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Interactions between Pseudomonas aeruginosa and Streptococcus salivarius and effects on the host immune response

Award Number: F31HL162487
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 02/01/2022
PERIOD OF PERFORMANCE END DATE: 08/18/2023

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Interactions between Pseudomonas aeruginosa and Streptococcus salivarius and effects on the host immune response - PROJECT SUMMARY Pseudomonas aeruginosa is a multi-drug resistant pathogen which causes chronic lung infections and is a leading cause of mortality in cystic fibrosis (CF) patients. P. aeruginosa produces a biofilm matrix which protects the bacterium from antimicrobials and aids in host immune evasion. The main component of this biofilm matrix are three exopolysaccharides- Pel, Psl, and alginate. Additionally, P. aeruginosa contributes to inflammation and lung damage by activating the pro-inflammatory NF-κB pathway in host cells, leading to the production of inflammatory cytokines and recruitment of inflammatory immune cells to the lungs, causing subsequent tissue damage. NF-κB activation is naturally elevated in the lungs of CF patients, which is further exacerbated by P. aeruginosa infection. Although P. aeruginosa is generally studied as an isolated infection, other species colonize the lungs of CF patients and could potentially modulate P. aeruginosa virulence. Colonization of oral streptococci in the lungs has recently been associated with CF lung stability. Of these oral streptococci, Streptococcus salivarius, was found to be the most prevalent streptococcal species in the lungs of CF patients. S. salivarius has been shown to inhibit growth of multiple respiratory pathogens, as well as inhibit activation of the NF-κB pathway in human bronchial epithelial cells. Although S. salivarius has been correlated with stable lung function in CF patients, no studies have examined interactions between S. salivarius and P. aeruginosa and their impact on the host response. To characterize the interactions between the two species, we first measured changes in biofilm formation of the two species when co-cultured. Our preliminary results demonstrated that S. salivarius biofilm formation is significantly increased in the presence of the exopolysaccharide Psl, which is produced by the non-mucoid P. aeruginosa strain PAO1. Additionally, the S. salivarius maltose-binding protein MalE was overexpressed in the presence of P. aeruginosa. Aim 1 will test the hypothesis that MalE interacts with Psl to promote biofilm formation of S. salivarius. Whole-cell ELISA and isothermal titration calorimetry will be used to characterize the binding affinity of the two targets. Our preliminary data also demonstrated that Drosophila melanogaster were protected from P. aeruginosa-mediated killing in the presence of S. salivarius, highlighting the need to further examine the impact of S. salivarius on P. aeruginosa pathogenesis. Aim 2 will test the hypothesis that the presence of S. salivarius in the CF lung improves lung function by downregulating pro- inflammatory cytokines downstream of NF-κB produced in response to P. aeruginosa infection. We will develop a CF rat model of co-infection in which we measure specific pro-inflammatory cytokines, neutrophil recruitment, and lung histopathology during P. aeruginosa infection in the presence or absence of S. salivarius. Data generated from this proposal will promote our understanding of how S. salivarius incorporates into the P. aeruginosa biofilm and modulates the host response to a P. aeruginosa infection.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2024 ( Subtotal = -$19,911 )
2024	2023	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Lung Diseases Research	000	2	1/27/2024	NON-COMPETING CONTINUATION	-$19,911
2024	2023	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Lung Diseases Research	001	2	6/24/2024	NON-COMPETING CONTINUATION	$0
														Subtotal = -$19,911

Issue Date FY: 2023 ( Subtotal = $38,984 )
2023	2023	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Lung Diseases Research	000	2	3/20/2023	NON-COMPETING CONTINUATION	$38,984
														Subtotal = $38,984

Issue Date FY: 2022 ( Subtotal = $38,042 )
2022	2022	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Lung Diseases Research	000	1	1/5/2022	NEW	$37,326
2022	2022	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH ST	BIRMINGHAM	AL	35294	JEFFERSON	USA	Lung Diseases Research	001	1	7/1/2022	NEW	$716
														Subtotal = $38,042

Grand Total All Awards = $57,115

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Interactions between Pseudomonas aeruginosa and Streptococcus salivarius and effects on the host immune response

Award Number: F31HL162487

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 02/01/2022

PERIOD OF PERFORMANCE END DATE: 08/18/2023

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