The interaction of secreted phospholipase A2-IIA with the microbiota alters its lipidome and promotes inflammation Article Swipe
Étienne Doré
,
Charles Joly-Beauparlant
,
Satoshi Morozumi
,
Alban Mathieu
,
Tania Lévesque
,
Isabelle Allaeys
,
Anne‐Claire Duchez
,
Nathalie Cloutier
,
Mickaël Leclercq
,
Antoine Bodein
,
Christine Payré
,
Cyril Martin
,
Agnès Petit-Paitel
,
Michael H. Gelb
,
Manu Rangachari
,
Makoto Murakami
,
Laëtitia Davidovic
,
Nicolas Flamand
,
Makoto Arita
,
Gérard Lambeau
,
Arnaud Droit
,
Éric Boilard
·
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1172/jci.insight.152638
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1172/jci.insight.152638
Secreted phospholipase A2-IIA (sPLA2-IIA) hydrolyzes phospholipids to liberate lysophospholipids and fatty acids. Given its poor activity toward eukaryotic cell membranes, its role in the generation of proinflammatory lipid mediators is unclear. Conversely, sPLA2-IIA efficiently hydrolyzes bacterial membranes. Here, we show that sPLA2-IIA affects the immune system by acting on the intestinal microbial flora. Using mice overexpressing transgene-driven human sPLA2-IIA, we found that the intestinal microbiota was critical for both induction of an immune phenotype and promotion of inflammatory arthritis. The expression of sPLA2-IIA led to alterations of the intestinal microbiota composition, but housing in a more stringent pathogen-free facility revealed that its expression could affect the immune system in the absence of changes to the composition of this flora. In contrast, untargeted lipidomic analysis focusing on bacteria-derived lipid mediators revealed that sPLA2-IIA could profoundly alter the fecal lipidome. The data suggest that a singular protein, sPLA2-IIA, produces systemic effects on the immune system through its activity on the microbiota and its lipidome.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1172/jci.insight.152638
- http://insight.jci.org/articles/view/152638/files/pdf
- OA Status
- gold
- Cited By
- 46
- References
- 138
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4206902780
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4206902780Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1172/jci.insight.152638Digital Object Identifier
- Title
-
The interaction of secreted phospholipase A2-IIA with the microbiota alters its lipidome and promotes inflammationWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2022Year of publication
- Publication date
-
2022-01-24Full publication date if available
- Authors
-
Étienne Doré, Charles Joly-Beauparlant, Satoshi Morozumi, Alban Mathieu, Tania Lévesque, Isabelle Allaeys, Anne‐Claire Duchez, Nathalie Cloutier, Mickaël Leclercq, Antoine Bodein, Christine Payré, Cyril Martin, Agnès Petit-Paitel, Michael H. Gelb, Manu Rangachari, Makoto Murakami, Laëtitia Davidovic, Nicolas Flamand, Makoto Arita, Gérard Lambeau, Arnaud Droit, Éric BoilardList of authors in order
- Landing page
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https://doi.org/10.1172/jci.insight.152638Publisher landing page
- PDF URL
-
https://insight.jci.org/articles/view/152638/files/pdfDirect link to full text PDF
- Open access
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
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https://insight.jci.org/articles/view/152638/files/pdfDirect OA link when available
- Concepts
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Lipidome, Immune system, Gut flora, Proinflammatory cytokine, Lipid signaling, Inflammation, Biology, Phospholipase A2, Cell biology, Microbiology, Chemistry, Lipidomics, Immunology, Biochemistry, EnzymeTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
46Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 7, 2024: 12, 2023: 19, 2022: 8Per-year citation counts (last 5 years)
- References (count)
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138Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.the | 23, 43, 49, 62, 87, 105, 109, 114, 135, 150, 157 |
| abstract_inverted_index.was | 65 |
| abstract_inverted_index.both | 68 |
