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Earlier assessment of the role played by bacteria in acute exacerbations was compromised by a deficiency of quality data and the use of parameters more relevant to invasive infection. Data are reviewed to support a hypothesis that states intrabronchial inflammation reflects an excessive and inappropriate host response (largely mediated by Th17 cells derived from gut\u2010associated lymphoid tissues) to colonising bacteria acting as an \u2018antigen sump\u2019 (in essence, a hypersensitivity reaction). It is proposed that both viral and bacterial infections exacerbate inflammation through a common pathway that involves colonising bacteria. An oral vaccine containing inactivated non\u2010typeable <jats:italic>Haemophilus influenzae<\/jats:italic> augments a protective loop that involves the aspiration of bronchus content into the gut and reduces the severity of acute exacerbations including the need for hospital admission by reducing the \u2018load\u2019 of bacteria comprising this final common path. The positive clinical results from trials using oral NTHi support both the concept that bacterial colonisation of damaged airways is a potent second pathogenic pathway and that oral immunotherapy provides a significant therapeutic advance in limiting damage in chronic obstructive pulmonary disease.<\/jats:p>","DOI":"10.1111\/j.1445-5994.2012.02752.x","type":"journal-article","created":{"date-parts":[[2012,2,28]],"date-time":"2012-02-28T14:05:08Z","timestamp":1330437908000},"page":"607-613","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Towards a vaccine for chronic obstructive pulmonary disease"],"prefix":"10.1111","volume":"42","author":[{"given":"R. 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