Role of complement in defense of the middle ear revealed by restoring the virulence of nontypeable Haemophilus influenzae siaB mutants.

Role of complement in defense of the middle ear revealed by restoring the virulence of nontypeable Haemophilus influenzae siaB mutants. Research Abstract Details 

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Role of complement in defense of the middle ear revealed by restoring the virulence of nontypeable Haemophilus influenzae siaB mutants. Abstract Text:

Marisol A Figueira,Sanjay Ram,Richard Goldstein,Derek W Hood,E Richard Moxon,Stephen I Pelton,

Nontypeable (NT) Haemophilus influenzae is an important cause of otitis media in children. We have shown previously that NT H. influenzae mutants defective in their ability to sialylate lipopolysaccharide (LPS), called siaB mutants, show attenuated virulence in a chinchilla model of experimental otitis media (EOM). We show that complement is a key arm of host innate immunity against NT H. influenzae-induced EOM. Depleting complement in chinchillas by use of cobra venom factor (CoVF) rendered two otherwise avirulent siaB mutants fully virulent and able to cause EOM with severity similar to that of wild-type strains. Clearance of infection caused by siaB mutants in CoVF-treated animals coincided with reappearance of C3. Wild-type strains were more resistant to direct complement-mediated killing than their siaB mutants. The serum-resistant strain bound less C3 and C4 than the serum-sensitive strain. Neither NT H. influenzae strain tested bound factor H (alternative complement pathway regulator). Selective activation of the alternative pathway resulted in more C3 binding to siaB mutants. LPS sialylation had a more profound impact on the amount of alternative-pathway-mediated C3 binding ( approximately 5-fold decrease in fluorescence) when LPS was the main C3 target, as occurred on the more serum-resistant strain. In contrast, only an approximately 1.5-fold decrease in fluorescence intensity of C3 binding was seen with the serum-sensitive strain, where surface proteins predominantly bound C3. Differences in binding sites for C3 and C4 may account for variations in serum resistance between NT H. influenzae strains, which in turn may impact their virulence. These data demonstrate a central role for complement in innate immune defenses against NT H. influenzae infections and specifically EOM.

Role of complement in defense of the middle ear revealed by restoring the virulence of nontypeable Haemophilus influenzae siaB mutants. Publishing Authors By Initials

MA Figueira,S Ram,R Goldstein,DW Hood,ER Moxon,SI Pelton,

For similar biological phenomena, cell phenomena, and immunity: biological phenomena: microbiologic phenomena: virulence research abstracts see: biological phenomena, cell phenomena, and immunity: biological phenomena: microbiologic phenomena: virulence research

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Role of complement in defense of the middle ear revealed by restoring the virulence of nontypeable Haemophilus influenzae siaB mutants. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Infection and immunity

VOLUME: 75

Page Numbers: 325-33

Journal Abbreviation: Infect. Immun.

ISSN: 0019-9567

DAY: 6

MONTH: 11

YEAR: 2006

Role of complement in defense of the middle ear revealed by restoring the virulence of nontypeable Haemophilus influenzae siaB mutants. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 246127

Role of complement in defense of the middle ear revealed by restoring the virulence of nontypeable Haemophilus influenzae siaB mutants. Keywords Mesh Terms:

KEYWORDS: Virulence

MESH TERMS: microbiology

Chemical & Substance for Abstract: Role of complement in defense of the middle ear revealed by restoring the virulence of nontypeable Haemophilus influenzae siaB mutants. Information

Substance Name: Complement System Proteins

Registry Number: 9007-36-7

Grant and Affiliation Information for Role of complement in defense of the middle ear revealed by restoring the virulence of nontypeable Haemophilus influenzae siaB mutants.

AFFILIATION: Section of Pediatric Infectious Diseases, Maxwell Finland Laboratory for Infectious Diseases, Room 508, 774 Albany Street, Boston Medical Center, Boston, MA 02118, USA. maf6559@bu.edu

Country: United States

AGENCY: United States NIDCD

GRANT: DC005855

ACRONYM: DC

MEDLINETA: Infect Immun

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