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Structural Basis for Burkholderia cepacia Complex Pili Mediated Adherence in Cystic Fibrosis

Award Number: F31AI198428
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 04/23/2026
PERIOD OF PERFORMANCE END DATE: 03/31/2028

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Structural Basis for Burkholderia cepacia Complex Pili Mediated Adherence in Cystic Fibrosis - Abstract Cystic fibrosis (CF) is caused by a dysfunctional cystic fibrosis transmembrane conductance regulator (CFTR) protein, leading to impaired mucociliary clearance and the accumulation of thick mucus in the airway, often resulting in chronic bacterial infections. Bacteria within the Burkholderia cepacia complex (BCC) are associated with severe infections in people with CF (pwCF). BCC species are inherently antibiotic-resistant, making effective treatments for BCC infections scarce. One potential therapeutic target for BCC treatment is the pili that mediate virulence factors like adherence and biofilm formation. One type of chaperone usher pathway (CUP) pilus, known as cable pilus, is often implicated in facilitating host adherence and drive biofilm formation in the BCC. However, it remains unknown whether the cable pilus is the sole pilus type produced during different stages of BCC infections, and no structures of BCC pili have been characterized. Currently, highly effective CFTR modulator therapies (HEMT) are commonly used in pwCF. However, the influence and interaction of BCC infection with host cells under HEMT remain unclear. This F31 proposal aims to elucidate the dynamics of BCC pili production and characterize the functions of these pili in CF infection. We hypothesize that multiple types of BCC pili are present and contribute differently at various stages of infection, including adherence, colonization, and biofilm formation. Aim 1 of this proposal explores the effect of different growth conditions on BCC pili production and the roles of pili in adherence to epithelial cells. We will utilize cryogenic-electron microscopy (cryo-EM) and adherence assays, and mutagenesis methods to characterize the pili produced by BCC and their role in adherence. Aim 2 investigates the interaction of BCC cells with CF epithelial cells in situ. We will use cryo-electron tomography (cryo-ET) to visualize interfaces of CF cells with BCC in the presence and absence of ETI HEMT.


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: 2026 ( Subtotal = $43,769 )
2026	2026	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Allergy and Infectious Diseases Research	001	1	4/21/2026	NEW	$0
2026	2026	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Allergy and Infectious Diseases Research	000	1	4/21/2026	NEW	$43,769
														Subtotal = $43,769

Grand Total All Awards = $43,769

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Structural Basis for Burkholderia cepacia Complex Pili Mediated Adherence in Cystic Fibrosis

Award Number: F31AI198428

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 04/23/2026

PERIOD OF PERFORMANCE END DATE: 03/31/2028

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