Plasma and BAL fluid concentrations of antimicrobial peptides in patients with Mycobacterium avium-intracellulare infection

Citation
J. Ashitani et al., Plasma and BAL fluid concentrations of antimicrobial peptides in patients with Mycobacterium avium-intracellulare infection, CHEST, 119(4), 2001, pp. 1131-1137
Citations number
29
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CHEST
ISSN journal
00123692 → ACNP
Volume
119
Issue
4
Year of publication
2001
Pages
1131 - 1137
Database
ISI
SICI code
0012-3692(200104)119:4<1131:PABFCO>2.0.ZU;2-0
Abstract
Study objectives: To investigate the roles of human alpha -defensin (HAD), human beta -defensin (HBD)-1, and HBD-2, novel antimicrobial peptides, in p atients with Mycobacterium avium-intracellulare infection (MAI), Patients: The study included 25 patients (10 men) with MAI who visited our hospital between June 1998 and August 1999, Measurements and results: In patients with pulmonary MAI, we measured HAD a nd HBD-1, and HBD-2 levels in plasma and in BAL fluid (BALF) by radioimmuno assay. Plasma concentrations of HAD and HBD-2 in those patients were higher than those in control subjects, whereas HBD-1 levels were similar to those in the control subjects. High levels of HAD and HBD-2, but not HBD-1, also were observed in the BALF of MAI patients. There was a positive correlatio n between HAD and interleukin (IL)-8 concentrations in the BALF of patients with MAI, BALF HBD-2 concentrations also correlated positively with those of plasma HBD-2 and BALF IL-1 beta in MAI patients. Patients with cavity fo rmation on the chest roentgenogram had higher HAD and HBD-2 levels in their BALF than those of patients without cavity formation. Treatment with clari thromycin combined with two or three other antibiotics, including ethambuto l, rifampicin, ofloxacin, or ciprofloxacin, for at least 6 months resulted in a significant fall in plasma HBD-2 concentrations in responders, but not in nonresponders. Conclusion: Our findings suggest that HAD and HBD-2 may participate in host defense and local remodeling of the respiratory tract in patients with MAI and that plasma HBD-2 levels map be a useful marker of disease activity in patients with pulmonary MAI.