IL-36 induces cytokine IL-6 and chemokine CXCL8 expression in human lung tissue cells: Implications for pulmonary inflammatory responses

Zhang, Juan; Yin, Yibing; Lin, Xue; Yan, Xingxing; Xia, Yun; Zhang, Liping; Cao, Ju

doi:10.1016/j.cyto.2017.08.022

Cited by 37 publications

(36 citation statements)

References 29 publications

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“…These concentrations are consistent with prior reports in the literature studying IL-36γ in the lung, skin, and intestines [25, 38–41]. Aggregates were treated with acyclovir (ACV; GlaxoSmithKline, Research Triangle Park, NC) at 20 μg/ml as a positive control, or left untreated as a negative control.…”

Section: Methodssupporting

confidence: 86%

“…Three-dimensional aggregates were treated with poly(I:C) (Invivogen, San Diego, CA) at 100 μg/ml, recombinant human IL-36γ (Peprotech, Rocky Hill, NJ) at 100 or 500 ng/ml as previously described [12], or recombinant IL-36Ra (BioLegend, San Diego, CA) at 100 ng/ml. These concentrations are consistent with prior reports in the literature studying IL-36γ in the lung, skin, and intestines [25, 38–41]. Aggregates were treated with acyclovir (ACV; GlaxoSmithKline, Research Triangle Park, NC) at 20 μg/ml as a positive control, or left untreated as a negative control.…”

Section: Methodssupporting

confidence: 86%

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IL-36γ induces a transient HSV-2 resistant environment that protects against genital disease and pathogenesis

Gardner

Herbst-Kralovetz

2018

Cytokine

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Herpes simplex virus 2 (HSV-2) causes a persistent, lifelong infection that increases risk for sexually transmitted infection acquisition. Both the lack of a vaccine and the need for chronic suppressive therapies to control infection presents the need to further understand immune mechanisms in response to acute HSV-2 infection. The IL-36 cytokines are recently identified members of the IL-1 family and function as inflammatory mediators at epithelial sites. Here, we first used a well-characterized three-dimensional (3-D) human vaginal epithelial cell (VEC) model to understand the role of IL-36γ in the context of HSV-2 infection. In 3-D VEC, IL-36γ is induced by HSV-2 infection, and pretreatment with exogenous IL-36γ significantly reduced HSV-2 replication. To assess the impact of IL-36γ treatment on HSV-2 disease pathogenesis, we employed a lethal genital infection model. We showed that IL-36γ treatment in mice prior to lethal intravaginal challenge significantly limited vaginal viral replication, delayed disease onset, decreased disease severity, and significantly increased survival. We demonstrated that IL-36γ treatment transiently induced pro-inflammatory cytokines, chemokines, and antimicrobial peptides in murine lower female reproductive tract (FRT) tissue and vaginal lavages. Induction of the chemokines CCL20 and KC in IL-36γ treated mice also corresponded with increased polymorphonuclear (PMN) leukocyte infiltration observed in vaginal smears. Altogether, these studies demonstrate that IL-36γ drives the transient production of immune mediators and promotes PMN recruitment in the vaginal microenvironment that increases resistance to HSV-2 infection and disease. Our data indicate that IL-36γ may participate as a key player in host defense mechanisms against invading pathogens in the FRT.

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Section: Methodssupporting

confidence: 86%

Section: Methodssupporting

confidence: 86%

IL-36γ induces a transient HSV-2 resistant environment that protects against genital disease and pathogenesis

Gardner

Herbst-Kralovetz

2018

Cytokine

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“…Immunohistochemistry analyses further confirmed that IL-8 was overexpressed in AGEP compared with MPR and healthy skin and that cells of the infiltrate in pustular regions of AGEP skin were the main source of IL-8 (Figure 5a, right panels). As previously reported, IL-36 is an inducer of IL-8 (Marrakchi et al, 2011;Towne et al, 2011;Zhang et al, 2017). Consistently, the exposure of PBMCs from AGEP patients to their respective culprit drugs resulted in IL-8 production that was inhibited by recombinant IL-36Ra in a dose-dependent manner (see Supplementary Figure S5 online).…”

Section: Il-36 Secretion By Agep Patients' Pbmcs Is Induced By Toll-lsupporting

confidence: 84%

Culprit Drugs Induce Specific IL-36 Overexpression in Acute Generalized Exanthematous Pustulosis

