Cargando…

Bone Status in a Mouse Model of Experimental Autoimmune-Orchitis

Investigations in male patients with fertility disorders revealed a greater risk of osteoporosis. The rodent model of experimental autoimmune-orchitis (EAO) was established to analyze the underlying mechanisms of male infertility and causes of reduced testosterone concentration. Hence, we investigat...

Descripción completa

Detalles Bibliográficos
Autores principales: Hemm, Fabian, Fijak, Monika, Belikan, Jan, Kampschulte, Marian, El Khassawna, Thaqif, Pilatz, Adrian, Heiss, Christian, Lips, Katrin Susanne
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8346031/
https://www.ncbi.nlm.nih.gov/pubmed/34360623
http://dx.doi.org/10.3390/ijms22157858
_version_ 1783734771750273024
author Hemm, Fabian
Fijak, Monika
Belikan, Jan
Kampschulte, Marian
El Khassawna, Thaqif
Pilatz, Adrian
Heiss, Christian
Lips, Katrin Susanne
author_facet Hemm, Fabian
Fijak, Monika
Belikan, Jan
Kampschulte, Marian
El Khassawna, Thaqif
Pilatz, Adrian
Heiss, Christian
Lips, Katrin Susanne
author_sort Hemm, Fabian
collection PubMed
description Investigations in male patients with fertility disorders revealed a greater risk of osteoporosis. The rodent model of experimental autoimmune-orchitis (EAO) was established to analyze the underlying mechanisms of male infertility and causes of reduced testosterone concentration. Hence, we investigated the impact of testicular dysfunction in EAO on bone status. Male mice were immunized with testicular homogenate in adjuvant to induce EAO (n = 5). Age-matched mice were treated with adjuvant alone (adjuvant, n = 6) or remained untreated (control, n = 7). Fifty days after the first immunization specimens were harvested. Real-time reverse transcription-PCR indicated decreased bone metabolism by alkaline phosphatase and Cathepsin K as well as remodeling of cell-contacts by Connexin-43. Micro computed tomography demonstrated a loss of bone mass and mineralization. These findings were supported by histomorphometric results. Additionally, biomechanical properties of femora in a three-point bending test were significantly altered. In summary, the present study illustrates the induction of osteoporosis in the investigated mouse model. However, results suggest that the major effects on bone status were mainly caused by the complete Freund’s adjuvant rather than the autoimmune-orchitis itself. Therefore, the benefit of the EAO model to transfer laboratory findings regarding bone metabolism in context with orchitis into a clinical application is limited.
format Online
Article
Text
id pubmed-8346031
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-83460312021-08-07 Bone Status in a Mouse Model of Experimental Autoimmune-Orchitis Hemm, Fabian Fijak, Monika Belikan, Jan Kampschulte, Marian El Khassawna, Thaqif Pilatz, Adrian Heiss, Christian Lips, Katrin Susanne Int J Mol Sci Article Investigations in male patients with fertility disorders revealed a greater risk of osteoporosis. The rodent model of experimental autoimmune-orchitis (EAO) was established to analyze the underlying mechanisms of male infertility and causes of reduced testosterone concentration. Hence, we investigated the impact of testicular dysfunction in EAO on bone status. Male mice were immunized with testicular homogenate in adjuvant to induce EAO (n = 5). Age-matched mice were treated with adjuvant alone (adjuvant, n = 6) or remained untreated (control, n = 7). Fifty days after the first immunization specimens were harvested. Real-time reverse transcription-PCR indicated decreased bone metabolism by alkaline phosphatase and Cathepsin K as well as remodeling of cell-contacts by Connexin-43. Micro computed tomography demonstrated a loss of bone mass and mineralization. These findings were supported by histomorphometric results. Additionally, biomechanical properties of femora in a three-point bending test were significantly altered. In summary, the present study illustrates the induction of osteoporosis in the investigated mouse model. However, results suggest that the major effects on bone status were mainly caused by the complete Freund’s adjuvant rather than the autoimmune-orchitis itself. Therefore, the benefit of the EAO model to transfer laboratory findings regarding bone metabolism in context with orchitis into a clinical application is limited. MDPI 2021-07-23 /pmc/articles/PMC8346031/ /pubmed/34360623 http://dx.doi.org/10.3390/ijms22157858 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Hemm, Fabian
Fijak, Monika
Belikan, Jan
Kampschulte, Marian
El Khassawna, Thaqif
Pilatz, Adrian
Heiss, Christian
Lips, Katrin Susanne
Bone Status in a Mouse Model of Experimental Autoimmune-Orchitis
title Bone Status in a Mouse Model of Experimental Autoimmune-Orchitis
title_full Bone Status in a Mouse Model of Experimental Autoimmune-Orchitis
title_fullStr Bone Status in a Mouse Model of Experimental Autoimmune-Orchitis
title_full_unstemmed Bone Status in a Mouse Model of Experimental Autoimmune-Orchitis
title_short Bone Status in a Mouse Model of Experimental Autoimmune-Orchitis
title_sort bone status in a mouse model of experimental autoimmune-orchitis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8346031/
https://www.ncbi.nlm.nih.gov/pubmed/34360623
http://dx.doi.org/10.3390/ijms22157858
work_keys_str_mv AT hemmfabian bonestatusinamousemodelofexperimentalautoimmuneorchitis
AT fijakmonika bonestatusinamousemodelofexperimentalautoimmuneorchitis
AT belikanjan bonestatusinamousemodelofexperimentalautoimmuneorchitis
AT kampschultemarian bonestatusinamousemodelofexperimentalautoimmuneorchitis
AT elkhassawnathaqif bonestatusinamousemodelofexperimentalautoimmuneorchitis
AT pilatzadrian bonestatusinamousemodelofexperimentalautoimmuneorchitis
AT heisschristian bonestatusinamousemodelofexperimentalautoimmuneorchitis
AT lipskatrinsusanne bonestatusinamousemodelofexperimentalautoimmuneorchitis