Interleukin-23 (IL-23) deficiency disrupts Th17 and Th1-related defenses against Streptococcus pneumoniae infection

Kim, Byung Jin; Lee, Suheung; Berg, Rance E.; Simecka, Jerry W.; Jones, Harlan P.

doi:10.1016/j.cyto.2013.05.013

Cited by 23 publications

(18 citation statements)

References 65 publications

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“…These data were consistent with observations that Il23a expression is induced by subacute O 3 exposure (Mathews et al, 2014a) and with data of other investigators showing that IL-23 promotes pulmonary IL-17A expression induced by other stimuli, including infection with Streptococcus pneumonia or Pseudomonas aeruginosa (Dubin et al, 2012; Kim et al, 2013). However, while Il17a mRNA was substantially reduced (≈ 70% reduction) in IL-23 −/− vs. WT mice (Figure 2A), it was not completely abolished.…”

Section: Discussionsupporting

confidence: 93%

Regulation of IL-17A expression in mice following subacute ozone exposure

Brand¹,

Mathews²,

Kasahara³

et al. 2016

Journal of Immunotoxicology

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Exposure to subacute ozone (O3) causes pulmonary neutrophil recruitment. In mice, this recruitment requires IL-17A. Ozone also causes expression of IL-23 and IL-1, which can induce IL-17A. The purpose of this study was to examine the hypothesis that IL-23 and IL-1 contribute to IL-17A expression and subsequent neutrophil recruitment after subacute O3 exposure. Wild-type, IL-23−/−, and Flt3l−/− mice were exposed to air or 0.3 ppm O3 for 72 hr. Flt3l−/− mice lack conventional dendritic cells (cDC) that can express IL-23 and IL-1. Other wild-type mice were pre-treated with saline or the IL-1R1 antagonist anakinra prior to O3 exposure. After exposure, bronchoalveolar lavage (BAL) was performed and lung tissue harvested. The results indicated that pulmonary Il17a mRNA abundance and IL-17A+ F4/80+ cells were significantly reduced in O3-exposed IL-23−/− vs. in wild-type mice. In contrast, anakinra had no effect on Il23a or Il17a pulmonary mRNA abundance or on BAL concentrations of the neutrophil survival factor G-CSF, but anakinra did reduce BAL neutrophil numbers, likely because anakinra also reduced BAL IL-6. Compared to air, O3 caused a significant increase in DC numbers in wild-type but not in Flt3−/− mice. However, there was no significant difference in Il23a or Il17a mRNA abundance or in BAL neutrophil count in O3-exposed Flt3−/− vs. in wild-type mice. From these results, we conclude that IL-23 but not IL-1 contributes to the IL-17A expression induced by subacute O3 exposure. Induction of IL-23 by O3 does not appear to require cDC.

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Section: Discussionsupporting

confidence: 93%

Regulation of IL-17A expression in mice following subacute ozone exposure

Brand¹,

Mathews²,

Kasahara³

et al. 2016

Journal of Immunotoxicology

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“…could indicate that the clearance of S. pneumoniae is more IL-17 dependent, and this has been suggested in studies that have carried out in mice and in humans. 10,24,25 The frequency of IL-17A G-152A has not been reported in Finnish population, but it is similar to a study carried out by OcejoVinyals et al 17 in which the reported frequency was 39% for G/G, 47% for G/A and 14% for A/A in a healthy Spanish population.…”

Section: Discussionsupporting

confidence: 88%

The Gene Polymorphism of IL-17 G-152A is Associated with Increased Colonization of Streptococcus pneumoniae in Young Finnish Children

Vuononvirta

Peltola²,

Ilonen³

et al. 2015

Pediatric Infectious Disease Journal

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“…DCs promote the development of protective type-1 and IL-17 immune responses by elaboration of cytokines. 5 , 6 Additionally, DCs highly express IL-36R. 28 We therefore examined whether IL-36γ could directly induce type-1 cytokines from BMDC in vitro .…”

Section: Resultsmentioning

confidence: 99%

“…Lung dendritic cells (DCs) promote the development of type-1 immune responses via elaboration of interleukin-12 (IL-12) and IL-23. 5 , 6 IL-12 induces interferon-γ (IFNγ), which is important for effective innate immunity against a variety of bacterial pathogens. 7 , 8 IL-23 drives type-1 and IL-17-mediated responses, which are protective in bacterial pneumonia.…”

Section: Introductionmentioning

confidence: 99%

IL-36γ is a crucial proximal component of protective type-1-mediated lung mucosal immunity in Gram-positive and -negative bacterial pneumonia

et al. 2017

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IL-36γ is a member of novel IL-1-like pro-inflammatory cytokine family that are highly expressed in epithelial tissues and several myeloid-derived cell types. Little is known about the role of the IL-36 family in mucosal immunity, including lung antibacterial responses. We utilized murine models of IL-36γ deficiency to assess the contribution of IL-36γ in the lung during experimental pneumonia. Induction of IL-36γ was observed in the lung in response to Streptococcus pneumoniae (Sp) infection, and mature IL-36γ protein was secreted primarily in microparticles. IL-36γ-deficient mice challenged with Sp demonstrated increased mortality, decreased lung bacterial clearance and increased bacterial dissemination, in association with reduced local expression of type-1 cytokines, and impaired lung macrophage M1 polarization. IL-36γ directly stimulated type-1 cytokine induction from dendritic cells in-vitro in a MyD88-dependent fashion. Similar protective effects of IL-36γ were observed in a Gram-negative pneumonia model (Klebsiella pneumoniae). Intrapulmonary delivery of IL-36γ-containing microparticles reconstituted immunity in IL-36γ−/ − mice. Enhanced expression of IL-36γ was also observed in plasma and BALF of patients with ARDS due to pneumonia. These studies indicate that IL-36γ assumes a vital proximal role in the lung innate mucosal immunity during bacterial pneumonia by driving protective type 1 responses and classical macrophage activation.

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Interleukin-23 (IL-23) deficiency disrupts Th17 and Th1-related defenses against Streptococcus pneumoniae infection

Cited by 23 publications

References 65 publications

Regulation of IL-17A expression in mice following subacute ozone exposure

Regulation of IL-17A expression in mice following subacute ozone exposure

The Gene Polymorphism of IL-17 G-152A is Associated with Increased Colonization of Streptococcus pneumoniae in Young Finnish Children

IL-36γ is a crucial proximal component of protective type-1-mediated lung mucosal immunity in Gram-positive and -negative bacterial pneumonia

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