title: Impaired Expression of MAPK Is Associated with the Downregulation of TNF-α, IL-6, and IL-10 in Mycobacterium abscessus Lung Disease.
abstract: BACKGROUND
  Healthy individuals who develop nontuberculous mycobacteria (NTM) lung disease are likely to have specific susceptibility factors which can lead to a NTM infection. The aim of the present study was to investigate the mechanism underlying innate immune responses, including the role of mitogen-activated protein kinase (MAPK), in Mycobacterium abscessus lung disease.
  
  
  METHODS
  Extracellular signal-regulated kinase (ERK1/2) and p38 MAPK expression in monocytes from peripheral blood mononuclear cells were measured by Western blot analysis after stimulation by Mycobacterium avium in five patients with M. abscessus lung disease and seven healthy controls. A M. avium-induced cytokine assay was performed after inhibition of ERK1/2 and p38 MAPK pathways.
  
  
  RESULTS
  Mycobacterium avium induced p38 and ERK1/2 expression in monocytes from healthy controls and subsequently upregulated tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 production. In monocytes from patients with M. abscessus lung disease, however, induction of p38 and ERK1/2 expression, and the production of TNF-α, IL-6, and IL-10 were significantly lower.
  
  
  CONCLUSIONS
  Decreased activity of MAPK and cytokine secretion in monocytes from patients with M. abscessus lung disease may provide an explanation regarding host susceptibility to these uncommon infections.
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
authors.forename: Yun Su
authors.initials: YS
authors.lastname: Sim
authors.forename: Su-Young
authors.initials: SY
authors.lastname: Kim
authors.forename: Eun Joo
authors.initials: EJ
authors.lastname: Kim
authors.forename: Sung Jae
authors.initials: SJ
authors.lastname: Shin
authors.forename: Won-Jung
authors.initials: WJ
authors.lastname: Koh