scholarly journals Short‐chain fatty acids modulate cytokine‐induced inflammation in human oral epithelial cells

2019 ◽  
Vol 30 (S19) ◽  
pp. 6-7
Author(s):  
Gabriel Magrin ◽  
Rami Rasho ◽  
Anna Somweber ◽  
Cesar Benfatti ◽  
Reinhard Gruber
2020 ◽  
Vol 21 (14) ◽  
pp. 4895
Author(s):  
Gabriel Leonardo Magrin ◽  
Franz Josef Strauss ◽  
Cesar Augusto Magalhães Benfatti ◽  
Lucianne Cople Maia ◽  
Reinhard Gruber

Short-chain fatty acids (SCFA), bacterial metabolites released from dental biofilm, are supposed to target the oral epithelium. There is, however, no consensus on how SCFA affect the oral epithelial cells. The objective of the present study was to systematically review the available in vitro evidence of the impact of SCFA on human oral epithelial cells in the context of periodontal disease. A comprehensive electronic search using five databases along with a grey literature search was performed. In vitro studies that evaluated the effects of SCFA on human oral epithelial cells were eligible for inclusion. Risk of bias was assessed by the University of Bristol’s tool for assessing risk of bias in cell culture studies. Certainty in cumulative evidence was evaluated using GRADE criteria (grading of recommendations assessment, development, and evaluation). Of 3591 records identified, 10 were eligible for inclusion. A meta-analysis was not possible due to the heterogeneity between the studies. The risk of bias across the studies was considered “serious” due to the presence of methodological biases. Despite these limitations, this review showed that SCFA negatively affect the viability of oral epithelial cells by activating a series of cellular events that includes apoptosis, autophagy, and pyroptosis. SCFA impair the integrity and presumably the transmigration of leucocytes through the epithelial layer by changing junctional and adhesion protein expression, respectively. SCFA also affect the expression of chemokines and cytokines in oral epithelial cells. Future research needs to identify the underlying signaling cascades and to translate the in vitro findings into preclinical models.


2021 ◽  
Author(s):  
Mihaela Anca Serbanescu

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is a gastrointestinal pathogen which causes hemorrhagic colitis and can lead to neurological damage, acute kidney failure (hemolytic uremic syndrome and vascular lesions. During intestinal colonization EHEC is exposed to a variety of stresses including bile salts (BS) in the small intestine and short chain fatty acids (SCFA) in the large intestine; little is known about how these stresses affect this pathogen's virulence properties. The goal of this study was to investigate the impact of exposure of E. coli O157:H7 to physiologically relevant concentrations of BS and SCFA alone and in mixtures on bacterial survival, verotoxin production and adhesion to human epithelial cells. The results indicated that BS treatments significantly enhanced several virulence properties including survival and adhesion to human epthelial cell lines including colonic epithelial cells. Verotoxin production was not affected by any of the BS treatments. Bacterial pretreatment with erythromycin at a sub-minimal inhibitory concentration eliminated the adhesion enhancement after BS treatment, suggesting that protein synthesis was required for enhanced adhesion of BS treated organisms. Using the isogenci mutant of the known adhesions, intimin and iha it was established that there was no role for intimin or iha in the BS-induced adhesion enhancement. SCFA treatments reduced bacterial viability but significantly enhanced both adhesion to human epithelial cells and verotoxin production. The results of this research indicate that ingestion stresses such as BS and SCFA, which are part of the host's natural chemical assault on foreign organisms, may actually enhance the viulence properties of this pathogen and contribute to, rather than, prevent infection. Furthermore, they suggest that this pathogen may use these ingestion stresses to cue the expression of numerous virulence factors for successful infection of local microenvironments.


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