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dc.contributor.authorFeng, Wenchao
dc.contributor.authorMinor, Dylan
dc.contributor.authorLiu, Mengyao
dc.contributor.authorLei, Benfang
dc.date.accessioned2018-07-11T14:59:21Z
dc.date.available2018-07-11T14:59:21Z
dc.date.issued2017-09
dc.identifier.citationFeng, Wenchao, Dylan Minor, Mengyao Liu, and Benfang Lei. "Requirement and Synergistic Contribution of PAF acetylhydrolase Sse and Streptolysin S to Inhibition of Neutrophil Recruitment and Systemic Infection by Hypervirulent emm3 Group A Streptococcus...." Infection and Immunity (September 2017). DOI: 10.1128/IAI.00530-17.en_US
dc.identifier.issn1098-5522
dc.identifier.urihttps://scholarworks.montana.edu/xmlui/handle/1/14633
dc.description.abstractHypervirulent group A streptococcus (GAS) can inhibit neutrophil recruitment and cause systemic infection in a mouse model of skin infection. The purpose of this study was to determine whether platelet-activating factor acetylhydrolase Sse and streptolysin S (SLS) have synergistic contributions to inhibition of neutrophil recruitment and systemic infection in subcutaneous infection of mice by MGAS315, a hypervirulent genotype emm3 GAS strain. Deletion of sse and sagA in MGAS315 synergistically reduced the skin lesion size and GAS burden in the liver and spleen. However, the mutants were persistent at skin sites and had similar growth factors in nonimmune blood. Thus, the low numbers of Δsse ΔsagA mutants in the liver and spleen were likely due to their reduction in the systemic dissemination. Few intact and necrotic neutrophils were detected at MGAS315 infection sites. In contrast, many neutrophils and necrotic cells were present at the edge of Δsse mutant infection sites on day 1 and at the edge of and inside Δsse mutant infection sites on day 2. ΔsagA mutant infection sites had massive numbers of and few intact neutrophils at the edge and center of the infection sites, respectively, on day 1 and were full of intact neutrophils or necrotic cells on day 2. Δsse ΔsagA mutant infection sites had massive numbers of intact neutrophils throughout the whole infection site. These sse and sagA deletion-caused changes in the histological pattern at skin infection sites could be complemented. Thus, the sse and sagA deletions synergistically enhance neutrophil recruitment. These findings indicate that both Sse and SLS are required but that neither is sufficient for inhibition of neutrophil recruitment and systemic infection by hypervirulent GAS.en_US
dc.rightsThis Item is protected by copyright and/or related rights. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).en_US
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en_US
dc.titleRequirement and Synergistic Contribution of Platelet-Activating Factor Acetylhydrolase Sse and Streptolysin S to Inhibition of Neutrophil Recruitment and Systemic Infection by Hypervirulent emm3 Group A Streptococcus in Subcutaneous Infection of Miceen_US
dc.typeArticleen_US
mus.citation.extentfirstpagee00530-17en_US
mus.citation.issue12en_US
mus.citation.journaltitleInfection and Immunityen_US
mus.citation.volume85en_US
mus.identifier.categoryLife Sciences & Earth Sciencesen_US
mus.identifier.doi10.1128/IAI.00530-17en_US
mus.relation.collegeCollege of Agricultureen_US
mus.relation.collegeCollege of Letters & Scienceen_US
mus.relation.departmentMicrobiology & Immunology.en_US
mus.relation.universityMontana State University - Bozemanen_US
mus.data.thumbpage27en_US


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