Altered inactivation of commensal LPS due to acyloxyacyl hydrolase deficiency in colonic dendritic cells impairs mucosal Th17 immunity

Janelsins, Brian M.; Lu, Mingfang; Datta, Sandip K.

doi:10.1073/pnas.1311987111

Cited by 56T-cell and B-cell ImmunologyPsoriasis: Treatment and PathogenesisImmunotherapy and Immune Responses

Altered inactivation of commensal LPS due to acyloxyacyl hydrolase deficiency in colonic dendritic cells impairs mucosal Th17 immunity

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Janelsins, Brian M., Lu, Mingfang, Datta, Sandip K.·2014·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.1311987111PMC PMC3890863

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Abstract

Significance: Th17 cells are a subset of T cells that secrete the cytokine IL-17 and play a role in mucosal immunity. LPS is a bacterial product that can influence the development of Th17 responses. We find that acyloxyacyl hydrolase (AOAH), a mammalian enzyme that inactivates LPS, is uniquely expressed in a subset of colonic dendritic cells and acts to maintain dendritic cell responsiveness to LPS expressed by commensal bacteria. This dendritic cell responsiveness is required to promote Th17 responses. These data identify the ability of AOAH to modulate microbial signals that influence mucosal T cell immunity, and suggest that host pathways to handle microbial products may be targeted to modulate Th17 responses in the context of inflammation or infection at mucosal surfaces.

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LPS in the human intestine is generally considered harmless because commensal Gram-negative microbiota routinely produce it, but it is at least partially inactivated by mammalian cell-derived acyloxyacyl hydrolase in vivo.
“The level of LPS found in the human intestine is generally considered harmless because the commensal Gram-negative gut microbiota routinely produce it, but it is at least partially inactivated by mammalian cell-derived acyloxyacyl hydrolase in vivo (37).”
From Contributions of microbiome and mechanical deformation to intestinal bacterial overgrowth and inflammation in a human gut-on-a-chip (2016) · cites this paper as [37]
The Abstract says mammalian-cell AOAH inactivates LPS in host tissues and identifies Gram-negative intestinal microbiota as an LPS source. The Discussion describes the gut findings as murine; it does not say that LPS levels in the human intestine are generally harmless or explain harmlessness by routine commensal production. The indexed passages do not specify page numbers. (LLM, conf=0.87)
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AOAH encodes acyloxycyl hydrolase, which is an enzyme expressed in antigen-presenting cells that deacylates and inactivates endotoxin.
“AOAH encodes acyloxycyl hydrolase, which is an enzyme expressed in antigen-presenting cells that deacylates and inactivates endotoxin.61”
From APOE*E2 allele delays age of onset in PSEN1 E280A Alzheimer’s disease (2016) · cites this paper as [61]

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Authors: Janelsins, B. M., Lu, M., & Datta, S. K.
Affiliations: National Institutes of Health (US)
Bacterial Pathogenesis Unit and
ORCID: Lu, Mingfang
Datta, Sandip K.
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2013-12-16
Volume: 111
Issue: 1
Pages: 373-378
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.1311987111
PMC: PMC3890863
OpenAlex: W2105139638
Cited by: 56
References: 48
Citations by year: 2026: 2 · 2025: 6 · 2024: 6 · 2023: 4 · 2022: 2 · 2021: 3 · 2020: 5 · 2019: 4 · 2018: 5 · 2017: 5 · 2016: 3 · 2015: 8 · 2014: 2 · 2013: 1
FWCI: 2.58
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
Topics: Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
Keywords: acyloxyacyl hydrolase, Th17 cell differentiation, mucosal immunity, interleukin-6, regulatory T cells, gut microbiota, Gram-negative bacteria, autoimmunity
MeSH terms: Animals, Antigen-Presenting Cells, Bone Marrow Cells, Carboxylic Ester Hydrolases, Colon, Dendritic Cells, Endotoxins, Female, Flow Cytometry, Inflammation, Intestinal Mucosa, Lipopolysaccharides, Lung, Male, Mice, Inbred C57BL, Phenotype, Recombinant Proteins, T-Lymphocytes, CD4-Positive T-Lymphocytes, Antigens, CD, Interleukin-6, Mice, Knockout, Integrin alpha Chains, CD11b Antigen, Toll-Like Receptors, Mice, Th17 Cells

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Altered inactivation of commensal LPS due to acyloxyacyl hydrolase deficiency in colonic dendritic cells impairs mucosal Th17 immunity

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