# Gene Expression Profiles in the Optic Nerve of Mice with Systemic Acanthamoebiasis

**Authors:** Ignacy Marcin Wiliński, Patrycja Tomasiak, Michał Czerewaty, Natalia Łanocha-Arendarczyk, Danuta Kosik-Bogacka, Karolina Kot

PMC · DOI: 10.3390/ijms27052382 · 2026-03-04

## TL;DR

This study explores how Acanthamoeba infection affects gene activity in mice optic nerves, revealing immune response changes under different immune conditions.

## Contribution

The study identifies specific gene expression patterns in the optic nerve during Acanthamoeba infection under immunocompetent and immunosuppressed conditions.

## Key findings

- In immunocompetent mice, Ptgs2 and Ifng were upregulated early in infection.
- In immunosuppressed mice, multiple inflammatory genes showed increased expression compared to controls.
- Immunosuppression promotes prolonged inflammation in the optic nerve via altered immune responses.

## Abstract

Systemic infection with Acanthamoeba spp. can induce inflammatory responses within the visual axis, yet the underlying molecular mechanisms in the optic nerve remain poorly understood. The aim of the study was to determine the gene expression of Nlrp3 (encoding NOD-, LRP- and pyrin domain-containing protein 3, NLRP3), Ptgs2 (encoding cyclooxygenase-2, COX-2), Rela (encoding nuclear factor kappa B, NF-κB), and several cytokines in the optic nerve of mice during disseminated infection with Acanthamoeba sp. (T16 genotype) under various immunological conditions. In immunocompetent mice, Ptgs2 and Ifng expressions were upregulated at the beginning of infection. In the late stages, we found increased levels of Il10 and Nlrp3. In immunosuppressed mice, higher expressions of Nlrp3, Ptgs2, Rela, Il1b, Il10, Il17a, Il21, and Ifng were found in the infected mice compared to the control group. These results indicate that immunosuppression promotes prolonged inflammation by altering innate and adaptive immune responses, contributing to sustained neuroinflammatory processes affecting the optic nerve. This study provides mechanistic insight into host–pathogen interactions in the optic nerve during systemic Acanthamoeba infection. Due to the analysis being based on mRNA expression levels, direct inference regarding protein levels and the actual activity of the investigated immunological pathways is limited.

## Linked entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548], PTGS2 (prostaglandin-endoperoxide synthase 2) [NCBI Gene 5743], RELA (RELA proto-oncogene, NF-kB subunit) [NCBI Gene 5970], IFNG (interferon gamma) [NCBI Gene 3458], IL10 (interleukin 10) [NCBI Gene 3586], IL1B (interleukin 1 beta) [NCBI Gene 3553], IL17A (interleukin 17A) [NCBI Gene 3605], IL21 (interleukin 21) [NCBI Gene 59067]
- **Proteins:** IL10 (interleukin 10), IL21 (interleukin 21)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Nlrp3 (NLR family, pyrin domain containing 3) [NCBI Gene 216799] {aka AGTAVPRL, AII/AVP, Cias1, FCAS, FCU, MWS}, Il21 (interleukin 21) [NCBI Gene 60505] {aka IL-21}, COX2 (cytochrome c oxidase subunit II) [NCBI Gene 17709], Il10 (interleukin 10) [NCBI Gene 16153] {aka CSIF, If2a, Il-10}, Ifng (interferon gamma) [NCBI Gene 15978] {aka IFN-g, If2f, Ifg}, Il1b (interleukin 1 beta) [NCBI Gene 16176] {aka IL-1beta, Il-1b}, Ptgs2 (prostaglandin-endoperoxide synthase 2) [NCBI Gene 19225] {aka COX2, Cox-2, PES-2, PGHS-2, PHS II, PHS-2}, Rela (Rela proto-oncogene, NFKB subunit) [NCBI Gene 19697] {aka p65, p65 NF-kappa B, p65 NFkB}, Il17a (interleukin 17A) [NCBI Gene 16171] {aka Ctla-8, Ctla8, IL-17, IL-17A, Il17}, Nfkb1 (nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105) [NCBI Gene 18033] {aka NF-KB1, NF-kappaB, NF-kappaB1, p105, p50, p50/p105}
- **Diseases:** inflammation (MESH:D007249), infection (MESH:D007239), Acanthamoeba infection (MESH:D000562), neuroinflammatory (MESH:D000090862)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Acanthamoeba sp. (species) [taxon 5756]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12985907/full.md

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Source: https://tomesphere.com/paper/PMC12985907