title: Changes in serum immunomolecules during antibiotic therapy for Mycobacterium avium complex lung disease.
abstract: Little information is available regarding changes in immune status for patients with Mycobacterium avium complex (MAC) lung disease during antibiotic therapy. Serum immunomolecules from 42 patients with MAC lung disease were assayed comparatively using an array-based system according to (i) patients with MAC lung disease at the time of diagnosis versus healthy controls and (ii) alterations after 12 months of antibiotic therapy in the MAC lung disease group. In addition, cytokine analyses were performed to determine whether cytokine responses were associated specifically with the disease phenotype, treatment outcome and aetiological agent. Notably, the serum concentrations of type 1 cytokine-associated molecules, such as CD40L, interferon (IFN)-γ, interleukin (IL)-8 and IL-23, were decreased significantly in patients at the time of diagnosis, suggesting that these molecules may serve as indicators of host susceptibility to MAC disease. Although the overall serum level of T helper type 1 (Th1)-related molecules, such as CD40L and IFN-γ, was restored after treatment, Th17-related cytokines, such as IL-17 and IL-23, were down-regulated significantly at 12 months post-treatment compared to pretreatment. Furthermore, these cytokine patterns differed among patient subgroups. Decreased serum concentrations of IL-17 and/or IL-23 were associated with failure of sputum conversion, the fibrocavitary disease phenotype and M. intracellulare lung disease. Thus, the reciprocal balance between Th1 and Th17 immunity during antibiotic therapy for MAC lung disease is critical for dictating the treatment response. In conclusion, a low level of Th1-related immunomolecules may perpetuate MAC lung disease, and the serum concentrations of Th17-related cytokines can reflect the treatment outcome, disease phenotype and aetiological agent.
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea.
authors.forename: S-Y
authors.initials: SY
authors.lastname: Kim
authors.forename: W-J
authors.initials: WJ
authors.lastname: Koh
authors.forename: H Y
authors.initials: HY
authors.lastname: Park
authors.forename: K
authors.initials: K
authors.lastname: Jeon
authors.forename: O J
authors.initials: OJ
authors.lastname: Kwon
authors.forename: S-N
authors.initials: SN
authors.lastname: Cho
authors.forename: S J
authors.initials: SJ
authors.lastname: Shin
mesh_terms: D000368:Aged; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D017291:Clarithromycin / Q000627:therapeutic use; D016207:Cytokines / Q000097:blood / Q000276:immunology; D004359:Drug Therapy, Combination; D004977:Ethambutol / Q000627:therapeutic use; D005260:Female; D006801:Humans; D008171:Lung Diseases / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D015269:Mycobacterium avium Complex / Q000187:drug effects* / Q000276:immunology; D015270:Mycobacterium avium-intracellulare Infection / Q000188:drug therapy* / Q000276:immunology / Q000382:microbiology; D011446:Prospective Studies; D012293:Rifampin / Q000627:therapeutic use; D018417:Th1 Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D058504:Th17 Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism
chemical_list: D000900:Anti-Bacterial Agents; D016207:Cytokines; D004977:Ethambutol; D017291:Clarithromycin; D012293:Rifampin
keywords: Mycobacterium avium complex; Th1 immunity; Th17 immunity; immunomolecules; lung disease