High glucose represents a good environment for bacterial growth on the skin, on the ocular surface (OS) and in the tears of type 2 diabetes mellitus (T2DM) patients, affecting the conjunctival bacterial community. This study aimed to investigate the OS bacterial flora of T2DM patients and healthy subjects using 16S rRNA sequencing-based bacterial identification. Among 23 healthy subjects (CON) and 31 T2DM patients, 54 eyes were examined to investigate the OS bacterial community. Factors potentially affecting the microbial growth were controlled. Results showed the OS microbiota presented higher diversity in the T2DM group than in the CON group. Bioinformatic analysis showed a lower abundance of
Proteobacteria
and a higher abundance of
Bacteroidetes
at the phyla level as well as a significantly increased abundance of
Acinetobacter
and
Pseudomonas
at the genus level in the T2DM group. The difference in OS microbiota at taxonomic level was associated with Ocular Surface Disease Index and course of T2DM. These findings indicate the OS flora in T2DM patients is significantly different from that in healthy subjects, which may be closely associated with OS discomfort and course of T2DM.
The aim of the present study was to investigate the role of histatin 1 (Hst1) in human corneal epithelial cells (HCECs) exposed to ultraviolet (UV) radiation. Prior to UV irradiation for various durations, HCECs were pre-treated with different concentrations of Hst1 and the effect on cell apoptosis and cell viability were examined by flow cytometry, alamarBlue® and MTT assays to determine the optimal concentration of Hst1 and UV dose. Cells were then subjected to quantitative PCR, ELISA and western blot analysis to determine the expression of cell damage-associated genes. HCECs exposed to UV light for 1 h displayed decreased viability when compared to that of control cells, and a 3 h UV exposure markedly increased the apoptotic rate of HECEs, while apoptosis was inhibited by pre-treatment with Hst1. UV radiation downregulated expression of insulin-like growth factor (IGF)-1 and B-cell lymphoma 2 (Bcl-2), while it upregulated Bcl-2-associated X protein (Bax) expression. Hst1 protected HCECs against UV-induced damage by upregulating the expression of IGF-1 protein and increasing the Bcl-2/Bax ratio. In conclusion, Hst1 may prevent UV-induced damage to corneal epithelial tissue injury and promote its healing.
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