Publications
216 results found
Ascough S, Ingram RJ, Metan G, et al., 2012, Comment on "Frequency of Epitope-Specific Naive CD4<SUP>+</SUP> T Cells Correlates with Immunodominance in the Human Memory Repertoire", JOURNAL OF IMMUNOLOGY, Vol: 188, Pages: 5205-5206, ISSN: 0022-1767
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- Citations: 1
Steer JA, Lamagni T, Healy B, et al., 2012, Guidelines for prevention and control of group A streptococcal infection in acute healthcare and maternity settings in the UK, JOURNAL OF INFECTION, Vol: 64, Pages: 1-18, ISSN: 0163-4453
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- Citations: 43
Sriskandan S, 2011, Severe peripartum sepsis., J R Coll Physicians Edinb, Vol: 41, Pages: 339-346
Despite global efforts to reduce maternal mortality, maternal deaths from bacterial sepsis have actually risen in the UK. The group A streptococcus, also known as Streptococcus pyogenes, is the leading cause of infection-related death in pregnancy and the puerperium. Many clinicians remain unaware of the risks posed to this particular group of otherwise fit, healthy patients despite the fact that S. pyogenes has been the leading infective cause of puerperal deaths since records began. S. pyogenes has a specific but unexplained predilection for the recently pregnant woman, and has an attributable mortality greater than many other invasive bacteria. Here, the epidemiology, aetiology, and management of severe peripartum sepsis are discussed, as are potential approaches to reduce risks. While fundamental changes in healthcare access can lead to dramatic reductions in maternal deaths in developing countries, an improvement in maternal sepsis deaths in the UK will require heightened awareness among both hospital and community-based clinical staff.
Lynskey NN, Lawrenson RA, Sriskandan S, 2011, New understandings in <i>Streptococcus pyogenes</i>, CURRENT OPINION IN INFECTIOUS DISEASES, Vol: 24, Pages: 196-202, ISSN: 0951-7375
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- Citations: 43
Garland P, de Lavallade H, Sekine T, et al., 2011, Humoral and Cellular Immunity to Primary H1N1 Infection in Patients with Hematologic Malignancies following Stem Cell Transplantation, BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION, Vol: 17, Pages: 632-639, ISSN: 1083-8791
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- Citations: 11
Chong DLW, Sriskandan S, 2011, Pro-Inflammatory Mechanisms in Sepsis, SEPSIS - PRO-INFLAMMATORY AND ANTI-INFLAMMATORY RESPONSES: GOOD, BAD OR UGLY?, Vol: 17, Pages: 86-107, ISSN: 1420-9519
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- Citations: 54
Musson JA, Ingram R, Durand G, et al., 2010, Repertoire of HLA-DR1-Restricted CD4 T-Cell Responses to Capsular Caf1 Antigen of <i>Yersinia pestis</i> in Human Leukocyte Antigen Transgenic Mice, INFECTION AND IMMUNITY, Vol: 78, Pages: 4356-4362, ISSN: 0019-9567
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- Citations: 14
Yuste J, Sen A, Truedsson L, et al., 2010, Impaired opsonization with complement and phagocytosis of <i>Streptococcus pyogenes</i> in sera from subjects with inherited C2 deficiency, MICROBES AND INFECTION, Vol: 12, Pages: 626-634, ISSN: 1286-4579
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- Citations: 3
Kurupati P, Turner CE, Tziona I, et al., 2010, Chemokine-cleaving Streptococcus pyogenes protease SpyCEP is necessary and sufficient for bacterial dissemination within soft tissues and the respiratory tract., Mol Microbiol, Vol: 76, Pages: 1387-1397, ISSN: 1365-2958
SpyCEP is a Streptococcus pyogenes protease that cleaves CXCL8/IL-8 and its activity is associated with human invasive disease severity. We investigated the role of SpyCEP in S. pyogenes necrotizing fasciitis and respiratory tract infection in mice using isogenic strains differing only in SpyCEP expression. SpyCEP cleaved human CXCL1, 2, 6 and 8 plus murine CXCL1 and 2 at a structurally conserved site. Mice were infected in thigh muscle with a strain of S. pyogenes that expresses a high level of SpyCEP, or with an isogenic non-SpyCEP expressing strain. SpyCEP expression by S. pyogenes hindered bacterial clearance from muscle, and enhanced bacterial spread, associated with cleavage of murine chemoattractant CXCL1. Mice were then infected with Lactococcus lactis strains that differed only in SpyCEP expression. In contrast to the parent L. lactis strain (lacks SpyCEP), which was avirulent when administered intramuscularly, infection with a strain that expressed SpyCEP heterologously led to dramatic systemic illness within 24 h, failure to clear bacteria from muscle and marked dissemination to other organs. In the upper airways, SpyCEP expression was required for survival of L. lactis but not S. pyogenes. However, dissemination of S. pyogenes to the lung was SpyCEP-dependent and was associated with evidence of chemokine cleavage. Taken together, the studies provide clear evidence that SpyCEP is necessary and sufficient for systemic bacterial dissemination from a soft tissue focus in this model and also underlies dissemination in the respiratory tract.
