IL-1ß is a key inflammatory cytokine that weakens lactation-specific tight junctions of mammary epithelial cells.
Exp Cell Res
; 409(2): 112938, 2021 12 15.
Article
en En
| MEDLINE
| ID: mdl-34800541
ABSTRACT
In lactating mammary glands, alveolar mammary epithelial cells (MECs) produce milk and form less-permeable tight junctions (TJs). However, alveolar TJs are weakened with a reduction in milk production in mammary glands due to mastitis or weaning in the presence of high levels of IL-1ß, IL-6, or TNF-α. In this study, using in vitro cultured model of MECs with milk-producing ability and lactation-specific TJs, we investigated whether the aforementioned cytokines affect MEC TJs. The results showed that TNF-α, IL-1ß, and IL-6 affected lactation-specific TJs in different ways. In particular, upon activation of p38 and JNK signalling, IL-1ß caused rapid disruption of TJs at tricellular contact points. IL-1ß treatment led to decreased CLDN3, CLDN4, and OCLN levels and a weakened TJ barrier. The adverse effects of IL-1ß on TJs were mimicked by anisomycin, which is an activator of p38 and JNK signalling, and were blocked by MEC pretreatment with a p38 inhibitor but not a JNK inhibitor. The mislocalization of tricellulin at tricellular contact areas was confirmed in MECs treated with IL-1ß or anisomycin. These results indicate that IL-1ß is a key cytokine that adversely affects the TJs between MECs by activating p38.
Palabras clave
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Lactancia
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Uniones Estrechas
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Interleucina-1beta
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Claudina-3
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Claudina-4
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Glándulas Mamarias Animales
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Anisomicina
Idioma:
En
Revista:
Exp Cell Res
Año:
2021
Tipo del documento:
Article