IL-33/ST2 Axis Plays a Protective Effect in Streptococcus pyogenes Infection through Strengthening of the Innate Immunity
| Autor: | Yu-Hsuan Tsai, Wei-Yu Chen, Chih-Feng Kuo, Ya-Chu Chang, Nina Tsao, Chih Peng Chang, Hai-Han Yu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Neutrophils
Streptococcus pyogenes the innate immunity QH301-705.5 Biology medicine.disease_cause Article Catalysis Microbiology Proinflammatory cytokine Inorganic Chemistry Cell Movement Streptococcal Infections medicine Animals Humans Viability assay Physical and Theoretical Chemistry Biology (General) Molecular Biology QD1-999 Spectroscopy Gene knockout Inflammation Mice Knockout Innate immune system Streptococcus Effector Organic Chemistry General Medicine Interleukin-33 medicine.disease Group A Streptococcus (GAS) Interleukin-1 Receptor-Like 1 Protein suppression of tumorigenicity 2 (ST2) Immunity Innate Computer Science Applications Mice Inbred C57BL Interleukin 33 Disease Models Animal interleukin-33 (IL-33) Chemistry Cytokines Cytokine storm Signal Transduction |
| Zdroj: | International Journal of Molecular Sciences, Vol 22, Iss 10566, p 10566 (2021) International Journal of Molecular Sciences Volume 22 Issue 19 |
| ISSN: | 1661-6596 1422-0067 |
| Popis: | Group A Streptococcus (GAS) causes invasive human diseases with the cytokine storm. Interleukin-33 (IL-33)/suppression of tumorigenicity 2 (ST2) axis is known to drive TH2 response, while its effect on GAS infection is unclear. We used an air pouch model to examine the effect of the IL-33/ST2 axis on GAS-induced necrotizing fasciitis. GAS infection induced IL-33 expression in wild-type (WT) C57BL/6 mice, whereas the IL-33- and ST2-knockout mice had higher mortality rates, more severe skin lesions and higher bacterial loads in the air pouches than those of WT mice after infection. Surveys of infiltrating cells in the air pouch of GAS-infected mice at the early stage found that the number and cell viability of infiltrating cells in both gene knockout mice were lower than those of WT mice. The predominant effector cells in GAS-infected air pouches were neutrophils. Absence of the IL-33/ST2 axis enhanced the expression of inflammatory cytokines, but not TH1 or TH2 cytokines, in the air pouch after infection. Using in vitro assays, we found that the IL-33/ST2 axis not only enhanced neutrophil migration but also strengthened the bactericidal activity of both sera and neutrophils. These results suggest that the IL-33/ST2 axis provided the protective effect on GAS infection through enhancing the innate immunity. |
| Databáze: | OpenAIRE |
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