Differential tissue-specific damage caused by bacterial epididymo-orchitis in the mouse.
Animals
Epididymis
/ immunology
Epididymitis
/ immunology
Escherichia coli Infections
/ immunology
GPI-Linked Proteins
/ metabolism
Gene Expression Profiling
Immunity
/ genetics
Male
Mice
Mice, Inbred C57BL
Orchitis
/ immunology
Testis
/ immunology
Urinary Tract Infections
/ immunology
Uropathogenic Escherichia coli
beta-Defensins
/ metabolism
LYPD8
beta-defensin
epididymis
epididymo-orchitis
spermatogenesis
testis
uropathogenic E. coli
Journal
Molecular human reproduction
ISSN: 1460-2407
Titre abrégé: Mol Hum Reprod
Pays: England
ID NLM: 9513710
Informations de publication
Date de publication:
24 04 2020
24 04 2020
Historique:
received:
30
07
2019
revised:
13
01
2020
accepted:
08
01
2020
pubmed:
6
2
2020
medline:
27
5
2021
entrez:
4
2
2020
Statut:
ppublish
Résumé
Ascending bacterial urinary tract infections can cause epididymo-orchitis. In the cauda epididymidis, this frequently leads to persistent tissue damage. Less coherent data is available concerning the functional consequences of epididymo-orchitis on testis and caput epididymidis. This in vivo study addresses the functional and spatial differences in responsiveness of murine epididymis and testis to infection with uropathogenic Escherichia coli (UPEC). Whole transcriptome analysis (WTA) was performed on testis, caput, corpus and cauda epididymidis of adult C57BL/6 J wildtype mice. Following UPEC-induced epididymo-orchitis in these mice, epididymal and testicular tissue damage was evaluated histologically and semi-quantitatively at 10 days and 31 days post-inoculation. Expression of inflammatory markers and candidate antimicrobial genes were analysed by RT-qPCR. WTA revealed distinct differences in gene signatures between caput and cauda epididymidis, particularly amonst immunity-related genes. Cellular and molecular signs of testicular inflammation and disruption of spermatogenesis were noticed at day 10, but recovery was observed by day 31. In contrast to the cauda, the caput epididymidis did not reveal any signs of gross morphological damage or presence of pro-inflammatory processes despite confirmed infection. In contrast to beta-defensins, known UPEC-associated antimicrobial peptides (AMP), like Lcn2, Camp and Lypd8, were inherently highly expressed or upregulated in the caput following infection, potentially allowing an early luminal protection from UPEC. At the time points investigated, the caput epididymidis was protected from any obvious infection/inflammation-derived tissue damage. Studies addressing earlier time-points will conclude whether in the caput epididymidis a pro-inflammatory response is indeed not essential for effective protection from UPEC.
Identifiants
pubmed: 32011693
pii: 5721557
doi: 10.1093/molehr/gaaa011
pmc: PMC7187874
doi:
Substances chimiques
GPI-Linked Proteins
0
Ly6-PLAUR domain containing 8 protein, mouse
0
beta-Defensins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
215-227Informations de copyright
© The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology.
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