| abstract_inverted_index.cell | 18 |
| abstract_inverted_index.data | 139 |
| abstract_inverted_index.mice | 54 |
| abstract_inverted_index.more | 95 |
| abstract_inverted_index.poor | 14 |
| abstract_inverted_index.role | 21 |
| abstract_inverted_index.show | 39 |
| abstract_inverted_index.that | 40, 61, 100, 130, 141 |
| abstract_inverted_index.this | 117 |
| abstract_inverted_index.Given | 12 |
| abstract_inverted_index.Here, | 37 |
| abstract_inverted_index.Using | 53 |
| abstract_inverted_index.alter | 134 |
| abstract_inverted_index.could | 103, 132 |
| abstract_inverted_index.fatty | 10 |
| abstract_inverted_index.fecal | 136 |
| abstract_inverted_index.found | 60 |
| abstract_inverted_index.human | 57 |
| abstract_inverted_index.lipid | 27, 127 |
| abstract_inverted_index.A2-IIA | 2 |
| abstract_inverted_index.acids. | 11 |
| abstract_inverted_index.acting | 47 |
| abstract_inverted_index.affect | 104 |
| abstract_inverted_index.flora. | 52, 118 |
| abstract_inverted_index.immune | 44, 72, 106, 151 |
| abstract_inverted_index.system | 45, 107, 152 |
| abstract_inverted_index.toward | 16 |
| abstract_inverted_index.absence | 110 |
| abstract_inverted_index.affects | 42 |
| abstract_inverted_index.changes | 112 |
| abstract_inverted_index.effects | 148 |
| abstract_inverted_index.housing | 92 |
| abstract_inverted_index.suggest | 140 |
| abstract_inverted_index.through | 153 |
| abstract_inverted_index.Secreted | 0 |
| abstract_inverted_index.activity | 15, 155 |
| abstract_inverted_index.analysis | 123 |
| abstract_inverted_index.critical | 66 |
| abstract_inverted_index.facility | 98 |
| abstract_inverted_index.focusing | 124 |
| abstract_inverted_index.liberate | 7 |
| abstract_inverted_index.produces | 146 |
| abstract_inverted_index.protein, | 144 |
| abstract_inverted_index.revealed | 99, 129 |
| abstract_inverted_index.singular | 143 |
| abstract_inverted_index.systemic | 147 |
| abstract_inverted_index.unclear. | 30 |
| abstract_inverted_index.bacterial | 35 |
| abstract_inverted_index.contrast, | 120 |
| abstract_inverted_index.induction | 69 |
| abstract_inverted_index.lipidome. | 137, 161 |
| abstract_inverted_index.lipidomic | 122 |
| abstract_inverted_index.mediators | 28, 128 |
| abstract_inverted_index.microbial | 51 |
| abstract_inverted_index.phenotype | 73 |
| abstract_inverted_index.promotion | 75 |
| abstract_inverted_index.sPLA2-IIA | 32, 41, 82, 131 |
| abstract_inverted_index.stringent | 96 |
| abstract_inverted_index.arthritis. | 78 |
| abstract_inverted_index.eukaryotic | 17 |
| abstract_inverted_index.expression | 80, 102 |
| abstract_inverted_index.generation | 24 |
| abstract_inverted_index.hydrolyzes | 4, 34 |
| abstract_inverted_index.intestinal | 50, 63, 88 |
| abstract_inverted_index.membranes, | 19 |
| abstract_inverted_index.membranes. | 36 |
| abstract_inverted_index.microbiota | 64, 89, 158 |
| abstract_inverted_index.profoundly | 133 |
| abstract_inverted_index.sPLA2-IIA, | 58, 145 |
| abstract_inverted_index.untargeted | 121 |
| abstract_inverted_index.(sPLA2-IIA) | 3 |
| abstract_inverted_index.Conversely, | 31 |
| abstract_inverted_index.alterations | 85 |
| abstract_inverted_index.composition | 115 |
| abstract_inverted_index.efficiently | 33 |
| abstract_inverted_index.composition, | 90 |
| abstract_inverted_index.inflammatory | 77 |
| abstract_inverted_index.pathogen-free | 97 |
| abstract_inverted_index.phospholipase | 1 |
| abstract_inverted_index.phospholipids | 5 |
| abstract_inverted_index.overexpressing | 55 |
| abstract_inverted_index.proinflammatory | 26 |
| abstract_inverted_index.bacteria-derived | 126 |
| abstract_inverted_index.transgene-driven | 56 |
| abstract_inverted_index.lysophospholipids | 8 |
| cited_by_percentile_year.max | 100 |
| cited_by_percentile_year.min | 99 |
| corresponding_author_ids | https://openalex.org/A5042606678 |
| countries_distinct_count | 4 |
| institutions_distinct_count | 22 |
| corresponding_institution_ids | https://openalex.org/I43406934 |
| citation_normalized_percentile.value | 0.95856769 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |