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• W2901426400 abstract "It is recognized that air pollution is associated with the pathogenesis of airway allergy.1Esposito S. Tenconi R. Lelii M. Preti V. Nazzari E. Consolo S. et al.Possible molecular mechanisms linking air pollution and asthma in children.BMC Pulm Med. 2014; 14: 31Crossref PubMed Scopus (102) Google Scholar, 2Guarnieri M. Balmes J.R. Outdoor air pollution and asthma.Lancet. 2014; 383: 1581-1592Abstract Full Text Full Text PDF PubMed Scopus (1066) Google Scholar Diesel exhaust particles are recognized as one of the major sources of air pollution.3Delfino R.J. Wu J. Tjoa T. Gullesserian S.K. Nickerson B. Gillen D.L. Asthma morbidity and ambient air pollution: effect modification by residential traffic-related air pollution.Epidemiology. 2014; 25: 48-57Crossref PubMed Scopus (95) Google Scholar 3-Methyl-4-nitrophenol (MNP) is a component of diesel exhaust particles,2Guarnieri M. Balmes J.R. Outdoor air pollution and asthma.Lancet. 2014; 383: 1581-1592Abstract Full Text Full Text PDF PubMed Scopus (1066) Google Scholar as well as the primary breakdown product of the excessively used insecticide fenitrothion.4Min J. Lu Y. Hu X. Zhou N.Y. Biochemical Characterization of 3-methyl-4-nitrophenol degradation in Burkholderia sp. Strain SJ98.Front Microbiol. 2016; 7: 791Crossref PubMed Scopus (15) Google Scholar Although the association between air pollution and airway allergy has been recognized,5Alexis N.E. Carlsten C. Interplay of air pollution and asthma immunopathogenesis: a focused review of diesel exhaust and ozone.Int Immunopharmacol. 2014; 23: 347-355Google Scholar the underlying mechanism remains to be further investigated. This study aims to elucidate the role of MNP in regulation of dendritic cell (DC) properties and facilitation of allergic rhinitis. Mouse bone marrow–derived dendritic cells (BMDCs) were prepared with established procedures.6Feng B.S. Zheng P.Y. Chen X. Liao X.Q. Yang P.C. Investigation of the role of cholera toxin in assisting the initiation of the antigen-specific Th2 response.Immunol Invest. 2008; 37: 782-797Crossref PubMed Scopus (0) Google Scholar BMDCs were exposed to MNP in the culture at gradient concentrations for 48 hours. Cell extracts were prepared and analyzed by using quantitative RT-PCR and Western blotting. The results showed that exposure to MNP markedly increased levels of TIM4 (T cell immunoglobulin mucin domain molecule-4), Bcl2L12, MHC class II, and CD80 in BMDCs in an MNP concentration–dependent manner (Fig 1). The results indicate that exposure to MNP increases expression of Bcl2L12 and other TH2 response–relevant costimulatory molecules in DCs. BMDCs were cultured with ovalbumin (OVA) and MNP for 48 hours. Cells were collected at the end of culture. Cell extracts were prepared and analyzed by means of co-immunoprecipitation (IP). The results showed that a triple complex of MHC class II/Bcl2L12/OVA was detected in DCs exposed to both OVA and MNP (Fig 2, A), levels of which were much less in those treated with OVA alone (Fig 2, B). The results suggest that Bcl2L12 facilitates formation of the MHC class II/OVA complex in DCs. BMDCs were generated with bone marrow of mice with the Bcl2L12 gene knockout (KO; see Fig E1 in this article's Online Repository at www.jacionline.org) to corroborate these results. KO DCs were treated with MNP and OVA in culture for 48 hours. Indeed, levels of the MHC class II/OVA complex were much less in KO BMDCs (Fig 2, C) compared with those in wild-type (WT) DCs (Fig 2, A). The results indicate that Bcl2L12 facilitates formation of the MHC class II/OVA complex in DCs. His-MHC class II–expressing and Flag-Bcl2L12–expressing plasmids were constructed and transfected into BMDCs to produce recombinant MHC class II and recombinant Bcl2L12 for corroboration of these results. BMDCs were exposed to OVA in culture for 48 hours. Cells were then analyzed by means of co-IP with antibodies of His, Flag, and OVA or isotype IgG as IP antibodies. The results showed that a complex in the extracts of the BMDCs was precipitated by antibodies