Increased soluble CD14 in bronchoalveolar lavage fluid of stable lung transplant recipients

Abstract

Macrophages, neutrophils and infection have been implicated in the genesis of the bronchiolitis obliterans syndrome (BOS) post lung transplantation. sCD14 is a soluble form of a shed-cell surface protein. It is capable of promoting cytokine-induced inflammation and it9s presence in clinically stable lung transplant recipients (LTR) might be important as an early marker of BOS.Bronchalveolar lavage (BAL) and blood samples were taken from 26 stable LTR, at or near their best forced expiratory volume in one second who were free from infection. sCD14 levels were measured via enzyme-linked immunosorbent assay. Cell counts were performed on unfiltered BAL.LTR neutrophil count, BAL sCD14 and serum sCD14 levels were higher than controls (median 3.8% versus 1.3%, pv0.05; 11.5 ng?mL -1 versus 6 ng?mL -1 , pv0.001; 6.2 mg?mL -1 versus 2.4 mg?mL -1 , pv0.05, respectively). BAL albumin and sCD14 correlated (regression coefficient: 0.77, pv0.001).In this hypothesis-generating, cross-sectional study, the authors have described for the first time soluble CD14 levels in the bronchoalveolar lavage and serum of stable lung transplant recipients, and show that these are elevated compared to controls. This is a practicable candidate marker system, which can be tested for a predictive role in bronchiolitis obliterans syndrome following lung transplantation. The origin of this cellular protein and its temporal relationship to the development of the bronchiolitis obliterans syndrome remains to be elucidated in more definitive longitudinal studies, which should include other measurements potentially relevant to the innate immune system, such as bronchoalveolar lavage endotoxin levels.

Lipopolysaccharide-binding protein and CD14 are increased in the bronchoalveolar lavage fluid of smokers

“…Previous studies have shown the presence of LBP and sCD14 in the airways of healthy subjects [12,23]. Moreover, evidence indicates that LBP and sCD14 levels increase in patients with lung diseases [8,12,23] yet, to the best of the present authors' knowledge, the current study is the first showing elevated levels of both molecules in smokers.…”

“…Moreover, evidence indicates that LBP and sCD14 levels increase in patients with lung diseases [8,12,23] yet, to the best of the present authors' knowledge, the current study is the first showing elevated levels of both molecules in smokers. The fact that the levels of LBP and sCD14 were not significantly different between smokers and COPD patients suggests that both proteins might not play an important role in the development of COPD.…”

“…It has been hypothesised that cigarette smoking may impair lung immune function against respiratory infections by, for example, affecting the recognition of pathogens and hence the activation of host defence mechanisms. Given the positive correlations between smoking and inflammation and between the latter and the levels of LBP and sCD14 [8][9][10][11][12], the present authors hypothesised that levels of these proteins in the lungs from smokers would be higher than those in lungs from never-smokers.…”

“…Several studies have reported that serum levels of LBP and sCD14 increase in inflammatory conditions and there is a correlation between severity of disease and the levels of these proteins [8][9][10][11][12]. Some of these studies suggest that these increased levels of both proteins might amplify the cellular response to LPS and Gram-negative bacteria.…”

Delayed Pulmonary Arterial Hypertension in Relation to Pulmonary Damage Score after Pneumonectomy under Protective Ventilation: Experimental Study

“…Previous studies assessed pulmonary endothelial intercellular junction disruption [26] or loss of integrity of the proteoglycan components of the interstitial space [7] immediately after overflow, followed by rapid (12 h) endothelial cell remodeling and reestablishment of cell junction [27]. In our study, precapillary pulmonary hypertension correlated with interstitial edema at H48, indicating that delayed endothelium injury may be mainly caused by overflow.…”