Legionella pneumophila (Lp.), the causative agent of Legionnaires’ disease, has been well known for infecting and replicating inside airway macrophages. Previous results from our laboratory indicated that Lp. attaches to non-polarized lung epithelial cells by binding and activating E-cadherin and β1-integrin.
However, in the polarized alveolar epithelia these receptors are segregated from the apical cell surface by tight junctions (TJs).
Our results showed that Lp. behaves as an opportunistic pathogen that efficiently targets disrupted, but not integrated epithelial cell monolayer. In such conditions,
Lp. can reach its host-cell receptors and consequently invade and replicate intracellularly, producing large amount of bacterial progeny. These results and
clinical evidence suggest the contribution of damaged airway epithelia to Legionellosis by providing a replication reservoir for the bacteria.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:OTU.1807/33549 |
| Date | 27 November 2012 |
| Creators | Tabatabaeiyazdi, Zohreh |
| Contributors | Terebiznik, Mauricio |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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