of either His (for MHC class II), Flag (for Bcl2L12), or OVA, respectively (Fig 2, D), indicating that recombinant MHC class II, recombinant Bcl2L12, and OVA can be processed by BMDCs to form a triple complex. Recombinant MHC class II bound OVA to form a complex in BMDCs (Fig 2, E), but the amounts were much less than that in the presence of Bcl2L12 (Fig 2, D). These results demonstrate that Bcl2L12 enhances formation of the MHC class II/OVA complex, whereas inhibition of Bcl2L12 does not affect the baseline of MHC class II/OVA complex formation in DCs. BMDCs were prepared and primed by means of exposure to MNP and OVA for 48 hours to generate the MHC class II/OVA complex on the surfaces of DCs (Fig 2, A). Primed BMDCs were cultured with CD4+ T cells (effector T [Teff] cells; isolated from the DO11.10 mouse spleen) for 3 days. As analyzed by using flow cytometry, coculture with primed BMDCs induced marked Teff cell proliferation (see Fig E2, A and B, in this article's Online Repository at www.jacionline.org). Levels of IL-4, IL-5, and IL-13, but not IFN-γ, were increased significantly in culture supernatants (see Fig E2, C-F). Results demonstrate that Bcl2L12 facilitates antigen presentation of DCs, whereas BMDCs generated from KO mice did not show such ability to present antigens to T cells (see Fig E2). BMDCs were prepared and primed by incubating with MNP and OVA, OVA alone, or saline in culture for 48 hours. Grouped BALB/c mice were adoptively transferred with primed BMDCs through tail vein injection, which was repeated 1 week later. The mice were killed 1 week after the second transfer. Teff cells were isolated from lung mononuclear cells (LMC) and splenic cells and analyzed by using the carboxyfluorescein succinimidyl ester (CFSE) dilution assay. The results showed that mice that received BMDCs primed with both MNP and OVA, but not either one alone, were sensitized to OVA because a high frequency of OVA-specific CD4+ T cells was detected in lung and spleen tissue (see Fig E3 in this article's Online Repository at www.jacionline.org). Next, primed WT BMDCs or KO BMDCs were adoptively transferred into naive BALB/c mice. Parameters relevant to nasal allergy were analyzed. The results showed that adoptive transfer of primed WT BMDCs induced nasal allergy–like changes in recipient mice, including rhinocnesmus, sneezing, and rhinorrhea, and increases in the content of OVA-specific IgE, TH2 cytokine, and mouse mast cell protease-1 (mMCP1) in the nasal mucosa, which did not occur in mice that received primed KO BMDCs (see Fig E4 in this article's Online Repository at www.jacionline.org). The data were corroborated by treating mice with a mixture of MNP and house mite extract in which WT mice were sensitized with nasal drops of MNP/house mite extract, whereas none of the Bcl2L12 KO mice were sensitized (see Fig E5 in this article's Online Repository at www.jacionline.org). The results demonstrate that MNP facilitates development of nasal allergy in mice, which can be prevented by inhibiting Bcl2L12 expression. MNP is a small molecule (molecular weight, 306.27) and somewhat similar to a hapten, such as dinitrophenyl, in induction of an immune response.7Holmdahl M. Ahlfors S.R. Holmdahl R. Hansson C. Structure-immune response relationships of hapten-modified collagen II peptides in a T-cell model of allergic contact dermatitis.Chem Res Toxicol. 2008; 21: 1514-1523Google Scholar Although a hapten has to conjugate with a large molecular carrier to initiate allergic responses,8Menard H.A. Demers J.C. Use of a hapten-carrier system in experimental immune arthritis in the rabbit.Arthritis Rheum. 