CGB - Universidad Mayor | English

04 April 2020

Aggregatibacter Actinomycetemcomitans Induces Autophagy in Human Junctional Epithelium Keratinocytes.

DOI : 10.3390/cells9051221


The adverse environmental conditions found in the periodontium during

periodontitis pathogenesis stimulate local autophagy responses, mainly due to a

continuous inflammatory response against the dysbiotic subgingival microbiome.

The junctional epithelium represents the main site of the initial interaction

between the host and the dysbiotic biofilm. Here, we investigated the role of

autophagy in junctional epithelium keratinocytes (JEKs) in response to

Aggregatibacter actinomycetemcomitans or its purified lipopolysaccharides (LPS).

Immunofluorescence confocal analysis revealed an extensive nuclear translocation

of transcription factor EB (TFEB) and consequently, an increase in autophagy

markers and LC3-turnover assessed by immunoblotting and qRT-PCR.

Correspondingly, challenged JEKs showed a punctuate cytosolic profile of LC3

protein contrasting with the diffuse distribution observed in untreated

controls. Three-dimensional reconstructions of confocal images displayed a close

association between intracellular bacteria and LC3-positive vesicles. Similarly,

a close association between autophagic vesicles and the protein p62 was observed

in challenged JEKs, indicating that p62 is the main adapter protein recruited

during A. actinomycetemcomitans infection. Finally, the pharmacological

inhibition of autophagy significantly increased the number of bacteria-infected

cells as well as their death, similar to treatment with LPS. Our results

indicate that A. actinomycetemcomitans infection induces autophagy in JEKs, and

this homeostatic process has a cytoprotective effect on the host cells during

the early stages of infection.

Participating Center Researchers



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