Changes in IgA Protease Expression Are Conferred by Changes in Genomes during Persistent Infection by Nontypeable Haemophilus influenzae in Chronic Obstructive Pulmonary Disease

Infection and Immunity
Mary C GalloTimothy F Murphy

Abstract

Nontypeable Haemophilus influenzae (NTHi) is an exclusively human pathobiont that plays a critical role in the course and pathogenesis of chronic obstructive pulmonary disease (COPD). NTHi causes acute exacerbations of COPD and also causes persistent infection of the lower airways. NTHi expresses four IgA protease variants (A1, A2, B1, and B2) that play different roles in virulence. Expression of IgA proteases varies among NTHi strains, but little is known about the frequency and mechanisms by which NTHi modulates IgA protease expression during infection in COPD. To assess expression of IgA protease during natural infection in COPD, we studied IgA protease expression by 101 persistent strains (median duration of persistence, 161 days; range, 2 to 1,422 days) collected longitudinally from patients enrolled in a 20-year study of COPD upon initial acquisition and immediately before clearance from the host. Upon acquisition, 89 (88%) expressed IgA protease. A total of 16 of 101 (16%) strains of NTHi altered expression of IgA protease during persistence. Indels and slipped-strand mispairing of mononucleotide repeats conferred changes in expression of igaA1, igaA2, and igaB1 Strains with igaB2 underwent frequent changes in expression...Continue Reading

References

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Citations

Oct 13, 2020·Critical Reviews in Microbiology·Jiexing LiuZhangyong Song
Feb 10, 2021·Infection and Immunity·Von Vergel L TorresTimothy J Wells
Apr 24, 2021·European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology·Niels Nørskov-LauritsenUNKNOWN ODiD Consortium
Jun 18, 2021·Computational and Structural Biotechnology Journal·Nahikari López-LópezJunkal Garmendia
Sep 10, 2021·Frontiers in Cellular and Infection Microbiology·Jodie AcklandKarl J Staples

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