Abstract
We investigated cell cycle progression in epithelial cervical ME-180 cells during colonization of three different Lactobacillus species utilizing live cell microscopy, bromodeoxyuridine incorporation assays, and flow cytometry. The colonization of these ME-180 cells by L. rhamnosus and L. reuteri, originating from human gastric epithelia and saliva, respectively, was shown to reduce cell cycle progression and to cause host cells to accumulate in the G1 phase of the cell cycle. The G1 phase accumulation in L. rhamnosus-colonized cells was accompanied by the up-regulation and nuclear accumulation of p21. By contrast, the vaginal isolate L. crispatus did not affect cell cycle progression. Furthermore, both the supernatants from the lactic acid-producing L. rhamnosus colonies and lactic acid added to cell culture media were able to reduce the proliferation of ME-180 cells. In this study, we reveal the diversity of the Lactobacillus species to affect host cell cycle progression and demonstrate that L. rhamnosus and L. reuteri exert anti-proliferative effects on human cervical carcinoma cells.
Highlights
Non-keratinizing cervical epithelial cells of the human body are a well-functioning barricade against the outer surroundings, protecting the human body against harmful external agents and damage
55% of the ME-180 cells that were colonized by L. crispatus had completed cytokinesis after 16 hours; these cells did not differ from untreated ME-180 cells with respect to cell cycle progression
Time points of Lactobacillus colonization that were longer than 16 hours were not feasible, because the dense layer of bacteria that covered the epithelial cells at colonization durations that were longer than 16 hours produced an impaired ability to visually monitor all of the cytokinesis events
Summary
Non-keratinizing cervical epithelial cells of the human body are a well-functioning barricade against the outer surroundings, protecting the human body against harmful external agents and damage. To maintain the fidelity of this barrier, epithelial cells are renewed by cell division. The cell cycle is divided into four phases, gap 1 (G1), synthesis (S), gap 2 (G2) and mitosis (M), and the epithelium consists of cells continuously progressing through the four different cell cycle phases [1]. Cell cycle progression is driven by cyclin-dependent kinases (CDKs) and cyclins. The regulation of CDK-cyclin complex activity occurs through cyclin-dependent kinase inhibitors (CKIs), such as p21, at checkpoints that can halt cell cycle progression [2]. Cells may cease active growth permanently or temporarily due to various influences, including contact inhibition and high cellular confluence; under these conditions, non-transformed cells enter a state of quiescence known as G0
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