World journal of surgery
October 18, 2026 · via Europe PMC
Thyroid Nodule Colloid Is Associated With a Pro-Inflammatory Response in THP-1-Derived Macrophages: An Exploratory In Vitro Study.
Rai MK, Jagannath S, Sabaretnam M, Chand G, Mishra A, Misra DP, Agarwal V, Agarwal G.
AI summary — for doctors, generated from the abstract only
Fluid from benign thyroid nodules triggered a pro-inflammatory M1-type response in cultured macrophages in vitro, but causality and specificity are unproven.
What was studied
Exploratory in vitro study exposing THP-1-derived macrophages to colloid from 10 benign nodules, matched patient serum, or healthy donor serum, measuring gene expression by qPCR and cytokines by ELISA.
Key findings
- Colloid upregulated M1 markers IL12B, IL23A, NOS2 and CD80 versus serum controls
- M2-associated genes IL10, CD163 and CD68 were reduced
- Colloid-exposed macrophages secreted more IL-1 beta, IL-6 and IL-17; IL-10 was unchanged
Clinical relevance
Suggests the nodule microenvironment may contribute to local inflammation, a hypothesis-generating finding with no direct clinical application yet.
Who should care
Limitations
Small sample (n = 10), a cell line model, and no non-nodular thyroid colloid comparator, so specificity and in vivo relevance cannot be established.
No change in practice; treat this as preliminary mechanistic data.
This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.
Abstract
Background
Benign thyroid nodules are common, but the contribution of the intranodular microenvironment to local inflammation remains incompletely understood. Thyroid colloid has traditionally been regarded primarily as a reservoir for thyroid hormone precursors, although it may also contain inflammatory mediators. We therefore explored the response of THP-1-derived macrophages to colloid obtained from benign thyroid nodules and compared this response with exposure to matched patient serum and healthy donor serum.
Methods
Thyroid colloid and serum samples (n = 10) were collected from patients undergoing hemithyroidectomy for benign nodules. Additionally, serum samples from age- and sex-matched healthy controls (n = 10) were obtained. They were centrifuged at 1500 rpm for 10 minutes and stored at -80°C. THP-1 monocytes were differentiated into macrophages using phorbol-12-myristate-13-acetate (PMA) and exposed to thyroid colloid, matched patient serum, or healthy donor serum. Expression of M1-associated (IL12 B, IL23 A, NOS2, and CD80) and M2-associated (ARG1, CD206, CD163, CD68, and IL10) genes was quantified by quantitative real-time PCR. Cytokine secretion was determined using an enzyme-linked immunosorbent assay.
Results
THP-1-derived macrophages exposed to thyroid nodule colloid showed significant upregulation of M1-associated markers, including IL12 B, IL23 A, NOS2, and CD80, compared with macrophages exposed to patient serum or healthy donor serum. Expression of several M2-associated genes, including IL10, CD163, and CD68, was reduced following colloid exposure. Colloid-exposed macrophages also showed higher secretion of IL-1β, IL-6, and IL-17, whereas IL-10 levels remained unchanged. These findings indicate a pro-inflammatory M1-associated transcriptional and secretory response to thyroid nodule colloid under the present in vitro conditions.
Conclusions
Exposure to benign thyroid nodule colloid was associated with a pro-inflammatory M1-associated response in THP-1-derived macrophages in vitro. Because non-nodular thyroid colloid was not available as a biologically matched comparator, these findings cannot establish that this response is specific to nodule-derived colloid or that colloid is a causal driver of inflammation in vivo. Studies using non-nodular thyroid comparators and primary patient-derived macrophages are required to validate the specificity and biological relevance of this observation.
Trial registry registration no
8638 dated January 22, 2023.
DOI
10.1002/wjs.70635
PMID
42894427
Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.
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