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Clinical Investigations: ANTIBIOTICS |

Plasma and BAL Fluid Concentrations of Antimicrobial Peptides in Patients With Mycobacterium avium- intracellulare Infection*

Jun-ichi Ashitani, MD; Hiroshi Mukae, MD; Takeaki Hiratsuka, MD; Masamitsu Nakazato, MD; Kenshi Kumamoto, MD; Shigeru Matsukura, MD
Author and Funding Information

*From the National Sanatorium Miyazakihigashi Hospital (Drs. Ashitani and Kumamoto), Miyazaki, Japan; and the Third Department of Internal Medicine (Drs. Mukae, Hiratsuka, Nakazato, and Matsukaura), Miyazaki Medical College, Miyazaki, Japan.

Correspondence to: Hiroshi Mukae, MD, Third Department of Internal Medicine, Miyazaki Medical College, Kihara 5200, Kiyotake, Miyazaki 889-1692, Japan; e-mail: hmukae@post.miyazaki-med.ac.jp



Chest. 2001;119(4):1131-1137. doi:10.1378/chest.119.4.1131
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Study objectives: To investigate the roles of humanα -defensin (HAD), human β-defensin (HBD)-1, and HBD-2, novel antimicrobial peptides, in patients 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 and HBD-1, and HBD-2 levels in plasma and in BAL fluid (BALF) by radioimmunoassay. 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 correlation 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-1β in MAI patients. Patients with cavity formation on the chest roentgenogram had higher HAD and HBD-2 levels in their BALF than those of patients without cavity formation. Treatment with clarithromycin combined with two or three other antibiotics, including ethambutol, 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 may be a useful marker of disease activity in patients with pulmonary MAI.

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