Skip to main content
. 2015 Nov 18;5:80. doi: 10.3389/fcimb.2015.00080

Figure 1.

Figure 1

A visualization of the known host-pathogen interactions of Burkholderia spp. with host epithelial cells. (A) Bacterial factors known to interact with host epithelial cells. Items in bold are specific for Burkholderia pseudomallei and/or mallei. Invasion of bacteria is driven by several bacterial factors; capsule (Phewkliang et al., 2010), cable pili (Sajjan and Forstner, 1992, 1993), pilA (Essex-Lopresti et al., 2005), adhesins [boaA/B (Balder et al., 2010; Lu et al., 2012) and other auto-transporter adhesins (Mil-Homens and Fialho, 2012; Lafontaine et al., 2014)], LPS (Dziarski and Gupta, 2000), Lipid A (Dziarski and Gupta, 2000), flagella (Tomich et al., 2002; Chuaygud et al., 2008; Allwood et al., 2011), irl locus (Jones et al., 1997), a 22kDa adhesion (Sajjan and Forstner, 1993), lipase (Mullen et al., 2007), and the metalloprotease ZmpA (Gingues et al., 2005). Receptor binding events on epithelial cells occur via mucin (Sajjan and Forstner, 1992), the asialogangliosides GM1/2 (Gori et al., 1999), toll-like receptors (West et al., 2009, 2013), and cytokeratin 13 (Sajjan et al., 2002). Bacterial escape from vacuoles is driven by the T3SS (Pilatz et al., 2006; Gong et al., 2011) and once the bacteria are cytosolic BimA affects host actin polymerization (Stevens et al., 2005; Sitthidet et al., 2011). Direct entry into epithelial cells has also been linked to the T3SS and the effector protein BopE which also affects host actin (Rudolph et al., 1999; Stevens et al., 2003; Muangsombut et al., 2008; Muangman et al., 2011). (B) The host response to Burkholderia infection from epithelial cells. Inflammation is driven by Nfk-B induction (Dziarski and Gupta, 2000) of IL-8 (Palfreyman et al., 1997; Fink et al., 2003; Utaisincharoen et al., 2005; Sim et al., 2009; Lu et al., 2012), IL-6 (Sim et al., 2009; Lu et al., 2012) and IL-1β (Sim et al., 2009; Lu et al., 2012; Gillette et al., 2013), TNF-α, MCP-1 and CCL20 (Sim et al., 2009; Lu et al., 2012). Tight junctions are disrupted (Kim et al., 2005; Duff et al., 2006; Ferreira et al., 2015) and extracellular matrix components degraded by matrix metalloproteases (Wright et al., 2011).