TY - JOUR
T1 - Respiratory epithelial cells release IL-8 in response to thermophilic bacteria causing hypersensitivity pneumonitis.
AU - Guðmundsson, Gunnar
AU - Hunninghake, Gary W
N1 - Funding Information: Received 3 March 1998 ; accepted 22 July 198. 9 G. Gudmundsnsisofunded by a Research Training Fellowship Grant from the American Lung Ascsiatioon ofIowa, a NATO Science Fellowship, an American Heart Ascsiatioon of Ioa wResrech a Training Fellowship grant, and the National Institute for Environmental Health Sciences through the University of Iowa Environmental Health Sciences Research Cer eNIEHnS/NtIH P30 ESO5. This560 manuscript isalso supported by VA Merit Grant, NIH HL-317, 2and1NHAII3085. 1We thank Anita Riggan for outstanding secretarial assistance. Address correspondence to Gary W. Hunninghake, University of Iowa CllegeooMfedicin, e C-33, 200 Hawkins Drive, Iowa City, IA 542, U2SA2. E-mail : [email protected]
PY - 1999
Y1 - 1999
N2 - Hypersensitivity pneumonitis (HP) is a granulomatous inflammatory lung disease that is usually triggered by organic antigens. At early time points after inhalation of antigen, neutrophilic inflammation is prominent in the lungs. Interleukin (IL)-8 is a potent chemoattractant for neutrophils and it is known that alveolar macrophages can release IL-8 after exposure to organic antigens. However, the role of respiratory epithelial cells in the production of IL-8 in HP is unknown. We exposed A 549 epithelial cells to the thermophilic bacteria Saccharopolyspora rectivirgula (SR), and measured IL-8 release via enzyme-linked immunosorbent assay (ELISA) and IL-8 messenger RNA (mRNA) induction via Northern analysis. We observed a dose- and time- dependent release of IL-8 in response to SR. The maximal release of IL-8 was measured at 24-48 hours after exposure. There was also an increase in release of IL-6 in a time-dependent fashion. SR induced a peak increase in IL-8 mRNA at 12-24 hours. SR also triggered expression of the DNA-binding activity of NF-κB, a transcription factor that mediates activation of the IL-8 gene. Both corticosteroids and IL-10 blocked the production of IL-8. The release of IL8 was not mediated through IL-1β. These data suggest that SR-induced IL-8 production in airway epithelium may play a role in the initial inflammatory response in HP.
AB - Hypersensitivity pneumonitis (HP) is a granulomatous inflammatory lung disease that is usually triggered by organic antigens. At early time points after inhalation of antigen, neutrophilic inflammation is prominent in the lungs. Interleukin (IL)-8 is a potent chemoattractant for neutrophils and it is known that alveolar macrophages can release IL-8 after exposure to organic antigens. However, the role of respiratory epithelial cells in the production of IL-8 in HP is unknown. We exposed A 549 epithelial cells to the thermophilic bacteria Saccharopolyspora rectivirgula (SR), and measured IL-8 release via enzyme-linked immunosorbent assay (ELISA) and IL-8 messenger RNA (mRNA) induction via Northern analysis. We observed a dose- and time- dependent release of IL-8 in response to SR. The maximal release of IL-8 was measured at 24-48 hours after exposure. There was also an increase in release of IL-6 in a time-dependent fashion. SR induced a peak increase in IL-8 mRNA at 12-24 hours. SR also triggered expression of the DNA-binding activity of NF-κB, a transcription factor that mediates activation of the IL-8 gene. Both corticosteroids and IL-10 blocked the production of IL-8. The release of IL8 was not mediated through IL-1β. These data suggest that SR-induced IL-8 production in airway epithelium may play a role in the initial inflammatory response in HP.
KW - Hypersensitivity pneumonitis
KW - Inflammation
KW - Interleukin-8
KW - Respiratory epithelial cells
UR - https://www.scopus.com/pages/publications/0032929098
U2 - 10.1080/019021499270277
DO - 10.1080/019021499270277
M3 - Article
C2 - 10352952
SN - 0190-2148
VL - 25
SP - 217
EP - 228
JO - Experimental Lung Research
JF - Experimental Lung Research
IS - 3
ER -