Prevalence of Antibody to Toxic Shock Syndrome Toxin-1 in Burn Patients

Park, Jiyoung; Kim, Jae‐Seok; Woo, Heungjeong

doi:10.3343/alm.2015.35.1.89

Cited by 8 publications

(4 citation statements)

References 20 publications

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“…This is unlikely to exist if memory T cells were constantly being driven into an anergic state by SAgs. Another key factor is the high prevalence of neutralising antibodies against staphylococcal SAgs, particularly the non- egc cluster SAgs such as TSST-1 and SElX [ 38 , 116 , 117 , 118 ]. This suggests that the helper T cell compartment is functional during and following S. aureus infection even when SAgs are expressed.…”

Section: Superantigens In S Aureus Pathogenesimentioning

confidence: 99%

Manipulation of Innate and Adaptive Immunity by Staphylococcal Superantigens

2018

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Staphylococcal superantigens (SAgs) constitute a family of potent exotoxins secreted by Staphylococcus aureus and other select staphylococcal species. SAgs function to cross-link major histocompatibility complex (MHC) class II molecules with T cell receptors (TCRs) to stimulate the uncontrolled activation of T lymphocytes, potentially leading to severe human illnesses such as toxic shock syndrome. The ubiquity of SAgs in clinical S. aureus isolates suggests that they likely make an important contribution to the evolutionary fitness of S. aureus. Although the apparent redundancy of SAgs in S. aureus has not been explained, the high level of sequence diversity within this toxin family may allow for SAgs to recognize an assorted range of TCR and MHC class II molecules, as well as aid in the avoidance of humoral immunity. Herein, we outline the major diseases associated with the staphylococcal SAgs and how a dysregulated immune system may contribute to pathology. We then highlight recent research that considers the importance of SAgs in the pathogenesis of S. aureus infections, demonstrating that SAgs are more than simply an immunological diversion. We suggest that SAgs can act as targeted modulators that drive the immune response away from an effective response, and thus aid in S. aureus persistence.

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Section: Superantigens In S Aureus Pathogenesimentioning

confidence: 99%

Manipulation of Innate and Adaptive Immunity by Staphylococcal Superantigens

2018

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“…aureus with insufficient antibody titers are at a greater risk of developing TSS [ 10 ]. Lack of detectable antibodies to TSS-1 in serum shows susceptibility to TSS [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

A Rare Case of Staphylococcal Toxic Shock Syndrome in a Neonate

Shrestha

Joshi

Hayashi

et al. 2022

Case Reports in Infectious Diseases

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Staphylococcus toxic shock syndrome (TSS) is not well described in neonates. The present criteria for diagnosis of TSS have not yet been validated in neonates. Here, we present a case of a 13-day-old female baby who presented with acute kidney injury (AKI). She had a pus-draining lesion on the head, and the pus grew Staphylococcus aureus. Based on the clinical criteria of fever, desquamation, hypotension, and AKI and laboratory criteria of absence of growth of any organisms in blood and cerebrospinal fluid, we diagnosed the case as TSS. She was treated with antibiotics, oxygen, and fluids, along with inotropic support and mechanical ventilation, and she recovered fully and was discharged on day 17 of admission. As there is no single test to diagnose TSS and it is uncommon in neonates, physicians should be familiar with the clinical presentation of the disease to make early diagnosis.

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“…The prevalence of antibody to TSST-1 in the population far outweighs the number of TSS cases. [ 26 , 27 ] The observed increased pro-inflammatory cytokine response to TLR 2 and NOD receptor stimulation in TSS may be due to either an underlying genetic immunological susceptibility or an altered immune response secondary to the past TSS illness. The possibility that our results reflect an underlying genetic immunological susceptibility is supported by the finding of a strong genetic influence on in vitro LPS-induced cytokine responses in meningococcal disease in a study of first degree relatives.…”

Section: Discussionmentioning

confidence: 99%

“…[ 25 ] Similar to KD, there is likely an underlying host immunological susceptibility as not all individuals exposed to the causative exotoxin develop TSS. [ 26 , 27 ] By including both diseases, we were able to study changes in innate immune responses following acute inflammatory illnesses more broadly.…”

Section: Introductionmentioning

confidence: 99%

Innate immune responses following Kawasaki disease and toxic shock syndrome

et al. 2018

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The pathogenesis of Kawasaki disease (KD) remains unknown and there is accumulating evidence for the importance of the innate immune system in initiating and mediating the host inflammatory response. We compared innate immune responses in KD and toxic shock syndrome (TSS) participants more than two years after their acute illness with control participants to investigate differences in their immune phenotype. Toxic shock syndrome shares many clinical features with KD; by including both disease groups we endeavoured to explore changes in innate immune responses following acute inflammatory illnesses more broadly. We measured the in vitro production of interferon (IFN)-γ, tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-1 receptor antagonist (IL-1ra), and IL-10 following whole blood stimulation with toll-like receptor and inflammasome ligands in 52 KD, 20 TSS, and 53 control participants in a case-control study. Analyses were adjusted for age, sex, and unstimulated cytokine concentrations. Compared to controls, KD participants have reduced IL-1ra production in response to stimulation with double stranded RNA (geometric mean ratio (GMR) 0.37, 95% CI 0.15, 0.89, p = 0.03) and increased IL-6 production in response to incubation with Lyovec™ (GMR 5.48, 95% CI 1.77, 16.98, p = 0.004). Compared to controls, TSS participants have increased IFN-γ production in response to peptidoglycan (GMR 4.07, 95% CI 1.82, 9.11, p = 0.001), increased IL-1β production to lipopolysaccharide (GMR 1.64, 95% CI 1.13, 2.38, p = 0.01) and peptidoglycan (GMR 1.61, 95% CI 1.11, 2.33, p = 0.01), and increased IL-6 production to peptidoglycan (GMR 1.45, 95% CI 1.10, 1.92, p = 0.01). Years following the acute illness, individuals with previous KD or TSS exhibit a pro-inflammatory innate immune phenotype suggesting a possible underlying immunological susceptibility or innate immune memory.

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Prevalence of Antibody to Toxic Shock Syndrome Toxin-1 in Burn Patients

Cited by 8 publications

References 20 publications

Manipulation of Innate and Adaptive Immunity by Staphylococcal Superantigens

Manipulation of Innate and Adaptive Immunity by Staphylococcal Superantigens

A Rare Case of Staphylococcal Toxic Shock Syndrome in a Neonate

Innate immune responses following Kawasaki disease and toxic shock syndrome

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