<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang L</submitter><funding>China Scholarship Council</funding><funding>Karolinska Institutet Research Foundation Grants</funding><funding>Scandinavian Society for Antimicrobial Chemotherapy Foundation</funding><pagination>589</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10975849</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(3)</volume><pubmed_abstract>Shiga toxin-producing &lt;i>Escherichia coli&lt;/i> (STEC) infection can cause a broad spectrum of symptoms spanning from asymptomatic shedding to mild and bloody diarrhea (BD) and even life-threatening hemolytic-uremic syndrome (HUS). As a member of the serine protease autotransporters of &lt;i>Enterobacteriaceae&lt;/i> (SPATE) family, EspP has the ability to degrade human coagulation factor V, leading to mucosal bleeding, and also plays a role in bacteria adhesion to the surface of host cells. Here, we investigated the prevalence and genetic diversity of &lt;i>espP&lt;/i> among clinical STEC isolates from patients with mild diarrhea, BD, and HUS, as well as from asymptomatic individuals, and assessed the presence of &lt;i>espP&lt;/i> and its subtypes in correlation to disease severity. We found that 130 out of 239 (54.4%) clinical STEC strains were &lt;i>espP&lt;/i> positive, and the presence of &lt;i>espP&lt;/i> was significantly associated with BD, HUS, and O157:H7 serotype. Eighteen unique &lt;i>espP&lt;/i> genotypes (GTs) were identified and categorized into four &lt;i>espP&lt;/i> subtypes, i.e., &lt;i>espP&lt;/i>α (119, 91.5%), &lt;i>espP&lt;/i>γ (5, 3.8%), &lt;i>espP&lt;/i>δ (4, 3.1%), and &lt;i>espP&lt;/i>ε (2, 1.5%). &lt;i>espP&lt;/i>α was widely distributed, especially in strains from patients with BD and HUS, and correlated with serotype O157:H7. Serogroup O26, O145, O121, and O103 strains carried &lt;i>espP&lt;/i>α only. Ten GTs were identified in &lt;i>espP&lt;/i>α, and &lt;i>espP&lt;/i>α/GT2 was significantly associated with severe disease, i.e., BD and HUS. Additionally, &lt;i>espP&lt;/i> was strongly linked to the presence of &lt;i>eae&lt;/i> gene, and the coexistence of &lt;i>espP&lt;/i>α and &lt;i>stx2&lt;/i>/&lt;i>stx2a&lt;/i> + &lt;i>stx2c&lt;/i> was closely related to HUS status. To sum up, our data demonstrated a high prevalence and genetic diversity of the &lt;i>espP&lt;/i> gene in clinical STEC strains in Sweden and revealed an association between the presence of &lt;i>espP&lt;/i>, &lt;i>espP&lt;/i> subtypes, and disease severity. &lt;i>espP&lt;/i>, particularly the &lt;i>espP&lt;/i>α subtype, was prone to be present in more virulent STEC strains, e.g., "top-six" serotypes strains.</pubmed_abstract><journal>Microorganisms</journal><pubmed_title>Prevalence and Characteristics of Plasmid-Encoded Serine Protease EspP in Clinical Shiga Toxin-Producing &lt;i>Escherichia coli&lt;/i> Strains from Patients in Sweden.</pubmed_title><pmcid>PMC10975849</pmcid><funding_grant_id>202109370052</funding_grant_id><funding_grant_id>SLS884041</funding_grant_id><funding_grant_id>2022-01818</funding_grant_id><pubmed_authors>Hua Y</pubmed_authors><pubmed_authors>Mernelius S</pubmed_authors><pubmed_authors>Hansson S</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Matussek A</pubmed_authors><pubmed_authors>Bai X</pubmed_authors><pubmed_authors>Chromek M</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Frykman A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Prevalence and Characteristics of Plasmid-Encoded Serine Protease EspP in Clinical Shiga Toxin-Producing &lt;i>Escherichia coli&lt;/i> Strains from Patients in Sweden.</name><description>Shiga toxin-producing &lt;i>Escherichia coli&lt;/i> (STEC) infection can cause a broad spectrum of symptoms spanning from asymptomatic shedding to mild and bloody diarrhea (BD) and even life-threatening hemolytic-uremic syndrome (HUS). As a member of the serine protease autotransporters of &lt;i>Enterobacteriaceae&lt;/i> (SPATE) family, EspP has the ability to degrade human coagulation factor V, leading to mucosal bleeding, and also plays a role in bacteria adhesion to the surface of host cells. Here, we investigated the prevalence and genetic diversity of &lt;i>espP&lt;/i> among clinical STEC isolates from patients with mild diarrhea, BD, and HUS, as well as from asymptomatic individuals, and assessed the presence of &lt;i>espP&lt;/i> and its subtypes in correlation to disease severity. We found that 130 out of 239 (54.4%) clinical STEC strains were &lt;i>espP&lt;/i> positive, and the presence of &lt;i>espP&lt;/i> was significantly associated with BD, HUS, and O157:H7 serotype. Eighteen unique &lt;i>espP&lt;/i> genotypes (GTs) were identified and categorized into four &lt;i>espP&lt;/i> subtypes, i.e., &lt;i>espP&lt;/i>α (119, 91.5%), &lt;i>espP&lt;/i>γ (5, 3.8%), &lt;i>espP&lt;/i>δ (4, 3.1%), and &lt;i>espP&lt;/i>ε (2, 1.5%). &lt;i>espP&lt;/i>α was widely distributed, especially in strains from patients with BD and HUS, and correlated with serotype O157:H7. Serogroup O26, O145, O121, and O103 strains carried &lt;i>espP&lt;/i>α only. Ten GTs were identified in &lt;i>espP&lt;/i>α, and &lt;i>espP&lt;/i>α/GT2 was significantly associated with severe disease, i.e., BD and HUS. Additionally, &lt;i>espP&lt;/i> was strongly linked to the presence of &lt;i>eae&lt;/i> gene, and the coexistence of &lt;i>espP&lt;/i>α and &lt;i>stx2&lt;/i>/&lt;i>stx2a&lt;/i> + &lt;i>stx2c&lt;/i> was closely related to HUS status. To sum up, our data demonstrated a high prevalence and genetic diversity of the &lt;i>espP&lt;/i> gene in clinical STEC strains in Sweden and revealed an association between the presence of &lt;i>espP&lt;/i>, &lt;i>espP&lt;/i> subtypes, and disease severity. &lt;i>espP&lt;/i>, particularly the &lt;i>espP&lt;/i>α subtype, was prone to be present in more virulent STEC strains, e.g., "top-six" serotypes strains.</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Mar</publication><modification>2025-04-26T11:21:08.672Z</modification><creation>2025-04-06T13:42:04.697Z</creation></dates><accession>S-EPMC10975849</accession><cross_references><pubmed>38543640</pubmed><doi>10.3390/microorganisms12030589</doi></cross_references></HashMap>