Increased expression of PRRs and NOS in patients with endometriosis (P3143)

In: The Journal of Immunology · 2013 · vol. 190(Supplement_1) , pp. 43.33 · doi:10.4049/jimmunol.190.supp.43.33 · W4313355099
article OA: closed CC0
View on OpenAlex View at publisher

Abstract

Abstract Objective: To assess these immune responses, we evaluated the levels of expression of Toll-like receptors (TLR)-1, -2, -4, -5, and -9; nucleotide-binding oligomerization domains (NOD)-1 and -2; interleukins-1β, -6, -8, -10, and -12; interferon-γ; tumor necrosis factor-α; inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS); and immunoglobulins (Igs) in patients with endometriosis. Methods: The levels of TLRs, NODs, cytokines, and NOS mRNAs in peritoneal effusion were assessed by real time polymerase chain reaction, and IgG, IgA and IgM concentrations were measured by enzyme-linked immunosorbent assays (ELISA) in 40 patients with and 40 without endometriosis. Findings from the two groups were compared. Results: We observed expression of all Pattern Recognition Receptors (PRRs), cytokines, and NOS mRNAs and immunoglobulins in the effusion fluid of patients with and without endometriosis. The levels of TLR-2 and -9; NOD-1 and -2; iNOS and eNOS mRNA and CA 125 were significantly higher in the endometriosis than in the non-endometriosis group (p<0.05 each). Moreover, PRRs, cytokine, and NOS showed significant correlations (p<0.05). Conclusions: PRRs, cytokines, and NOS, which act cooperatively in the innate immune response, are closely associated with endometriosis. Increased expression of PRRs and NOS in peritoneal fluid may be associated with endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosis

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
unpaywall
last seen: 2026-06-02T02:00:03.124865+00:00
License: CC0 · commercial use OK