Meier‐Schiesser

Feldmeyer

Janković

et al. 2019

Journal of Investigative Dermatology

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Acute generalized exanthematous pustulosis (AGEP) is a severe adverse cutaneous drug reaction. Although an involvement of drug-specific T cells has been reported, the physiopathology of AGEP and mechanism of neutrophilic skin inflammation remain incompletely understood. Recently, mutations in IL-36RN, the gene encoding the IL-36 receptor antagonist, have been reported to be more frequent in AGEP patients and pustular psoriasis. Here, we show that IL-36 cytokines, in particular IL-36g, are highly expressed in lesional skin of AGEP patients, keratinocytes and macrophages being a major source of IL-36g. Such an IL-36g overexpression was not observed in patients with drug-induced maculopapular rash. In vitro, the causative drug specifically induced IL-36g release either directly by the patient's peripheral blood monocytes or indirectly by keratinocytes in the presence of autologous peripheral blood mononuclear cells. Such culprit drug induction of IL-36g secretion in vitro was specific for AGEP and involved toll-like receptor 4 sensing the drug/albumin complex as a danger signal. Our results suggest that IL-36g secretion by monocytes/macrophages and keratinocytes in response to culprit drug exposure likely plays a key role in the pathogenesis of AGEP.

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“…Chemokines, a group of cytokines that attract and activate leucocytes into inflamed tissue, have been associated with the pathogenesis of a number of diseases, ranging from atherosclerosis to human immunodeficiency virus (HIV) infection [54], and CCL21 has been suggested as being involved in the pathogenesis of various inflammatory disorders including rheumatoid arthritis, inflammatory bowel diseases, and atherosclerosis [55]. Nutrigenomic analysis also identified several interleukins such as IL-36A that have pro-inflammatory properties and have been described as being involved in pulmonary inflammatory responses [56]. Several studies have shown that foods rich in BC or isolated BC such as hesperidin can regulate the expression of chemokines [7].…”

Section: Discussionmentioning

confidence: 99%

Acute Effects of the Consumption of Passiflora setacea Juice on Metabolic Risk Factors and Gene Expression Profile in Humans

et al. 2020

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Background: Passiflora setacea (PS) is a passionfruit variety of the Brazilian savannah and is a rich source of plant food bioactives with potential anti-inflammatory activity. This study aimed to investigate the effect of an acute intake of PS juice upon inflammation, metabolic parameters, and gene expression on circulating immune cells in humans. Methods: Overweight male volunteers (n = 12) were enrolled in two double-blind placebo-controlled studies. Blood samples were collected from fasting volunteers 3 h after the consumption of 250 mL of PS juice or placebo (PB). Metabolic parameters (insulin, glucose, total cholesterol, high-density lipoprotein (LDL), high-density lipoprotein (HDL), and total triglycerides) and circulating cytokines were evaluated (study 1). Peripheral blood mononuclear cell (PBMC) from the same subjects were isolated and RNA was extracted for transcriptomic analyses using microarrays (study 2). Results: Insulin and homeostatic model assessment for insulin resistance (HOMA-IR) levels decreased statistically after the PS juice intake, whereas HDL level increased significantly. Interleukin (IL)-17A level increased after placebo consumption, whereas its level remained unchanged after PS juice consumption. Nutrigenomic analyses revealed 1327 differentially expressed genes after PS consumption, with modulated genes involved in processes such as inflammation, cell adhesion, or cytokine–cytokine receptor. Conclusion: Taken together, these clinical results support the hypothesis that PS consumption may help the prevention of cardiometabolic diseases.

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IL-36 induces cytokine IL-6 and chemokine CXCL8 expression in human lung tissue cells: Implications for pulmonary inflammatory responses

Cited by 37 publications

References 29 publications

IL-36γ induces a transient HSV-2 resistant environment that protects against genital disease and pathogenesis

IL-36γ induces a transient HSV-2 resistant environment that protects against genital disease and pathogenesis

Culprit Drugs Induce Specific IL-36 Overexpression in Acute Generalized Exanthematous Pustulosis

Acute Effects of the Consumption of Passiflora setacea Juice on Metabolic Risk Factors and Gene Expression Profile in Humans

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