Intranasal streptococcal infection exacerbates psoriasis-like dermatitis via the induction of skin tissue-resident memory T cells

Ya Zhou; Ning Li; Xin Fan; Meiyi Xu; Beinan Wang

doi:10.1016/j.bbadis.2022.166629

Intranasal streptococcal infection exacerbates psoriasis-like dermatitis via the induction of skin tissue-resident memory T cells

Biochim Biophys Acta Mol Basis Dis. 2023 Mar;1869(3):166629. doi: 10.1016/j.bbadis.2022.166629. Epub 2022 Dec 20.

Authors

Ya Zhou¹, Ning Li², Xin Fan², Meiyi Xu³, Beinan Wang⁴

Affiliations

¹ CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China; Savaid Medical School, University of Chinese Academy of Sciences, Beijing, China.
² CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China.
³ CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China; Tianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin Central Hospital of Gynecology Obstetrics and Nankai University Affiliated Hospital of Obstetrics and Gynecology, Tianjin, China.
⁴ CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China; Savaid Medical School, University of Chinese Academy of Sciences, Beijing, China. Electronic address: wangbn@im.ac.cn.

PMID: 36563916
DOI: 10.1016/j.bbadis.2022.166629

Abstract

Recurrent streptococcal tonsillitis exacerbates psoriasis. Studies have indicated that T cells responding to streptococcal antigens in the skin are involved in the pathogenesis of the disease. However, a direct link between streptococcal tonsillitis and psoriasis has not been evidenced. In the present study, the impact of intranasal (i.n.) streptococcal infection on psoriasis was investigated using the imiquimod (IMQ) psoriasis mouse model. The results showed that repeated i.n. infection with group A Streptococcus (GAS) induced a robust and persistent Th17 response in the nasal-associated lymphoid tissue (NALT) and exacerbated IMQ-mediated psoriatic skin lesions. ELISpot and flow cytometry analyses revealed that GAS-reactive tissue-resident memory T cells (T_RM) were present in the skin of GAS-infected mice and produced IL-17/IL-23 axis cytokines in response to IMQ, compared to mice uninfected with GAS. In addition, i.n. infection with Streptococcus pneumoniae (Sp), a pathogen not associated with the development of psoriasis, also induced a persistent Th17 response in NALT but did not exacerbate IMQ-induced psoriatic inflammation nor elicited Sp-specific T cells in the skin. The results provide in vivo evidence that GAS-associated psoriasis is dependent on the skin GAS-specific T_RM cells induced by GAS nasopharyngeal infection and can be later activated by environmental triggers, leading to psoriatic inflammation. Reducing the reservoir of Th17 cells, which are source of skin T_RM cells, may constitute a promising treatment for psoriasis.

Keywords: Group A Streptococcus; Interleukin-17A; Psoriasis; Th17; Tissue-resident memory T cells.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Dermatitis*
Imiquimod
Inflammation
Memory T Cells
Mice
Psoriasis* / pathology
Streptococcal Infections* / complications
Tonsillitis*

Substances

Imiquimod