The lung is one of the important organs for adiponectin effects and consequently, adiponectin abnormalities may be related with lower airway disease such as asthma, CF and COPD [23–25].
Both airway infection and inflammation played role in the deterioration of CF lung disease and accordingly assessment of inflammatory cells, cytokines, and anti - inflammatory molecules is essential for monitoring the progression of chronic CF lung disease. It has been reported that elevated sputum concentrations of neutrophils and inflammatory biomarkers to be clinically relevant in patients with acute chest exacerbation compared with those who were clinically stable [26–27].
We investigated whether stable adult CF patients with mild CFTR genotype (homozygous I1234V mutation) with pancreatic sufficiency modulated sputum and plasma adiponectin levels. The finding of this study demonstrated no significant differences in total plasma adiponectin concentrations in stable adult CF patients compared to healthy controls, although the mean BMI was found to be higher in healthy controls compared to CF patients, however their differences were statistically insignificant.
To our knowledge, we reported for the first time in a cohort of stable adult CF patients with homozygous CFTR I1234V mutation which demonstrated a positive correlation between plasma and sputum adiponectin. However, a mean sputum and plasma adiponectin levels were higher in CF patients with pancreatic insufficiency compared to those CF patients with pancreatic sufficiency, which may suggest an augmented inflammatory process and possible disease severity more among CF patients with pancreatic insufficiency versus pancreatic sufficiency.
Adiponectin may have a potential role in inflammatory process in lower airway diseases such as asthma, COPD and CF as well as critical illnesses such as respiratory failure with and without sepsis [28]. The present study demonstrated no difference in plasma adiponectin between stable adult CF patients and healthy controls. Recent studies have shown conflicting findings on the role of adiponectin in inflammatory lung conditions and only few researches have been conducted on the role of circulating adiponectin in CF which was found be inconsistent among different studies [29–31]. In one report, CF patients were found to have elevated adiponectin levels despite increased visceral adipose tissue mass, higher serum CRP levels, and similar levels of insulin resistance compared with a control population matched by BMI, age, and sex [29]. Another study reported by Hammana et al demonstrated normal adiponectin levels a large cohort of CF patients despite abnormal glucose tolerance or diabetes and subclinical chronic inflammation [30]. Other study demonstrated lower adiponectin in CF children than in healthy children and higher resistin levels [31]. The discrepancy between studies can be explained by involved different age groups, ethnicity, variations, severity of disease and organ involvement including pancreatic status liver involvement, nutritional status, and metabolic disorders.
FEV1% is the currently used Spirometric predictor of morbidity and mortality in patients of CF. A recent study reported no association between adiponectin and lung function after adjusting for covariates related to adiposity in a population-based sample [32]. In contrast, the main findings of the present study demonstrated sputum and plasma adiponectin levels were inversely weakly correlated with Spirometric percentage predicted FEV1 and FVC suggesting that systemic and sputum inflammation might play a role in the development of airway obstruction. This is in agreement with other pulmonary disease as in COPD subjects where demonstrated systemic adiponectin levels inversely associated with FEV1 [28]. In contrast to a recent study in children with CF observed no correlation between BMI and spirometry and adiponectin levels [31].
The results of our study should be considered as preliminary findings with some limitations. First, this study was designed to be cross-sectional that limits a causal link between sputum and plasma adiponectin levels and lung function changes. Other limitation includes small number of adult CF patients with homozygous I1234V mutation, majority with pancreatic sufficiency and a varying degree of disease severity, making it a heterogeneous population in certain tribe.