Chest
Bronchial Inflammation: Its Relationship to Colonizing Microbial Load and α1-Antitrypsin Deficiency
Section snippets
Materials and Methods
We studied 55 patients with chronic obstructive bronchitis, 64 patients with a similar degree of airflow obstruction related to α1-AT deficiency (phenotype Pi Z), and 43 patients with idiopathic bronchiectasis diagnosed by high-resolution CT scan. Sputum was collected over a 4-h period from rising from each patient, and an aliquot was removed and assessed for the colonizing microbial load as described previously.4 The remaining sample was ultracentrifuged to obtain the sputum sol phase. These
Results
Inflammation in the airway was clearly associated with the presence and size of colonizing microbial load as indicated by the positive correlations with MPO (r = 0.58; p < 0.0005), NE activity (r = 0.43; p < 0.0005), interleukin-8 (r = 0.67; p < 0.0001), LTB4 (r = 0.48; p < 0.0005), sputum-serum albumin ratio (r = 0.43; p < 0.0005), and a negative correlation with SLPI (r = − 0.52; p < 0.0005). The relationship indicated a microbial threshold of 106 cfu below which inflammation was present but
Discussion
The results presented here confirmed that subjects with chronic bronchial disease have inflammation present in their airways as indicated by the presence of neutrophils (quantified by the MPO concentration) and leakage of the serum protein albumin. It is well known that patients with chronic bronchial disease can be colonized with bacteria even in the stable clinical state.6 The current data confirm that some patients are colonized and that the bacterial load may vary from 105 to > 108 cfu/mL.
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Small airways disease in patients with alpha-1 antitrypsin deficiency
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2014, Respiratory MedicineCitation Excerpt :In AATD lung disease, autoimmunity is not considered to play a significant role [21] and thus the pathophysiological processes may differ from usual COPD. Birring et al. discovered that sputum levels of IL8 and neutrophil counts were higher in patients with hypothyroidism compared to healthy control subjects [18], again suggesting an inflammatory link, and certainly lung inflammation is even more likely to be high in patients with AATD [22]. Therefore the potential association between patients with AATD and hypothyroidism may be more complex involving both autoimmunity and neutrophilic inflammatory processes.
α<inf>1</inf>-antitrypsin, old dog, new tricks: α<inf>1</inf>- antitrypsin exerts in vitro anti-inflammatory activity in human monocytes by elevating cAMP
2007, Journal of Biological ChemistryCitation Excerpt :However, AAT also reduces bacterial endotoxin and TNFα-induced lethality in vivo (11). In man, Prolastin® therapy has been shown to reduce LTB4 levels in patients with AAT-deficient emphysema (56, 57). Comparative studies in vivo looking at the efficacy of native and modified forms of AAT and low molecular weight serine protease inhibitors may help address the question regarding the dominant anti-inflammatory mechanism of AAT in vivo.
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2007, International Journal of Biochemistry and Cell Biology
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