Ingram RJ, Metan G, Maillere B, et al., 2010, Natural Exposure to Cutaneous Anthrax Gives Long-Lasting T Cell Immunity Encompassing Infection-Specific Epitopes, JOURNAL OF IMMUNOLOGY, Vol: 184, Pages: 3814-3821, ISSN: 0022-1767
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- Citations: 39
Alam F, Bateman C, Turner C, et al., 2010, Bioluminescence imaging of a clinical isolate of <i>Streptococcus pyogenes</i>, Publisher: JOHN WILEY & SONS LTD, Pages: 179-181, ISSN: 1522-7235
Sriskandan S, 2010, Management of candiduria in the ICU, Infectious Diseases: Third Edition, Pages: 759-760, ISBN: 9780323045797
Goldblatt J, Begum J, Brannigan E, et al., 2009, FEVER IN A RETURNED TRAVELLER, JOURNAL OF INFECTION, Vol: 59, Pages: S438-S439, ISSN: 0163-4453
Goldblatt J, Begum J, Brannigan E, et al., 2009, FEVER IN A RETURNED TRAVELLER, JOURNAL OF INFECTION, Vol: 59, Pages: S439-S440, ISSN: 0163-4453
Turner CE, Kurupati P, Jones MD, et al., 2009, Emerging role of the interleukin-8 cleaving enzyme SpyCEP in clinical Streptococcus pyogenes (The Journal of Infectious Diseases (2009) 200 (555-563)), Journal of Infectious Diseases, Vol: 200, ISSN: 0022-1899
Hopkins P, Sriskandan S, 2009, THE EFFECT OF LEAD TIME AND CLINICAL CONTEXT ON THE HUMAN INNATE IMMUNE RESPONSE TO SEVERE SEPSIS, 22nd Annual Congress of the European-Society-of-Intensive-Care-Medicine (ESICM), Publisher: SPRINGER, Pages: 248-248, ISSN: 0342-4642
Turner CE, Kurupati P, Jones MD, et al., 2009, Emerging Role of the Interleukin-8 Cleaving Enzyme SpyCEP in Clinical <i>Streptococcus pyogenes</i> Infection, JOURNAL OF INFECTIOUS DISEASES, Vol: 200, Pages: 555-563, ISSN: 0022-1899
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- Citations: 56
Turner CE, Kurupati P, Wiles S, et al., 2009, Impact of immunization against SpyCEP during invasive disease with two streptococcal species: <i>Streptococcus pyogenes</i> and <i>Streptococcus equi</i>, VACCINE, Vol: 27, Pages: 4923-4929, ISSN: 0264-410X
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- Citations: 52
Russell HH, Zhou L, Sriskandan S, 2009, Rapid screen for epithelial internalization of Tn917-mutagenized <i>Streptococcus pyogenes</i>, JOURNAL OF MICROBIOLOGICAL METHODS, Vol: 78, Pages: 34-39, ISSN: 0167-7012
Paul-Clark MJ, McMaster SK, Sorrentino R, et al., 2009, Toll-like Receptor 2 Is Essential for the Sensing of Oxidants during Inflammation, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, Pages: 299-306, ISSN: 1073-449X
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- Citations: 47
Ingram RJ, Chong DLW, Turner CE, et al., 2008, The role of T cells in acute <i>Streptococcus pyogenes</i> infection, Annual Congress of the British-Society-of-Immunology, Publisher: WILEY-BLACKWELL PUBLISHING, INC, Pages: 62-62, ISSN: 0019-2805
Ingram RJ, Chu K, Metan G, et al., 2008, T cell epitope mapping anthrax: the detection of CD<sub>4</sub> epitopes in lethal factor, Annual Congress of the British-Society-of-Immunology, Publisher: WILEY-BLACKWELL, Pages: 144-144, ISSN: 0019-2805
Davies F, Faulkner L, Kearns A, et al., 2008, NON-MENSTRUAL TOXIC SHOCK AND THE <i>IN VIVO</i> ROLES OF SEB AND IVIG, JOURNAL OF INFECTION, Vol: 57, Pages: 426-426, ISSN: 0163-4453
Zinkernagel AS, Timmer AM, Pence MA, et al., 2008, The IL-8 protease SpyCEP/ScpC of Group A <i>Streptococcus</i> promotes resistance to neutrophil killing, CELL HOST & MICROBE, Vol: 4, Pages: 170-178, ISSN: 1931-3128