1977; 20: 1402-1408Google Scholar MNP enhances allergic responses in a different way by facilitating expression of Bcl2L12, as shown by the present data. In summary, the present data show a previously unknown phenomenon that exposure to MNP, one of the components of diesel exhaust, enhances the ability of DCs to present antigen and drives DCs to produce allergy development–relevant factors. Bcl2L12 inhibition can diminish the ability of DCs to present antigen and the development of nasal allergy in mice. Experimental procedures are presented in the Methods section in this article's Online Repository at www.jacionline.org. Antibodies of TIM4, Bcl2L12, MHC class II, CD80, OVA, His, and Flag were purchased from Santa Cruz Biotechnology (Santa Cruz, Calif). ELISA kits of OVA-specific IgE, mMCP1, IL-4, IL-5, and IFN-γ were purchased from BioMart (Beijing, China). The MNP and materials and reagents for IP were purchased from Sigma-Aldrich (St Louis, Mo). Immune cell isolation kits were purchased from Miltenyi Biotech (San Diego, Calif). Male BALB/c mice (6-8 weeks old) were obtained from the Guangzhou Experimental Animal Center (Guangzhou, China). DO11.10 mice (BALB/c ground) were purchased from the Jackson Laboratory (Bar Harbor, Me). Bcl2L12 KO mice were provided by the Animal Institute of the Chinese Science Academy (Beijing, China). Mice were maintained in a specific pathogen-free facility with free access to water and food. Mice used in the present study were approved by the Animal Ethics Committee at Shenzhen University. BMDCs were prepared from bone marrow of BALB/c mice according to our established procedures.E1Feng B.S. Zheng P.Y. Chen X. Liao X.Q. Yang P.C. Investigation of the role of cholera toxin in assisting the initiation of the antigen-specific Th2 response.Immunol Invest. 2008; 37: 782-797Crossref PubMed Scopus (25) Google Scholar Cells were cultured in RPMI 1640 supplemented with 10% FBS, 0.1 mg/mL streptomycin, 100 U/mL penicillin, and 2 mmol/L glutamine. Medium was changed in 2 to 3 days. Cell viability was greater than 99%, as determined by using the Trypan blue exclusion assay. Cells were cultured in RPMI 1640 supplemented with 10% FBS (BSA), 100 U/mL penicillin, 0.1 mg/mL streptomycin, and 2 mmol/L glutamine. The medium was changed in 2 to 3 days. Cell viability was greater than 99%, as determined by using the Trypan blue exclusion assay. In some experiments MNP was added to the culture to stimulate immune cells. Concentrations of MNP in culture were referred to in other published articles.E2Mi Y. Zhang C. Li C. Taneda S. Watanabe G. Suzuki A.K. et al.Quercetin protects embryonic chicken spermatogonial cells from oxidative damage intoxicated with 3-methyl-4-nitrophenol in primary culture.Toxicol Lett. 2009; 190: 61-65Google Scholar, E3Mori Y. Kamata K. Toda N. Hayashi H. Seki K. Taneda S. et al.Isolation of nitrophenols from diesel exhaust particles (DEP) as vasodilatation compounds.Biol Pharm Bull. 2003; 26: 394-395Google Scholar, E4Ghio A.J. Smith C.B. Madden M.C. Diesel exhaust particles and airway inflammation.Curr Opin Pulm Med. 2012; 18: 144-150Crossref PubMed Scopus (97) Google Scholar Cytokine levels were determined by means of ELISA with commercial reagent kits, according to the manufacturer's instructions. Bcl2L12 KO mice on the BALB/c background were prepared by the Animal Institute of Chinese Science Academy (Beijing, China). Procedures of the Bcl2L12 KO mouse preparation are presented in our recent report.E5Li M.G. Liu X.Y. Liu Z.Q. Hong J.Y. Liu J.Q. Zhou C.J. et al.Bcl2L12 contributes to Th2-biased inflammation in the intestinal mucosa by regulating CD4+ T cell activities.J Immunol. 2018; 201: 725-733Crossref PubMed Scopus (15) Google Scholar Cells were collected from relevant experiments and incubated with a lysing buffer for 30 minutes. The supernatant was collected by means of centrifugation at 13,000 rpm for 10 minutes and used for cytosolic extracts. The remaining pellets were resuspended in nuclear lysing buffer and incubated for 30 minutes. The supernatant was collected by means of centrifugation at 13,000 rpm for 10 minutes and used for nuclear extracts. All procedures were performed at 4°C. Proteins were fractioned by using SDS-PAGE and transferred onto a polyvinylidene difluoride membrane. After blocking with 5% skim milk for 30 minutes, the membrane was incubated with the first antibodies of interest overnight at 4°C, followed by incubating with the second antibodies (labeled with peroxidase) for 2 hours at room temperature. The membrane was washed with Tris-buffered saline/Tween 20 after