tetano
Editor, Senior Moderator
Innfect Immun. 2017 Jan 17. pii: IAI.01044-16. doi: 10.1128/IAI.01044-16. [Epub ahead of print] Pneumococcal neuraminidase A (NanA) promotes biofilm formation and synergizes with influenza A virus in nasal colonization and middle ear infection.
Wren JT[SUP]1[/SUP], Blevins LK[SUP]1[/SUP], Pang B[SUP]1[/SUP], Basu Roy A[SUP]1,[/SUP][SUP]2[/SUP], Oliver MB[SUP]1,[/SUP][SUP]2[/SUP], Reimche JL[SUP]1[/SUP], Wozniak JE[SUP]1[/SUP], Alexander-Miller MA[SUP]1[/SUP], Swords WE[SUP]3,[/SUP][SUP]2[/SUP].
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Abstract
Even in the vaccine era, Streptococcus pneumoniae (pneumococcus) remains a leading cause of otitis media, a significant public health burden, in large because of its high prevalence of nasal colonization in children. The primary pneumococcal neuraminidase NanA, which is a sialidase that catalyzes the cleavage of terminal sialic acids from host glycoconjugates, is involved in both of these processes. Coinfection with influenza A virus, which also expresses a neuraminidase, exacerbates nasal colonization and disease by S. pneumoniae, in part via the synergistic contributions of the viral neuraminidase. The specific role of its pneumococcal counterpart NanA in this interaction, however, is less well-understood. We demonstrate in a mouse model that NanA-deficient pneumococci are impaired in both nasal colonization and middle ear infection. Coinfection with neuraminidase-expressing influenza virus potentiates both but not to wild-type levels, suggesting an intrinsic role of NanA. Using in vitro models, we show that while NanA contributes to both epithelial adherence and biofilm viability, its effect on the latter is actually independent of its sialidase activity. These data indicate that NanA contributes both enzymatically and non-enzymatically to pneumococcal pathogenesis and, as such, suggest that it is not a redundant bystander during coinfection with influenza A virus. Rather, that its expression is required for the full synergism between these two pathogens.
Copyright ? 2017 American Society for Microbiology.
PMID: 28096183 DOI: 10.1128/IAI.01044-16
[PubMed - as supplied by publisher]
Wren JT[SUP]1[/SUP], Blevins LK[SUP]1[/SUP], Pang B[SUP]1[/SUP], Basu Roy A[SUP]1,[/SUP][SUP]2[/SUP], Oliver MB[SUP]1,[/SUP][SUP]2[/SUP], Reimche JL[SUP]1[/SUP], Wozniak JE[SUP]1[/SUP], Alexander-Miller MA[SUP]1[/SUP], Swords WE[SUP]3,[/SUP][SUP]2[/SUP].
Author information
Abstract
Even in the vaccine era, Streptococcus pneumoniae (pneumococcus) remains a leading cause of otitis media, a significant public health burden, in large because of its high prevalence of nasal colonization in children. The primary pneumococcal neuraminidase NanA, which is a sialidase that catalyzes the cleavage of terminal sialic acids from host glycoconjugates, is involved in both of these processes. Coinfection with influenza A virus, which also expresses a neuraminidase, exacerbates nasal colonization and disease by S. pneumoniae, in part via the synergistic contributions of the viral neuraminidase. The specific role of its pneumococcal counterpart NanA in this interaction, however, is less well-understood. We demonstrate in a mouse model that NanA-deficient pneumococci are impaired in both nasal colonization and middle ear infection. Coinfection with neuraminidase-expressing influenza virus potentiates both but not to wild-type levels, suggesting an intrinsic role of NanA. Using in vitro models, we show that while NanA contributes to both epithelial adherence and biofilm viability, its effect on the latter is actually independent of its sialidase activity. These data indicate that NanA contributes both enzymatically and non-enzymatically to pneumococcal pathogenesis and, as such, suggest that it is not a redundant bystander during coinfection with influenza A virus. Rather, that its expression is required for the full synergism between these two pathogens.
Copyright ? 2017 American Society for Microbiology.
PMID: 28096183 DOI: 10.1128/IAI.01044-16
[PubMed - as supplied by publisher]
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