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- Citations: 129
Russell HH, Sriskandan S, 2008, Superantigens SPEA and SMEZ do not affect secretome expression in <i>Streptococcus pyogenes</i>, MICROBIAL PATHOGENESIS, Vol: 44, Pages: 537-543, ISSN: 0882-4010
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- Citations: 2
Sorrentino R, de Souza PM, Sriskandan S, et al., 2008, Pattern recognition receptors and interleukin-8 mediate effects of Gram-positive and Gram-negative bacteria on lung epithelial cell function, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 154, Pages: 864-871, ISSN: 0007-1188
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- Citations: 12
Issa R, Sorrentino R, Sukkar MB, et al., 2008, Differential regulation of CCL-II/eotaxin-I and CXCL-8/IL-8 by Gram-positive and Gram-negative bacteria in human airway smooth muscle cells, Respiratory Research, Vol: 9, ISSN: 1465-993X
Background: Bacterial infections are a cause of exacerbation of airway disease. Airway smoothmuscle cells (ASMC) are a source of inflammatory cytokines/chemokines that may propagate localairway inflammatory responses. We hypothesize that bacteria and bacterial products could inducecytokine/chemokine release from ASMC.Methods: Human ASMC were grown in culture and treated with whole bacteria or pathogenassociated molecular patterns (PAMPs) for 24 or 48 h. The release of eotaxin-1, CXCL-8 orGMCSF was measured by ELISA.Results: Gram-negative E. coli or Gram-positive S. aureus increased the release of CXCL-8, as didIL-1β, LPS, FSL-1 and Pam3CSK4, whereas FK565, MODLys18 or Poly I:C did not. E. coli inhibitedeotaxin-1 release under control conditions and after stimulation with IL-1β. S. aureus tended toinhibit eotaxin-1 release stimulated with IL-1β. E. coli or LPS, but not S. aureus, induced the releaseof GMCSF.Conclusion: Gram-positive or Gram-negative bacteria activate human ASMC to release CXCL-8.By contrast Gram-negative bacteria inhibited the release of eotaxin-1 from human ASMCs. E. coli,but not S. aureus induced GMCSF release from cells.Our findings that ASMC can respond directly to Gram-negative and Gram-positive bacteria byreleasing the neutrophil selective chemokine, CXCL-8, is consistent with what we know about therole of neutrophil recruitment in bacterial infections in the lung. Our findings that bacteria inhibitthe release of the eosinophil selective chemokine, eotaxin-1 may help to explain the mechanismsby which bacterial immunotherapy reduces allergic inflammation in the lung.
Hopkins PA, Pridmore AC, Ellmerich S, et al., 2008, Increased surface toll-like receptor 2 expression in superantigen shock, CRITICAL CARE MEDICINE, Vol: 36, Pages: 1267-1276, ISSN: 0090-3493
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- Citations: 16
McMaster SK, Paul-Clark MJ, Walters M, et al., 2008, Cigarette smoke inhibits macrophage sensing of Gram-negative bacteria and lipopolysaccharide: relative roles of nicotine and oxidant stress, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 153, Pages: 536-543, ISSN: 0007-1188
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- Citations: 33
Paul-Clark MJ, Sorrentino R, Bailey LK, et al., 2008, Gram-positive and gram-negative bacteria synergize with oxidants to release CXCL8 from innate immune cells, MOLECULAR MEDICINE, Vol: 14, Pages: 238-246, ISSN: 1076-1551
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- Citations: 15
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