opposed to obese nonasthmatic subjects. The investigators reported that the bariatric surgeries resulted in weight loss among all of those assessed and improved FEV1 values among both nonallergic and allergic obese asthmatic patients.
This result was noted by the research team as being supportive of the consensus that weight loss can benefit lung function among such individuals. In assessing the effects of the obese microenvironment on the human airway epithelial cells, the team found that cells which were exposed to plasma from obese participants at the point of baseline showed a heightened production of cytokines versus cells exposed to post-surgery plasma.
These latter findings point to the overall influence of weight loss among these patients on airway epithelial cell responses.
“To the best of our knowledge, this study is the first to address the gap in understanding the effects of circulating and adipocyte-derived factors through exposure to Ad-CM on relevant cellular drivers in asthma by utilizing samples from an ongoing longitudinal study following a cohort of asthmatic and nonasthmatic obese subjects over the course of 12 mo after undergoing bariatric surgery,” they wrote.