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Norepinephrine modulates the gene expression of iron-acquiring genes in Pseudomonas aeruginosa isolates.

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Pseudomonas aeruginosa (Pa) is an opportunistic pathogen that causes broad-spectrum diseases in stressed and immunocompromised patients. Norepinephrine (NE) is a stress hormone that enhances bacterial growth, but its mechanistic action is not well known. This research project was designed to determine the expression of iron-acquiring genes in non-mucoid (PAO1) and mucoid (2192) Pa isolates. We hypothesize that supplementing NE to a salt and glucose medium modulates the gene expression of iron-acquiring genes. Bacterial growth in the presence and absence of NE was performed to determine bacterial colony-forming units/ml in 24 hours. Our data shows that supplementation of NE resulted in a multifold increase in growth in the non-mucoid isolate compared to that of the mucoid isolate. Moreover, the gene expression of PvdS, RegA, ToxA, and RpsLd genes speculated in iron acquisition in bacteria have shown differential gene expression of the genes in mucoid and non-mucoid isolates.  Isolate PAO1 occurred to have an up-regulated expression of pvdS and rpsLd. In contrast, RpsLd was down-regulated in mucoid isolates; however, the expression of pvdS and ToxA was up-regulated. The effect of NE on the growth conditions of starved Pa isolates is underway. Overall, our results show that i) the NE has a positive growth effect on mucoid and non-mucoid isolates, and ii) the genes rpsLd and ToxA have different expression profiles in both isolates. Data obtained in this study will provide some understanding of the role of NE in iron acquisition that may enhance bacterial pathogenesis during stressful conditions.    
Title: Norepinephrine modulates the gene expression of iron-acquiring genes in Pseudomonas aeruginosa isolates.
Description:
Pseudomonas aeruginosa (Pa) is an opportunistic pathogen that causes broad-spectrum diseases in stressed and immunocompromised patients.
Norepinephrine (NE) is a stress hormone that enhances bacterial growth, but its mechanistic action is not well known.
This research project was designed to determine the expression of iron-acquiring genes in non-mucoid (PAO1) and mucoid (2192) Pa isolates.
We hypothesize that supplementing NE to a salt and glucose medium modulates the gene expression of iron-acquiring genes.
Bacterial growth in the presence and absence of NE was performed to determine bacterial colony-forming units/ml in 24 hours.
Our data shows that supplementation of NE resulted in a multifold increase in growth in the non-mucoid isolate compared to that of the mucoid isolate.
Moreover, the gene expression of PvdS, RegA, ToxA, and RpsLd genes speculated in iron acquisition in bacteria have shown differential gene expression of the genes in mucoid and non-mucoid isolates.
  Isolate PAO1 occurred to have an up-regulated expression of pvdS and rpsLd.
In contrast, RpsLd was down-regulated in mucoid isolates; however, the expression of pvdS and ToxA was up-regulated.
The effect of NE on the growth conditions of starved Pa isolates is underway.
Overall, our results show that i) the NE has a positive growth effect on mucoid and non-mucoid isolates, and ii) the genes rpsLd and ToxA have different expression profiles in both isolates.
Data obtained in this study will provide some understanding of the role of NE in iron acquisition that may enhance bacterial pathogenesis during stressful conditions.
   .

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