Abstract
SummaryCancer patients are known to be highly susceptible to Pseudomonas aeruginosa (Pa) infection, but it remains unknown whether alterations at the tumor cell level can contribute to infection. This study explored how cellular changes associated with tumor metastasis influence Pa infection using highly metastatic MTLn3 cells and non-metastatic MTC cells as cell culture models. MTLn3 cells were found to be more sensitive to Pa infection than MTC cells based on increased translocation of the type III secretion effector, ExoS, into MTLn3 cells. Subsequent studies found that higher levels of ExoS translocation into MTLn3 cells related to Pa entry and secretion of ExoS within MTLn3 cells, rather than conventional ExoS translocation by external Pa. ExoS includes both Rho GTPase activating protein (GAP) and ADP-ribosyltransferase (ADPRT) enzyme activities, and differences in MTLn3 and MTC cell responsiveness to ExoS were found to relate to the targeting of ExoS-GAP activity to Rho GTPases. MTLn3 cell migration is mediated by RhoA activation at the leading edge, and inhibition of RhoA activity decreased ExoS translocation into MTLn3 cells to levels similar to those of MTC cells. The ability of Pa to be internalized and transfer ExoS more efficiently in association with Rho activation during tumor metastasis confirms that alterations in cell migration that occur in conjunction with tumor metastasis contribute to Pa infection in cancer patients. This study also raises the possibility that Pa might serve as a biological tool for dissecting or detecting cellular alterations associated with tumor metastasis.
Highlights
The relationship between bacterial infections and cancer is complex
Summary Cancer patients are known to be highly susceptible to Pseudomonas aeruginosa (Pa) infection, but it remains unknown whether alterations at the tumor cell level can contribute to infection
This study explored how cellular changes associated with tumor metastasis influence Pa infection using highly metastatic MTLn3 cells and nonmetastatic MTC cells as cell culture models
Summary
The relationship between bacterial infections and cancer is complex Bacteria, such as Helicobacter pylori, are a proven carcinogen in the development of gastric cancer and mucosaassociated lymphoid tissue lymphoma (Crowe, 2005; Montalban et al, 2001). Other bacteria, such as Salmonella typhi, Streptococcus bovis and Chlamydia pneumoniae have been linked to the induction of specific types of cancers in association with chronic infection, inflammation or immune suppressive mechanisms (Dutta et al, 2000; Gold et al, 2004; Koyi et al, 2001; Kuper et al, 2000). Relationships between bacterial infection and tumor induction introduce the notion that there might be commonalities in mechanisms of bacterial pathogenesis and tumor induction that can be applied to an understanding of neoplastic processes
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