each incubation. Immunoblots on the membrane were developed by using enhanced chemiluminescence and photographed with an imaging device. Proteins were precleared by incubating with protein G agarose beads for 2 hours to remove the nonspecific immune complexes. Samples were then incubated with antibodies of interest or isotype IgG overnight. Immune complexes on beads were collected by means of centrifugation (13,000 rpm for 10 minutes) and eluted with an eluting buffer. Samples were then analyzed by using Western blotting. All procedures were performed at 4°C. BMDCs were prepared and primed by incubating with MNP (10 μg/mL) and OVA (10 μg/mL) for 48 hours. Primed or naive BMDCs were adoptively transplanted into mice (106 cells per mouse) by means of tail vein injection 2 times at 1 week apart. Mice were killed 1 week after the second injection. CD4+CD25− T cells (Teff) were isolated from the lungs and spleen. Teff cells were labeled with CFSE and cultured with DCs in the presence of OVA (5 μg/mL) or BSA (5 μg/mL) for 3 days. Cells were analyzed by using the CFSE-dilution assay. Levels of TH1 and TH2 cytokines in culture supernatants were determined by means of ELISA. The rate of Teff cell proliferation and TH2 cytokine levels in culture were used as indicators of mouse sensitization. One week after the second transplantation of primed DCs, mice were treated with nasal drops containing OVA (50 μg/mL) daily for 7 days. Parameters of nasal allergy in mice were assessed, including recording rhinocnesmus, sneezing, and rhinorrhea within 1 hour after the last nasal challenge with the specific antigen (OVA). Levels of OVA-specific IgE, mMCP1, TH2 cytokines, and the TH1 cytokine IFN-γ in nasal mucosal protein extracts were determined by means of ELISA. Lungs were excised from mice on death. Lung tissue was cut into small pieces and incubated with collagenase IV (1 mg/mL) at 37°C for 1 hour with mild agitation. Single cells were passed through a cell strainer (70 μm) and collected by means of centrifugation. Teff cells (CD3+CD4+CD25−) were isolated from splenic cells or LMCs by using magnetic cell sorting with purchased reagent kits, according to the manufacturer's instructions. If the purity of the cells did not reach 95%, magnetic cell sorting procedures were repeated with the cells. T-cell proliferation was assessed by using the CFSE dilution assay. Teff cells were isolated from the spleen and lung, labeled with CFSE, and cultured with DCs (Teff/DC ratio, 106:105/mL) in the presence of OVA (5 μg/mL) or BSA (5 μg/mL) for 3 days. Cells were analyzed by using flow cytometry. Data are presented as means ± SDs. The difference between 2 groups was determined by using the Student t test. ANOVA followed by the Dunnett t test or Student-Neuman-Keuls test was used for multiple comparisons. P values of less than .05 were considered statistically significant. The objective of this procedure was to create a Bcl2112 KO mouse model (C57BL/6) by using CRISPR/Cas-mediated genome engineering, which include the following. The mouse Bcl2112 gene (GenBank accession number: NM_029410.3; Ensembl: ENSMUSG00000003190) was located on mouse chromosome 7. Seven exons were identified, with the ATG start codon in exon 2 and the TGA stop codon in exon 7. Exon 2 to exon 3 and exon 3 were selected as target sites. Two pairs of gRNA-targeting vectors were constructed and confirmed by means of sequencing. Cas9 mRNA and gRNA generated by means of in vitro transcription were coinjected into fertilized eggs for KO mouse production. Pups were genotyped by using PCR, followed by sequence analysis. The genomic region of the mouse Bcl2112 locus is diagrammed below (the gene is oriented from left to right; total size, 6.36 kb). Solid bars represent open reading frames, and open bars present untranslated regions. Pair 1: gRNA1 (matches forward strand of gene), AGCGTG TACGCCAGTGCGACGGG; gRNA2 (matches forward strand of gene), TTCCGTGGTTGACC CGGGAGAGG. Pair 2: gRNA3 (matches reverse strand of gene), GGAGT TATCCCGAAGGGG TCTGG; gRNA4 (matches forward strand of gene), GTGGGACGTGTCCCG ATGGAGGG .Fig E2Bcl2L12 facilitates