Upregulation of IL-17A/F from human lung tissue explants with cigarette smoke exposure: implications for COPD View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-11-27

AUTHORS

Ying Chang, Laila Al-Alwan, Sama Alshakfa, Severine Audusseau, Andrea Karen Mogas, Fazila Chouiali, Parameswaran Nair, Carolyn J Baglole, Qutayba Hamid, David H Eidelman

ABSTRACT

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is an inflammatory disorder marked by relative resistance to steroids. The IL-17 superfamily, which mediates cross-talk between the adaptive and innate immune systems, has been associated with diminished responses to steroids. Increasing evidence supports elevated IL-17 expression in the lung of COPD subjects. However, whether cells of the immune system (systemic) and/or local lung cells are contributing to the elevated IL-17 remains unclear. To address this issue, we utilized a human parenchymal lung tissue explant culture system with cigarette smoke exposure to investigate the expression of IL-17 and the mechanisms involved. METHODS: Parenchymal lung tissue removed from 10 non-COPD and 8 COPD patients was sectioned and cultured with different concentrations of cigarette smoke extract (CSE) for 3 or 6 hours. Tissue viability was evaluated by LDH (lactate dehydrogenase) in culture supernatants. Western blot and real-time PCR were performed to evaluate IL-17A/F expression. To investigate the mechanisms, pharmacological inhibitors for MAPK p38, ERK1/2, NF-κB and PI3K pathways were added into the culture media. RESULTS: No tissue damage was observed after the cigarette smoke exposure for 3 h or 6 h compared with the control media. At the protein level, the expression of both IL-17A (2.4 ± 0.6 fold) and IL-17 F (3.7 ± 0.7 fold) in the tissue from non-COPD subjects was significantly increased by 5% of CSE at 3 h. For COPD subjects, IL-17A/F expression were significantly increased only at 6 h with 10% of CSE (IL-17A: 4.2 ± 0.8 fold; IL-17 F: 3.3 ± 0.8 fold). The increased expression of IL-17A/F is also regulated at the mRNA level. The inhibitors for NF-κB and PI3K pathways significantly inhibited CSE-induced IL-17A/F expression from lung tissue of non-COPD subjects. CONCLUSIONS: We found the evidence that the expression of both IL-17A and IL-17 F is increased by the cigarette smoke exposure in explants from both non-COPD and COPD subjects, supporting that local lung cells contribute IL-17 production. The elevated IL-17A/F expression is dependent on NF-κB and PI3K pathways. These observations add to the growing evidence which suggests that Th17 cytokines play a significant role in COPD. More... »

PAGES

145

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s12931-014-0145-7

DOI

http://dx.doi.org/10.1186/s12931-014-0145-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1005662096

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25427574


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34 schema:description BACKGROUND: Chronic obstructive pulmonary disease (COPD) is an inflammatory disorder marked by relative resistance to steroids. The IL-17 superfamily, which mediates cross-talk between the adaptive and innate immune systems, has been associated with diminished responses to steroids. Increasing evidence supports elevated IL-17 expression in the lung of COPD subjects. However, whether cells of the immune system (systemic) and/or local lung cells are contributing to the elevated IL-17 remains unclear. To address this issue, we utilized a human parenchymal lung tissue explant culture system with cigarette smoke exposure to investigate the expression of IL-17 and the mechanisms involved. METHODS: Parenchymal lung tissue removed from 10 non-COPD and 8 COPD patients was sectioned and cultured with different concentrations of cigarette smoke extract (CSE) for 3 or 6 hours. Tissue viability was evaluated by LDH (lactate dehydrogenase) in culture supernatants. Western blot and real-time PCR were performed to evaluate IL-17A/F expression. To investigate the mechanisms, pharmacological inhibitors for MAPK p38, ERK1/2, NF-κB and PI3K pathways were added into the culture media. RESULTS: No tissue damage was observed after the cigarette smoke exposure for 3 h or 6 h compared with the control media. At the protein level, the expression of both IL-17A (2.4 ± 0.6 fold) and IL-17 F (3.7 ± 0.7 fold) in the tissue from non-COPD subjects was significantly increased by 5% of CSE at 3 h. For COPD subjects, IL-17A/F expression were significantly increased only at 6 h with 10% of CSE (IL-17A: 4.2 ± 0.8 fold; IL-17 F: 3.3 ± 0.8 fold). The increased expression of IL-17A/F is also regulated at the mRNA level. The inhibitors for NF-κB and PI3K pathways significantly inhibited CSE-induced IL-17A/F expression from lung tissue of non-COPD subjects. CONCLUSIONS: We found the evidence that the expression of both IL-17A and IL-17 F is increased by the cigarette smoke exposure in explants from both non-COPD and COPD subjects, supporting that local lung cells contribute IL-17 production. The elevated IL-17A/F expression is dependent on NF-κB and PI3K pathways. These observations add to the growing evidence which suggests that Th17 cytokines play a significant role in COPD.
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42 COPD subjects
43 CSE-induced IL-17A/F expression
44 ERK1/2
45 F expression
46 IL-17
47 IL-17 F
48 IL-17 expression
49 IL-17 production
50 IL-17A
51 IL-17A/F
52 IL-17A/F expression
53 K pathways
54 LDH
55 MAPK p38
56 NF-κB
57 PCR
58 PI3K pathway
59 Western blot
60 blot
61 cells
62 chronic obstructive pulmonary disease
63 cigarette smoke exposure
64 cigarette smoke extract
65 concentration
66 control medium
67 culture medium
68 culture supernatants
69 culture system
70 cytokines
71 damage
72 different concentrations
73 diminished response
74 disease
75 disorders
76 elevated IL-17
77 elevated IL-17A/F expression
78 evidence
79 evidence support
80 explant culture system
81 explants
82 exposure
83 expression
84 expression of IL-17
85 extracts
86 hours
87 human lung tissue explants
88 human parenchymal lung tissue explant culture system
89 immune system
90 implications
91 increased expression
92 inflammatory disorders
93 inhibitors
94 innate immune system
95 issues
96 levels
97 local lung cells
98 lung
99 lung cells
100 lung tissue
101 lung tissue explant culture system
102 lung tissue explants
103 mRNA levels
104 mechanism
105 medium
106 non-COPD subjects
107 observations
108 obstructive pulmonary disease
109 p38
110 parenchymal lung tissue
111 parenchymal lung tissue explant culture system
112 pathway
113 patients
114 pharmacological inhibitors
115 production
116 protein levels
117 pulmonary disease
118 real-time PCR
119 relative resistance
120 resistance
121 response
122 role
123 significant role
124 smoke exposure
125 smoke extract
126 steroids
127 subjects
128 supernatant
129 support
130 system
131 tissue
132 tissue damage
133 tissue explant culture system
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135 tissue viability
136 upregulation
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