Asian sand dust enhances murine lung inflammation caused by Klebsiella pneumoniae

Journal Article · Sun Jan 15 04:00:00 EST 2012 · Toxicology and Applied Pharmacology

DOI:https://doi.org/10.1016/J.TAAP.2011.11.003· OSTI ID:22215217

He, Miao ^[1]; Ichinose, Takamichi; Yoshida, Seiichi ^[2]; Yamamoto, Shoji; Inoue, Ken-ichiro; Takano, Hirohisa; Yanagisawa, Rie ^[3]; Nishikawa, Masataka; Mori, Ikuko ^[4]; Sun, Guifan ^[1]; Shibamoto, Takayuki ^[5]

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1. Department of Environmental and Occupational Health, College of Public Health, China Medical University, 11001, Shenyang (China)
2. Department of Health Sciences, Oita University of Nursing and Health Sciences, 870-1201, Oita (Japan)
3. Pathophysiology Research Team, National Institute for Environmental Studies, 305-8506, Tsukuba, Ibaraki (Japan)
4. Environmental Chemistry Division, National Institute for Environmental Studies, 305-8506, Tsukuba, Ibaraki (Japan)
5. Department of Environmental Toxicology, University of California, Davis, CA 95616 (United States)

Inhaling concomitants from Asian sand dust (ASD) may result in exacerbation of pneumonia by the pathogen. The exacerbating effect of ASD on pneumonia induced by Klebsiella pneumoniae (KP) was investigated in ICR mice. The organic substances adsorbed onto ASD collected from the atmosphere of Iki-island in Japan were excluded by heat treatment at 360 °C for 30 min. ICR mice were instilled intratracheally with ASD at doses of 0.05 mg or 0.2 mg/mouse four times at 2-week intervals (total dose of 0.2 mg or 0.8 mg/mouse) and were administrated with ASD in the presence or absence of KP at the last intratracheal instillation. Pathologically, ASD caused exacerbation of pneumonia by KP as shown by increased inflammatory cells within the bronchiolar and the alveolar compartments. ASD enhanced the neutrophil number dose dependently as well as the expression of cytokines (IL-1β, IL-6, IL-12, IFN-γ, TNF-α) and chemokines (KC, MCP-1, MIP-1α) related to KP in BALF. In an in vitro study using RAW264.7 cells, combined treatment of ASD and KP increased gene expression of IL-1β, IL-6, IFN-β, KC, MCP-1, and MIP-1α. The same treatment tended to increase the protein level of IL-1β, TNF-α and MCP-1 in a culture medium compared to each treatment alone. The combined treatment tended to increase the gene expression of Toll-like receptor 2 (TLR2), and NALP3, ASC and caspase-1 compared with KP alone. These results suggest that the exacerbation of pneumonia by ASD + KP was due to the enhanced production of pro-inflammatory mediators via activation of TLR2 and NALP3 inflammasome pathways in alveolar macrophages.

• OSTI ID: 22215217
• Journal Information: Toxicology and Applied Pharmacology, Journal Name: Toxicology and Applied Pharmacology Journal Issue: 2 Vol. 258; ISSN TXAPA9; ISSN 0041-008X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
DUSTS
INFLAMMATION
ION CYCLOTRON-RESONANCE
KLEBSIELLA
LUNGS
LYMPHOKINES
MACROPHAGES
MICE
NEUTROPHILS
PNEUMONIA
RECEPTORS