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Serum killing of 'ureaplasma parvum' shows serovar-determined susceptibility for normal individuals and common variable immuno-deficiency patients

Beeton, Michael L., Daha, Mohamed R., El-Shanawany, Tariq, Jolles, Stephen, Kotecha, Sailesh ORCID: https://orcid.org/0000-0003-3535-7627 and Spiller, Owen Bradley ORCID: https://orcid.org/0000-0002-9117-6911 2012. Serum killing of 'ureaplasma parvum' shows serovar-determined susceptibility for normal individuals and common variable immuno-deficiency patients. Immunobiology 217 (2) , pp. 187-194. 10.1016/j.imbio.2011.07.009

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Abstract

Background: Many Gram-negative bacteria, unlike Gram-positive, are directly lysed by complement. Ureaplasma can cause septic arthritis and meningitis in immunocompromised individuals and induce premature birth. Ureaplasma has no cell wall, cannot be Gram-stain classified and its serum susceptibility is unknown. Methods: Survival of Ureaplasma serovars (SV) 1, 3, 6 and 14 (collectively Ureaplasma parvum) were measured following incubation with normal or immunoglobulin-deficient patient serum (relative to heat-inactivated controls). Blocking monoclonal anti-C1q antibody and depletion of calcium, immunoglobulins, or lectins were used to determine the complement pathway responsible for killing. Results: Eighty-three percent of normal sera killed SV1, 67% killed SV6 and 25% killed SV14; greater killing correlating to strong immunoblot identification of anti-Ureaplasma antibodies; killing was abrogated following ProteinA removal of IgG1. All normal sera killed SV3 in a C1q-dependent fashion, irrespective of immunoblot identification of anti-Ureaplasma antibodies; SV3 killing was unaffected by total IgG removal by ProteinG, where complement activity was retained. Only one of four common variable immunodeficient (CVID) patient sera failed to kill SV3, despite profound IgM and IgG deficiency for all; however, killing of SV3 and SV1 was restored with therapeutic intravenous immunoglobulin therapy. Conclusions: Only the classical complement pathway mediated Ureaplasma-cidal activity, sometimes in the absence of observable immunoblot reactive bands.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Subjects: Q Science > QR Microbiology > QR180 Immunology
R Medicine > RJ Pediatrics > RJ101 Child Health. Child health services
Uncontrolled Keywords: complement, common variable immuno-deficiency, hypogammaglobulinemia, innate immunity, ureaplasma
Additional Information: Special Issue COMPLEMENT UK
Publisher: Elsevier
ISSN: 0171-2985
Last Modified: 06 Dec 2022 09:40
URI: https://orca.cardiff.ac.uk/id/eprint/25487

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