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Pentraxin 3 exacerbates psoriasiform dermatitis through regulation of macrophage polarization
Jingwei Liu1, Cheng Qiu2, Zhonghua Zhou1
1Department of Pediatric Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, PR China.
Objective:
To elucidate the mechanism of Pentraxin 3 (PTX3) in the pathogenesis of psoriasiform dermatitis using Ptx3-knockout (Ptx3-KO) background mice.
Methods:
An Imiquimod (IMQ)-induced murine psoriatic model was created using Ptx3-KO (Ptx3-/-) and wild-type (Ptx3+/+) mice. Skin lesion severity and expression of inflammatory mediators (IL-6 and TNFα) were assessed using PASI score and ELISA, respectively. Cutaneous tissues from the two mice groups were subjected to histological analyses, including HE staining, Masson staining, and Immunohistochemistry (IHC). The PTX3, iNOS, COX2, and Arg1 expressions were quantified and compared between the two groups. We used RNA-seq to clarify the underlying mechanisms of the disease. Flow cytometry was used to analyze systemic Th17 cell differentiation and macrophage polarization.
Result:
The psoriatic region exhibited a higher PTX3 expression than the normal cutaneous area. Moreover, PTX3 was upregulated in HaCaT cells post-TNFα stimulation. Upon IMQ stimulation, Ptx3-/- mice displayed a lower degree of the psoriasiform dermatitis phenotype compared to Ptx3+/+ mice. Consistent with the RNA-seq results, further experiments confirmed that compared to the wild-type group, the PTX3-KO group exhibited a generally lower IL-6, TNFα, iNOS, and COX2 expression and a contrasting trend in macrophage polarization. However, no significant difference in Th17 cell activation was observed between the two groups.
Conclusions:
This study revealed that PTX3 was upregulated in psoriatic skin tissues and TNFα-stimulated HaCaT cells. We also discovered that PTX3 deficiency in mice ameliorated the psoriasiform dermatitis phenotype upon IMQ stimulation. Mechanistically, PTX3 exacerbates psoriasiform dermatitis by regulating macrophage polarization rather than Th17 cell differentiation.
Insights
Pentraxin 3 (PTX3) worsens psoriasiform dermatitis by altering macrophage polarization. PTX3 deficiency in mice reduced disease severity, indicating PTX3
Area of Science:
- Dermatology
- Immunology
- Molecular Biology
Background:
- Psoriasiform dermatitis is a skin condition with complex pathogenesis.
- Pentraxin 3 (PTX3) is an inflammatory mediator implicated in various diseases.
- The specific role of PTX3 in psoriasiform dermatitis remains to be fully elucidated.
Purpose of the Study:
- To investigate the mechanism of Pentraxin 3 (PTX3) in the pathogenesis of psoriasiform dermatitis.
- To compare disease severity and inflammatory responses in Ptx3-knockout (Ptx3-KO) and wild-type (Ptx3+/+) mice using an imiquimod (IMQ)-induced model.
Main Methods:
- Established an IMQ-induced psoriasiform dermatitis model in Ptx3-KO and wild-type mice.
- Assessed skin lesion severity (PASI score) and inflammatory mediators (IL-6, TNFα) via ELISA.
- Performed histological analyses (HE, Masson, IHC) and quantified protein expression (PTX3, iNOS, COX2, Arg1).
- Utilized RNA-seq for mechanistic insights and flow cytometry for Th17 cell and macrophage analysis.
Main Results:
- Psoriatic skin showed higher PTX3 expression; PTX3 was also upregulated in TNFα-stimulated HaCaT cells.
- Ptx3-KO mice exhibited a milder psoriasiform dermatitis phenotype compared to wild-type mice after IMQ stimulation.
- PTX3 deficiency led to reduced IL-6, TNFα, iNOS, and COX2 expression and altered macrophage polarization, but did not affect Th17 cell activation.
Conclusions:
- PTX3 is upregulated in psoriatic skin and upon TNFα stimulation.
- PTX3 deficiency ameliorates the psoriasiform dermatitis phenotype.
- PTX3 exacerbates psoriasiform dermatitis primarily by regulating macrophage polarization, not Th17 cell differentiation.
