scholarly journals Macrophages and Epithelial Cells Respond Differently to the Pseudomonas aeruginosa Type III Secretion System

1999 ◽  
Vol 67 (6) ◽  
pp. 3151-3154 ◽  
Author(s):  
Jenifer Coburn ◽  
Dara W. Frank
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Target Cell ◽  
Type Iii Secretion ◽  
Type Iii Secretion System ◽  
Secretion System ◽  
Lung Epithelial Cells ◽  
Cell Type ◽  
Type Iii ◽  
Lung Epithelial

ABSTRACT The multiple effects of Pseudomonas aeruginosa type III secretion have largely been attributed to variations in cytotoxin expression between strains. Here we show that the target cell type is also important. While lung epithelial cells showed significant changes in morphology but not viability when infected with P. aeruginosa, macrophages were efficiently killed by P. aeruginosa. Both responses were dependent on the type III secretion system.

scholarly journals The Posttranscriptional Regulator RsmA Plays a Role in the Interaction between Pseudomonas aeruginosa and Human Airway Epithelial Cells by Positively Regulating the Type III Secretion System

2006 ◽  
Vol 74 (5) ◽  
pp. 3012-3015 ◽  
Author(s):  
Heidi Mulcahy ◽  
Julie O'Callaghan ◽  
Eoin P. O'Grady ◽  
Claire Adams ◽  
Fergal O'Gara
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Type Iii Secretion ◽  
Posttranscriptional Regulation ◽  
Rna Binding ◽  
Type Iii Secretion System ◽  
Airway Epithelial Cells ◽  
Secretion System ◽  
Airway Epithelial ◽  
Type Iii

ABSTRACT Posttranscriptional regulation of certain virulence-related genes in Pseudomonas aeruginosa is brought about by RsmA, a small RNA-binding protein. During interaction with airway epithelial cells, RsmA promoted actin depolymerization, cytotoxicity, and anti-internalization of P. aeruginosa by positively regulating the virulence-associated type III secretion system.

scholarly journals The Pseudomonas aeruginosa Magnesium Transporter MgtE Inhibits Transcription of the Type III Secretion System

2009 ◽  
Vol 78 (3) ◽  
pp. 1239-1249 ◽  
Author(s):  
Gregory G. Anderson ◽  
Timothy L. Yahr ◽  
Rustin R. Lovewell ◽  
George A. O'Toole
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Type Iii Secretion ◽  
Biofilm Formation ◽  
Type Iii Secretion System ◽  
Secretion System ◽  
Bacterial Biofilm ◽  
Magnesium Transport ◽  
Type Iii ◽  
Magnesium Transporter

ABSTRACT Pseudomonas aeruginosa is an opportunistic pathogen that causes life-long pneumonia in individuals with cystic fibrosis (CF). These long-term infections are maintained by bacterial biofilm formation in the CF lung. We have recently developed a model of P. aeruginosa biofilm formation on cultured CF airway epithelial cells. Using this model, we discovered that mutation of a putative magnesium transporter gene, called mgtE, led to increased cytotoxicity of P. aeruginosa toward epithelial cells. This altered toxicity appeared to be dependent upon expression of the type III secretion system (T3SS). In this study, we found that mutation of mgtE results in increased T3SS gene transcription. Through epistasis analyses, we discovered that MgtE influences the ExsE-ExsC-ExsD-ExsA gene regulatory system of T3SS by either directly or indirectly inhibiting ExsA activity. While variations in calcium levels modulate T3SS gene expression in P. aeruginosa, we found that addition of exogenous magnesium did not inhibit T3SS activity. Furthermore, mgtE variants that were defective for magnesium transport could still complement the cytotoxicity effect. Thus, the magnesium transport function of MgtE does not fully explain the regulatory effects of MgtE on cytotoxicity. Overall, our results indicate that MgtE modulates expression of T3SS genes.

scholarly journals Effector ExoU from the Type III Secretion System Is an Important Modulator of Gene Expression in Lung Epithelial Cells in Response to Pseudomonas aeruginosa Infection

2003 ◽  
Vol 71 (10) ◽  
pp. 6035-6044 ◽  
Author(s):  
B. McMorran ◽  
L. Town ◽  
E. Costelloe ◽  
J. Palmer ◽  
J. Engel ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pseudomonas Aeruginosa ◽  
Transcription Factor ◽  
Epithelial Cells ◽  
Type Iii Secretion ◽  
Lung Epithelial Cells ◽  
Type Iii ◽  
Lung Epithelial ◽  
Factor C ◽  
Host Genes

ABSTRACT Pseudomonas aeruginosa is an important pathogen in immunocompromised patients and secretes a diverse set of virulence factors that aid colonization and influence host cell defenses. An important early step in the establishment of infection is the production of type III-secreted effectors translocated into host cells by the bacteria. We used cDNA microarrays to compare the transcriptomic response of lung epithelial cells to P. aeruginosa mutants defective in type IV pili, the type III secretion apparatus, or in the production of specific type III-secreted effectors. Of the 18,000 cDNA clones analyzed, 55 were induced or repressed after 4 h of infection and could be classified into four different expression patterns. These include (i) host genes that are induced or repressed in a type III secretion-independent manner (32 clones), (ii) host genes induced specifically by ExoU (20 clones), and (iii) host genes induced in an ExoU-independent but type III secretion dependent manner (3 clones). In particular, ExoU was essential for the expression of immediate-early response genes, including the transcription factor c-Fos. ExoU-dependent gene expression was mediated in part by early and transient activation of the AP1 transcription factor complex. In conclusion, the present study provides a detailed insight into the response of epithelial cells to infection and indicates the significant role played by the type III virulence mechanism in the initial host response.

scholarly journals Positive regulation of Type III secretion effectors and virulence by RyhB paralogs in Salmonella enterica serovar Enteritidis

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Binjie Chen ◽  
Xianchen Meng ◽  
Jie Ni ◽  
Mengping He ◽  
Yanfei Chen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Type Iii Secretion ◽  
Salmonella Enterica ◽  
Intestinal Epithelial Cells ◽  
Type Iii Secretion System ◽  
Secretion System ◽  
Intestinal Epithelial ◽  
Type Iii ◽  
Effector Gene ◽  
T3ss Effector

AbstractSmall non-coding RNA RyhB is a key regulator of iron homeostasis in bacteria by sensing iron availability in the environment. Although RyhB is known to influence bacterial virulence by interacting with iron metabolism related regulators, its interaction with virulence genes, especially the Type III secretion system (T3SS), has not been reported. Here, we demonstrate that two RyhB paralogs of Salmonella enterica serovar Enteritidis upregulate Type III secretion system (T3SS) effectors, and consequently affect Salmonella invasion into intestinal epithelial cells. Specifically, we found that RyhB-1 modulate Salmonella response to stress condition of iron deficiency and hypoxia, and stress in simulated intestinal environment (SIE). Under SIE culture conditions, both RyhB-1 and RyhB-2 are drastically induced and directly upregulate the expression of T3SS effector gene sipA by interacting with its 5′ untranslated region (5′ UTR) via an incomplete base-pairing mechanism. In addition, the RyhB paralogs upregulate the expression of T3SS effector gene sopE. By regulating the invasion-related genes, RyhBs in turn affect the ability of S. Enteritidis to adhere to and invade into intestinal epithelial cells. Our findings provide evidence that RyhBs function as critical virulence factors by directly regulating virulence-related gene expression. Thus, inhibition of RyhBs may be a potential strategy to attenuate Salmonella.

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