antigen presentation of DCs. BMDCs were generated from bone marrow of WT and Bcl2L12 KO mice. Cells were primed with MNP and OVA for 48 hours. Naive CD4+ T cells (Teff cells) were isolated from the spleens of DO11.10 mice. Teff cells were labeled with CFSE and cultured with primed BMDCs at gradient ratios for 3 days. Cells were analyzed by using flow cytometry. A, Gated histograms indicate proliferating Teff cells. B, Bars indicate summarized data of proliferating Teff cells in Fig E2, A. C-F, Bars indicate cytokine levels of CD4+ T cells in culture supernatants. Data shown in bars are presented as means ± SDs. *P < .01 compared with the “10:0” group. Data represent 3 independent experiments.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Fig E3MNP/OVA-primed DCs sensitize mice. BMDCs were prepared and primed by incubating with MNP (10 μg/mL) and OVA (μg/mL), OVA alone, or saline in culture for 48 hours. BALB/c mice (6 mice per group) were adoptively transferred with primed BMDCs (106 cells/mouse) through tail vein injection, which was repeated 1 week after. Mice were killed 1 week after the second transfer. Teff cells were isolated from LMCs and splenic cells and analyzed by using the CFSE dilution assay. A, Gated histograms indicate proliferating Teff cells after treating with reagents in culture as denoted above each panel in the presence of DCs and OVA (5 μg/mL) or BSA (#; 5 μg/mL). B, Bars indicate summarized data of proliferating Teff cells in Fig E3, A. Data shown in bars are presented as means ± SDs. *P < .01 compared with the saline group.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Fig E4Adoptive transfer with MNP/OVA-primed BMDCs induces allergic rhinitis in mice. BMDCs were prepared with bone marrow of WT and KO mice. Cells were primed by means of exposure to MNP/OVA in the culture for 48 hours. BMDCs (106 cells/mouse) or saline (control) were injected into BALB/c mice through tail vein puncture; injection was repeated 1 week later. One week after the second injection, mice were challenged with nasal drops containing OVA (5 mg/mL). A-C, Nasal symptoms (rhinocnesmus, sneezing, and rhinorrhea) were recorded within 1 hour after challenge with nasal drops. D-H, Mice were killed 1 hour after nasal challenge. Nasal mucosa was collected from each mouse and processed for protein extracts. Levels of specific IgE, mMCP1, IL-4, IL-5, and IFN-γ in protein extracts were determined by mean of ELISA, as shown in bars. Data shown in bars are presented as means ± SDs. *P < .01 compared with the saline group. Each group consists of 6 mice.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Fig E5Inhibition of Bcl2L12 abolishes MNP/house mite extract (HME)–induced allergic rhinitis in mice. BALB/c (WT) mice (n = 6) and Bcl2L12 KO mice (n = 6) were treated with a mixture of MNP (10 μg/mL) and HME (10 μg/mL) by using nasal drops (50 μL per nostril per time) daily for 21 consecutive days. Control mice were treated with saline nasal drops. Mice were killed on day 21, 1 hour after treating with nasal drops. A-C, AR clinical symptoms, rhinocnesmus (Fig E5, A), sneezing (Fig E5, B), and rhinorrhea (Fig E5, C), were recorded on day 21 at 0 to 60 minutes after treating with nasal drops. D and E, Blood samples were collected from each mouse. Sera were isolated from samples and analyzed by means of ELISA. Bars indicate serum levels of specific IgE (Fig E5, D) and mMCP1 (Fig E5, E). F-H, Nasal mucosa was collected from each mouse immediately after death. Protein extracts were prepared with nasal mucosal samples and analyzed by means of ELISA. Bars indicate levels of IL-4 (Fig E5, F), IL-5 (Fig E5, G), and IFN-γ (Fig E5, H) in nasal mucosal extracts. Data shown in bars are presented as means ± SDs. Samples from individual mice were analyzed separately in triplicates.View Large Image Figure ViewerDownload Hi-res image Download (PPT)" @default.
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• W2901426400 title "3-Methyl-4-nitrophenol triggers nasal allergy by modulating dendritic cell properties" @default.
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