Role of Pneumococcal NanA Neuraminidase Activity in Peripheral Blood

The most frequent form of hemolytic-uremic syndrome (HUS) is associated with infections caused by Shiga-like toxin-producing Enterohaemorrhagic (STEC). In rarer cases HUS can be triggered by . While production of Shiga-like toxins explains STEC-HUS, the mechanisms of pneumococcal HUS are less well-k...

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Bibliographic Details
Published in:Frontiers in cellular and infection microbiology 2019-06, Vol.9, p.218-218
Main Authors: Syed, Shahan, Hakala, Pipsa, Singh, Anirudh K, Lapatto, Helena A K, King, Samantha J, Meri, Seppo, Jokiranta, T Sakari, Haapasalo, Karita
Format: Article
Language:English
Subjects:
alternative pathway
Bacterial Proteins - genetics
Blood Platelets - metabolism
Cellular and Infection Microbiology
Complement System Proteins - drug effects
Erythrocytes
HEK293 Cells
Hemolysis
Hemolytic-Uremic Syndrome - microbiology
Humans
Inflammation
Neuraminidase - blood
Neuraminidase - genetics
Neuraminidase - metabolism
Neuraminidase - pharmacology
Pneumococcal Infections - microbiology
pneumococcus
pneumonia
Sequence Deletion
Sialic Acids
sialidase
Streptococcus pneumoniae - enzymology
Streptococcus pneumoniae - metabolism
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Summary:The most frequent form of hemolytic-uremic syndrome (HUS) is associated with infections caused by Shiga-like toxin-producing Enterohaemorrhagic (STEC). In rarer cases HUS can be triggered by . While production of Shiga-like toxins explains STEC-HUS, the mechanisms of pneumococcal HUS are less well-known produces neuraminidases with activity against cell surface sialic acids that are critical for factor H-mediated complement regulation on cells and platelets. The aim of this study was to find out whether neuraminidase NanA could trigger complement activation and hemolysis in whole blood. We studied clinical isolates and two laboratory strains, a wild-type strain expressing NanA, and a NanA deletion mutant for their ability to remove sialic acids from various human cells and platelets. Red blood cell lysis and activation of complement was measured by incubating whole blood with bacterial culture supernatants. We show here that NanA expressing strains and isolates are able to remove sialic acids from cells, and platelets. Removal of sialic acids by NanA increased complement activity in whole blood, while absence of NanA blocked complement triggering and hemolytic activity indicating that removal of sialic acids by NanA could potentially trigger pHUS.
ISSN:2235-2988
2235-2988
DOI:10.3389/fcimb.2019.00218