Increased oxidized methionine residues in BAL fluid proteins in acute or chronic bronchitis

Abstract

Phagocytic cells such as alveolar macrophages (AM) or polymorphonuclear neutrophils (PMN) in the bronchoalveolar tract are a potential source of the oxygen-derived free radicals which are presumed to be involved in lung tissue damage. Previous results have shown that the methionine sulphoxide (MET(O)) content of bronchoalveolar lavage fluid (BALF) protein is a reliable parameter to indicate oxidative processes in idiopathic pulmonary fibrosis (IPF). We measured the molar ratio between MET(O) and methionine (MET) in the BALF protein from healthy nonsmokers (control group), healthy smokers and patients with acute or chronic bronchitis (AB or CB). The MET(O)/MET ratio of the nonsmoking group (n = 11) was 0.046 +/- 0.008 (mean +/- SEM). Healthy smokers (n = 8) had similar values (0.042 +/- 0.008), even though they had strongly increased AM counts in BALF. Patients with AB (n = 12) showed an increased MET(O)/MET ratio (0.191 +/- 0.031) and had high PMN but normal AM counts in BALF. Patients with CB (n = 13) showed an increase in the MET(O)/MET ratio (0.086 +/- 0.010) and moderately increased PMN and markedly increased AM counts. Taking all results together, the MET(O)/MET ratio correlated positively with the relative PMN number (r = 0.70; p less than 0.0002) and inversely with the relative AM number (r = 0.67; p less than 0.0002). In the group with CB, the MET(O)/MET ratio correlated inversely with forced expiratory volume in one second (FEV1) % pred. (r = -0.77) and FEV1/inspiratory vital capacity (IVC) % pred. (r = -0.89).(ABSTRACT TRUNCATED AT 250 WORDS)

How the lung deals with oxidants

“…Accumulation of inflammatory cells, such as neutrophils or eosinophlls, in the airways results in an exaggerated release of reactive oxygen metabolites, representing a potential risk of lung tissue damage. Data have accumulated indicating an increased oxidant burden of neutrophilic origin in a number of lung diseases, such as the adult respiratory distress syndrome [7], idiopathic pulmonary fibrosis [8], bronchitis [9,10], cystic fibrosis (11], and immune complex injury [12]. The role of oxidants in the initial stage of lung diseases is stili unclear, but it is obvious that reactive oxygen metabolites must be removed rapidly from the organ, before they can cause cellular dysfunction or cell death resulting in impaired lung functions.…”