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Tyndallized bacteria prime bronchial epithelial cells to mount an effective innate immune response against infections

Serena Di Vincenzo; Caterina Di Sano; Claudia D’Anna; Maria Ferraro; Velia Malizia; Andreina Bruno; Marta Cristaldi; Chiara Cipollina; Valentina Lazzara; Paola Pinto; Stefania La Grutta; Elisabetta Pace
Human Cell · Vol. 37, Issue 4 · pp. 1080-1090 · 2024

Abstract

Airway epithelium represents a physical barrier against toxic substances and pathogens but also presents pattern recognition receptors on the epithelial cells that detect pathogens leading to molecule release and sending signals that activate both the innate and adaptive immune responses. Thus, impaired airway epithelial function and poor integrity may increase the recurrence of infections. Probiotic use in respiratory diseases as adjuvant of traditional therapy is increasingly widespread. There is growing interest in the use of non-viable heat-killed bacteria, such as tyndallized bacteria (TB), due to safety concerns and to their immunomodulatory properties. This study explores in vitro the effects of a TB blend on the immune activation of airway epithelium. 16HBE bronchial epithelial cells were exposed to different concentrations of TB. Cell viability, TB internalization, TLR2 expression, IL-6, IL-8 and TGF-βl expression/release, E-cadherin expression and wound healing were assessed. We found that TB were tolerated, internalized, increased TLR2, E-cadherin expression, IL-6 release and wound healing but decreased both IL-8 and TGF-βl release. In conclusion, TB activate TLR2 pathway without inducing a relevant pro-inflammatory response and improve barrier function, leading to the concept that TB preserve epithelial homeostasis and could be used as strategy to prevent and to manage respiratory infection, exacerbations included.

Bibliographic Information

JournalHuman Cell
PublisherSpringer
Publication Date2024-05-30
Publication Year2024
Volume37
Issue4
Pages1080-1090
Document TypeJournal Article
eISSN1749-0774
DOI10.1007/s13577-024-01080-z

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NARA Access Coverage2002-01-01~Current
Journal Homepagehttps://www.springer.com/journal/13577
Publisher PageOpen Publisher Page
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