IL-17A Synergizes with IFN-γ to Upregulate iNOS and NO Production and Inhibit Chlamydial Growth

Zhang, Yongci; Wang, Haiping; Ren, Jianyun; Tang, Xiaofei; Jing, Yingying; Xing, Donghong; Zhao, Guosheng; Yao, Zhi; Yang, Xi; Bai, Hong

doi:10.1371/journal.pone.0039214

Cited by 58 publications

(56 citation statements)

References 30 publications

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“…After IFN-␥ removal and subsequent tryptophan production, these persistent forms quickly differentiate into infectious elementary bodies. Furthermore, a recent study by Zhang and colleagues demonstrated that IFN-␥ and IL-17A synergistically inhibit Chlamydia muridarum replication by inducing intracellular iNOS and NO production (117).…”

Section: Ifn-␥mentioning

confidence: 99%

Genital Chlamydia trachomatis: Understanding the Roles of Innate and Adaptive Immunity in Vaccine Research

Vasilevsky¹,

Greub

Nardelli-Haefliger

et al. 2014

Clin Microbiol Rev

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SUMMARY Chlamydia trachomatis is the leading cause of bacterial sexually transmitted disease worldwide, and despite significant advances in chlamydial research, a prophylactic vaccine has yet to be developed. This Gram-negative obligate intracellular bacterium, which often causes asymptomatic infection, may cause pelvic inflammatory disease (PID), ectopic pregnancies, scarring of the fallopian tubes, miscarriage, and infertility when left untreated. In the genital tract, Chlamydia trachomatis infects primarily epithelial cells and requires Th1 immunity for optimal clearance. This review first focuses on the immune cells important in a chlamydial infection. Second, we summarize the research and challenges associated with developing a chlamydial vaccine that elicits a protective Th1-mediated immune response without inducing adverse immunopathologies.

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Section: Ifn-␥mentioning

confidence: 99%

Genital Chlamydia trachomatis: Understanding the Roles of Innate and Adaptive Immunity in Vaccine Research

Vasilevsky¹,

Greub

Nardelli-Haefliger

et al. 2014

Clin Microbiol Rev

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“…Notably, the role of Th17 cells in host defense against chlamydial lung infection has been recently realized. In particular, we recently reported that IFNγ and IL-17 can work synergistically to inhibit chlamydial growth (58). Therefore, the better protection in IL-10 KO mice is likely the synergistic effect of Th17 and Th1, which are both increased in these mice.…”

Section: Discussionmentioning

confidence: 95%

Enhanced Inducible Costimulator Ligand (ICOS-L) Expression on Dendritic Cells in Interleukin-10 Deficiency and Its Impact on T-Cell Subsets in Respiratory Tract Infection

Gao

Zhao

Wang

et al. 2013

Mol Med

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An association between inducible costimulator ligand (ICOS-L) expression and interleukin (IL)-10 production by dendritic cells (DCs) has been commonly found in infectious disease. DCs with higher ICOS-L expression and IL-10 production are reportedly more efficient in inducing regulatory T cells (Tregs). Here we use the Chlamydia muridarum (Cm) lung infection model in IL-10 knockout (KO) mice to test the relationship between IL-10 production and ICOS-L expression by DCs. We examined ICOS-L expression, the development of T-cell subsets, including Treg, Th17 and Th1 cell, in the background of IL-10 deficiency and its relationship with ICOS-L/ICOS signaling after infection. Surprisingly, we found that the IL-10 KO mice exhibited significantly higher ICOS-L expression by DCs. Moreover, IL-10 KO mice showed lower Tregs but higher Th17 and Th1 responses, but only the Th17 response depended on ICOS signaling. Consistently, most of the Th17 cells were ICOS + , whereas most of the Th1 cells were ICOS -in the infected mice. Furthermore, neutralization of IL-17 in IL-10 KO mice significantly exacerbated lung infection.

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“…IFN‐activated human mast cells secreted IL‐17A, which may have important roles in enhancing immunity. Indeed, IL‐17A and IFNγ can act synergistically to enhance macrophage function and inhibit bacterial growth 45. Minor increases in IL‐4, IL‐13, and IL‐12 were also observed following activation with IFNγ, but not IFNα2, demonstrating differential regulation by type I and II IFNs.…”

Section: Discussionmentioning

confidence: 98%

Interferon α2 and interferon γ induce the degranulation independent production of VEGF‐A and IL‐1 receptor antagonist and other mediators from human mast cells

Oldford

Salsman

Portales‐Cervantes

et al. 2017

Immunity Inflam & Disease

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BackgroundMast cells are resident immune effector cells, often studied in the context of allergic disease. Found in substantial numbers at sites of potential infection they are increased at sites of angiogenesis and can be pivotal for the sensing and clearance of a variety of pathogens. Interferons (IFNs) are cytokines that are critical for host defence against intracellular pathogens. Increased levels of IFNs are observed during viral infection and in autoimmune diseases. IFNs are also widely used therapeutically and have been examined in the therapy of severe asthma.ObjectiveTo define the selective human mast cell cytokine and chemokine response following activation with type I or type II IFN's.MethodsThe ability of both IFNα2 and IFNγ to induce cytokine production by human cord blood‐derived mast cells was examined in vitro. Cytokine and chemokine production at 6 and 24 h was assessed by multiplex protein analysis. Degranulation was assessed by β‐hexosaminidase release. Mast cells were also treated with reovirus or respiratory syncytial virus and their production of CXCL10, IL‐1 receptor antagonist (IL‐1Ra), and vascular endothelial growth factor (VEGF) examined after 24 h.ResultsIn addition to increased expression of classical IFN response genes, such as CXCL10, small but significant increases in CCL5 and IL‐17 production were observed following IFN activation. Notably, human mast cells produced both VEGF and IL‐1Ra in a dose dependent manner. These responses occurred in the absence of mast cell degranulation by a mechanism consistent with classical IFN signaling. Both reovirus and respiratory syncytial virus infection of mast cells, were also associated with IFN‐dependent IL‐1Ra expression.Conclusion and Clinical RelevanceOur findings demonstrate that IFNs have profound impact on cytokine and chemokine expression by human mast cells, alone or in the context of viral infection. Mast cell VEGF and IL‐1Ra responses to IFNs could impact the regulation of local inflammatory responses and subsequent tissue remodeling.

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IL-17A Synergizes with IFN-γ to Upregulate iNOS and NO Production and Inhibit Chlamydial Growth

Cited by 58 publications

References 30 publications

Genital Chlamydia trachomatis: Understanding the Roles of Innate and Adaptive Immunity in Vaccine Research

Genital Chlamydia trachomatis: Understanding the Roles of Innate and Adaptive Immunity in Vaccine Research

Enhanced Inducible Costimulator Ligand (ICOS-L) Expression on Dendritic Cells in Interleukin-10 Deficiency and Its Impact on T-Cell Subsets in Respiratory Tract Infection

Interferon α2 and interferon γ induce the degranulation independent production of VEGF‐A and IL‐1 receptor antagonist and other mediators from human mast cells

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