COVID-19 disrupts the blood-testis barrier through the induction of inflammatory cytokines and disruption of junctional proteins.
Autopsy
Blood-Testis Barrier
/ pathology
COVID-19
/ pathology
Claudins
/ metabolism
Connexin 43
/ metabolism
Cytokines
/ metabolism
Humans
Immunohistochemistry
Interleukin-1beta
/ metabolism
Interleukin-6
/ metabolism
Lung
/ pathology
Male
Middle Aged
Occludin
/ metabolism
RNA, Viral
/ analysis
Sertoli Cells
/ pathology
Testis
/ pathology
Tumor Necrosis Factor-alpha
/ metabolism
Blood–testis barrier
COVID-19
Inflammatory cytokines
Journal
Inflammation research : official journal of the European Histamine Research Society ... [et al.]
ISSN: 1420-908X
Titre abrégé: Inflamm Res
Pays: Switzerland
ID NLM: 9508160
Informations de publication
Date de publication:
Dec 2021
Dec 2021
Historique:
received:
03
06
2021
accepted:
20
08
2021
revised:
18
08
2021
pubmed:
27
8
2021
medline:
12
11
2021
entrez:
26
8
2021
Statut:
ppublish
Résumé
Junctional proteins are the most important component of the blood-testis barrier and maintaining the integrity of this barrier is essential for spermatogenesis and male fertility. The present study elucidated the effect of SARS-CoV-2 infection on the blood-testis barrier (BTB) in patients who died from severe acute respiratory syndrome coronavirus 2 (COVID-19) complications. In this study, lung and testis tissue was collected from autopsies of COVID-19 positive (n = 10) and negative men (n = 10) and was taken for stereology, immunocytochemistry, and RNA extraction. Evaluation of the lung tissue showed that the SARS-CoV-2 infection caused extensive damage to the lung tissue and also increases inflammation in testicular tissue and destruction of the testicular blood barrier. Autopsied testicular specimens of COVID-19 showed that COVID-19 infection significantly changes the spatial arrangement of testicular cells and notably decreased the number of Sertoli cells. Moreover, the immunohistochemistry results showed a significant reduction in the protein expression of occluding, claudin-11, and connexin-43 in the COVID-19 group. In addition, we also observed a remarkable enhancement in protein expression of CD68 in the testes of the COVID-19 group in comparison with the control group. Furthermore, the result showed that the expression of TNF-α, IL1β, and IL6 was significantly increased in COVID-19 cases as well as the expression of occludin, claudin-11, and connexin-43 was decreased in COVID-19 cases. Overall, the present study demonstrated that SARS-CoV-2 could induce the up-regulation of the pro-inflammatory cytokine and down-regulation of junctional proteins of the BTB, which can disrupt BTB and ultimately impair spermatogenesis.
Identifiants
pubmed: 34436630
doi: 10.1007/s00011-021-01497-4
pii: 10.1007/s00011-021-01497-4
pmc: PMC8387554
doi:
Substances chimiques
CLDN11 protein, human
0
Claudins
0
Connexin 43
0
Cytokines
0
GJA1 protein, human
0
IL1B protein, human
0
IL6 protein, human
0
Interleukin-1beta
0
Interleukin-6
0
Occludin
0
RNA, Viral
0
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1165-1175Subventions
Organisme : Shahid Beheshti University of Medical Sciences
ID : 1399. 26274
Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer Nature Switzerland AG.
Références
Philos Trans R Soc Lond B Biol Sci. 2010 May 27;365(1546):1607-20
pubmed: 20403873
Biol Reprod. 2012 Nov 29;87(5):122
pubmed: 23018187
Andrologia. 2020 Oct;52(9):e13712
pubmed: 32578263
Cells. 2020 Apr 09;9(4):
pubmed: 32283711
Proc Natl Acad Sci U S A. 2010 Oct 19;107(42):17998-8003
pubmed: 20921394
Theranostics. 2020 Jun 12;10(16):7448-7464
pubmed: 32642005
Urology. 2020 Aug;142:42
pubmed: 32343996
J Med Virol. 2021 Jan;93(1):250-256
pubmed: 32592501
Sci Rep. 2014 Mar 03;4:4260
pubmed: 24584780
Asian J Urol. 2021 Jul;8(3):324-326
pubmed: 32837913
Crit Rev Clin Lab Sci. 2020 Sep;57(6):365-388
pubmed: 32645276
Philos Trans R Soc Lond B Biol Sci. 2010 May 27;365(1546):1621-35
pubmed: 20403874
Microorganisms. 2020 Sep 28;8(10):
pubmed: 32998451
J Microsc. 2010 Jul 1;239(1):54-65
pubmed: 20579269
Am J Pathol. 2013 Dec;183(6):1871-1884
pubmed: 24121020
Front Immunol. 2020 Jun 16;11:1446
pubmed: 32612617
Philos Trans R Soc Lond B Biol Sci. 2010 May 27;365(1546):1593-605
pubmed: 20403872
J Reprod Immunol. 2020 Nov;142:103213
pubmed: 33080435
Mediators Inflamm. 2019 Feb 21;2019:2401081
pubmed: 30918468
Horm Metab Res. 2020 May;52(5):257-263
pubmed: 32340044
Andrologia. 2020 Jul;52(6):e13654
pubmed: 32436229
World J Urol. 2021 Mar;39(3):975-976
pubmed: 32318855
Curr Top Dev Biol. 2005;71:263-96
pubmed: 16344108
Endocrinology. 2000 Aug;141(8):3012-9
pubmed: 10919290
Trends Endocrinol Metab. 2005 Sep;16(7):300-6
pubmed: 16054834
J Infect. 2020 Jun;80(6):607-613
pubmed: 32283152
Acta Biomed. 2020 Mar 19;91(1):157-160
pubmed: 32191675
EClinicalMedicine. 2020 Nov;28:100604
pubmed: 33134901
Int J Infect Dis. 2020 Jul;96:467-474
pubmed: 32425643
J Basic Clin Physiol Pharmacol. 2020 Oct 5;31(6):
pubmed: 33006953
Endocr Rev. 2015 Oct;36(5):564-91
pubmed: 26357922
Am J Physiol Endocrinol Metab. 2020 Jun 1;318(6):E878-E880
pubmed: 32421367
Chem Immunol Allergy. 2005;88:1-14
pubmed: 16129933
J Endocrinol. 2006 Aug;190(2):313-29
pubmed: 16899565