Abstract
Background: Toll like receptor 9 (TLR9) agonist CpG-ODN is being explored as an anti-allergic drug for asthma. However TLR9 could play a role in COPD. Cigarette smoke induced IL-8 production is partly TLR9 mediated. Aim: To investigate the (extra)-pulmonary effects of CpG-ODN. We hypothesized that pulmonary TLR9 activation induces neutrophil influx which could lead to adverse effects. Methods: A single dose of 0.01, 0.05 or 0.25nMol/gBW GpGODN was targeted to balb/c mice lungs by aspiration (acute). Next 0.01nMol/gBW GpGODN was administered repeatedly for 5 days (subchronic) or 5 weeks (chronic). 24 hours after last exposures, measurements were done: lung function; hypertension and heart hypertrophy; lung weight; blood and bronchoalveolar lavage (BAL) analysis; morphology of unlavaged lungs. Results: Total BAL cells were increased in all CpG-ODN mice (p
| Original language | English |
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| Publication status | Published - 1 Sept 2011 |
Keywords
- CpG oligodeoxynucleotide
- toll like receptor 9
- cigarette smoke
- interleukin 8
- European
- society
- lung
- lymphocyte
- long term exposure
- lung weight
- neutrophil
- heart hypertrophy
- heart right ventricle
- blood
- aspiration
- Bagg albino mouse
- heart weight
- exposure
- hypertension
- single drug dose
- agonist
- adverse drug reaction
- asthma
- mouse
- morphology
- lung lavage
- peak expiratory flow
- airway resistance
- cardiovascular effect
- lung function