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Assessment of cellular immune parameters in paediatric toxic shock syndrome: a report of five cases
Olivier Dauwalder1, Fabienne Venet, Etienne Javouhey
1Centre National de Références des Staphylocoques, Faculté de Médecine Lyon Est, Université de Lyon, France. olivier.dauwalder@chu-lyon.fr
Insights
Toxic shock syndrome (TSS) and septic shock (SS) share symptoms, but TSS does not show the same immune suppression. TSS increases regulatory T cells (Treg), unlike septic shock, suggesting different immune responses.
Area of Science:
- Immunology
- Infectious Diseases
- Pediatrics
Background:
- Toxic shock syndrome (TSS) and septic shock (SS) present with similar clinical signs of severe inflammation.
- Septic shock is characterized by delayed immunosuppression, including lymphopenia and reduced HLA-DR expression on monocytes.
- Understanding the immune alterations in TSS is crucial for differentiating it from SS and guiding treatment.
Observation:
- This study monitored five children diagnosed with TSS.
- TSS cases were confirmed by clinical signs and specific Vbeta expansions linked to bacterial toxin genes.
- Regulatory T cell (Treg) percentages were measured in TSS patients.
Findings:
- Patients with TSS showed an increased percentage of circulating regulatory T cells (Treg).
- Unlike septic shock, TSS did not exhibit lymphopenia or decreased HLA-DR expression on monocytes.
- These findings suggest distinct immune alterations in TSS compared to SS, despite similar clinical presentations.
Implications:
- The distinct immune profiles of TSS and SS indicate different underlying pathophysiological mechanisms.
- Further research into Treg subsets in TSS is needed to elucidate the role of superantigens.
- Differentiating immune responses in TSS and SS could lead to more targeted therapeutic strategies.
Abstract:
Toxic shock syndrome (TSS) and septic shock (SS) share many clinical signs of an exacerbated inflammatory response. In this report, we investigated whether TSS presents similar features of delayed immunosuppression as described in SS. Five children with TSS from paediatric intensive care units in a university hospital were monitored. TSS cases were defined by the association of standardized clinical signs of TSS and confirmed by measurement of specific Vbeta expansions corresponding to toxin gene profile of the isolated strains. As in SS, an increased percentage of circulating regulatory T cells (Treg) was observed in patients with TSS. However, in contrast to SS, neither lymphopenia nor decreased HLA-DR expression on monocytes was measured. In conclusion, whereas SS and TSS exhibited similar clinical presentation, the present observation suggests that respective pathophysiological mechanisms induce different immune alterations. Future studies must isolate and better characterize the phenotypic and functional properties of Treg subsets during TSS to understand the mechanisms sustaining their increase, especially the putative role of superantigens.
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