HIF-1 expression is associated with CCL2 chemokine expression in airway inflammatory cells: implications in allergic airway inflammation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-07-23

AUTHORS

Guillermina J Baay-Guzman, Ilona G Bebenek, Michelle Zeidler, Rogelio Hernandez-Pando, Mario I Vega, Eduardo A Garcia-Zepeda, Gabriela Antonio-Andres, Benjamin Bonavida, Marc Riedl, Eric Kleerup, Donald P Tashkin, Oliver Hankinson, Sara Huerta-Yepez

ABSTRACT

BACKGROUND: The pathogenesis of allergic airway inflammation in asthmatic patients is complex and characterized by cellular infiltrates and activity of many cytokines and chemokines. Both the transcription factor hypoxia inducible factor-1 (HIF-1) and chemokine CCL2 have been shown to play pivotal roles in allergic airway inflammation. The interrelationship between these two factors is not known. We hypothesized that the expression of HIF-1 and CCL2 may be correlated and that the expression of CCL2 may be under the regulation of HIF-1. Several lines of evidence are presented to support this hypothesis. METHODS: The effects of treating wild-type OVA (ovalbumin)-sensitized/challenged mice with ethyl-3,4-dihydroxybenzoate (EDHB), which upregulate HIF, on CCL2 expression, were determined. Mice conditionally knocked out for HIF-1β was examined for their ability to mount an allergic inflammatory response and CCL2 expression in the lung after intratracheal exposure to ovalbumin. The association of HIF-1α and CCL2 levels was also measured in endobronchial biopsies and bronchial fluid of asthma patients after challenge. RESULTS: We show that both HIF-1α and CCL2 were upregulated during an OVA (ovalbumin)-induced allergic response in mice. The levels of HIF-1α and CCL2 were significantly increased following treatment with a pharmacological agent which upregulates HIF-1α, ethyl-3,4-dihydroxybenzoate (EDHB). In contrast, the expression levels of HIF-1α and CCL2 were decreased in the lungs of mice that have been conditionally knocked out for ARNT (HIF-1β) following sensitization with OVA when compared to levels in wild type mice. In asthma patients, the levels of HIF-1α and CCL2 increased after challenge with the allergen. CONCLUSIONS: These data suggest that CCL2 expression is regulated, in part, by HIF-1 in the lung. These findings also demonstrate that both CCL2 and HIF-1 are implicated in the pathogenesis of allergic airway inflammation. More... »

PAGES

60-60

Journal

TITLE

Respiratory Research

ISSUE

1

VOLUME

13

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1465-9921-13-60

DOI

http://dx.doi.org/10.1186/1465-9921-13-60

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1048406154

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22823210


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24 schema:description BACKGROUND: The pathogenesis of allergic airway inflammation in asthmatic patients is complex and characterized by cellular infiltrates and activity of many cytokines and chemokines. Both the transcription factor hypoxia inducible factor-1 (HIF-1) and chemokine CCL2 have been shown to play pivotal roles in allergic airway inflammation. The interrelationship between these two factors is not known. We hypothesized that the expression of HIF-1 and CCL2 may be correlated and that the expression of CCL2 may be under the regulation of HIF-1. Several lines of evidence are presented to support this hypothesis. METHODS: The effects of treating wild-type OVA (ovalbumin)-sensitized/challenged mice with ethyl-3,4-dihydroxybenzoate (EDHB), which upregulate HIF, on CCL2 expression, were determined. Mice conditionally knocked out for HIF-1β was examined for their ability to mount an allergic inflammatory response and CCL2 expression in the lung after intratracheal exposure to ovalbumin. The association of HIF-1α and CCL2 levels was also measured in endobronchial biopsies and bronchial fluid of asthma patients after challenge. RESULTS: We show that both HIF-1α and CCL2 were upregulated during an OVA (ovalbumin)-induced allergic response in mice. The levels of HIF-1α and CCL2 were significantly increased following treatment with a pharmacological agent which upregulates HIF-1α, ethyl-3,4-dihydroxybenzoate (EDHB). In contrast, the expression levels of HIF-1α and CCL2 were decreased in the lungs of mice that have been conditionally knocked out for ARNT (HIF-1β) following sensitization with OVA when compared to levels in wild type mice. In asthma patients, the levels of HIF-1α and CCL2 increased after challenge with the allergen. CONCLUSIONS: These data suggest that CCL2 expression is regulated, in part, by HIF-1 in the lung. These findings also demonstrate that both CCL2 and HIF-1 are implicated in the pathogenesis of allergic airway inflammation.
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32 CCL2
33 CCL2 chemokine expression
34 CCL2 expression
35 CCL2 levels
36 HIF
37 HIF-1 expression
38 HIF-1α
39 HIF-1β
40 OVA
41 ability
42 activity
43 agents
44 airway inflammation
45 airway inflammatory cells
46 allergens
47 allergic airway inflammation
48 allergic inflammatory response
49 allergic responses
50 association
51 asthma patients
52 asthmatic patients
53 biopsy
54 bronchial fluid
55 cells
56 cellular infiltrate
57 challenges
58 chemokine CCL2
59 chemokine expression
60 chemokines
61 contrast
62 cytokines
63 data
64 dihydroxybenzoate
65 effect
66 endobronchial biopsies
67 ethyl
68 evidence
69 exposure
70 expression
71 expression levels
72 expression of CCL2
73 factor 1
74 factor hypoxia inducible factor-1
75 factors
76 findings
77 fluid
78 hypothesis
79 hypoxia-inducible factor-1
80 implications
81 inducible factor-1
82 infiltrate
83 inflammation
84 inflammatory cells
85 inflammatory response
86 interrelationships
87 intratracheal exposure
88 levels
89 lines
90 lines of evidence
91 lung
92 lungs of mice
93 mice
94 part
95 pathogenesis
96 patients
97 pharmacological agents
98 pivotal role
99 regulation
100 response
101 role
102 sensitization
103 transcription factor hypoxia-inducible factor-1
104 treatment
105 type mice
106 wild-type OVA
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