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Strongyloides stercoralis infection reduces bacteria producing short-chain fatty acids and increases bacterial amino-acid biosynthesis in early CKD patients

ABSTRACT: Controlling the progression of chronic kidney disease (CKD) at an early stage is critical for reducing disease severity. A cross-sectional study of chronic kidney disease (CKD) patients at all stages with S. stercoralis infection found that helminth infection caused gut dysbiosis, which may be involved in CKD progression. Because of the variation of gut microbiome results with helminth infection, the cross-sectional study of 16S rRNA sequencing, therefore, is insufficient to draw valid conclusions and correct the effects of S. stercoralis on the early stages of CKD. Combination with other omics approach is warrant to be better understand the disease.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Sittiruk Roytrakul

PROVIDER: PXD039656 | JPOST Repository | Wed Jan 24 00:00:00 GMT 2024

REPOSITORIES: jPOST

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			Action	DRS
	CN01_BE3_01_31130.mzXML	Mzxml
	CN01_BE3_01_31131.mzXML	Mzxml
	CN01_BE3_01_31132.mzXML	Mzxml
	CN02_BE4_01_31133.mzXML	Mzxml
	CN02_BE4_01_31134.mzXML	Mzxml

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Project description:Background: Short-chain fatty acids (SCFAs), mainly acetate, propionate and butyrate, are produced by gut microbiota through fermentation of complex carbohydrates that cannot be digested by the human host. They affect gut health and can contribute at the distal level to the pathophysiology of several diseases, including renal pathologies. Methods: SCFA levels were measured in chronic kidney disease (CKD) patients (n = 54) at different stages of the disease and associations with renal function and inflammation parameters were examined. The impact of propionate and butyrate in pathways triggered in tubular cells under inflammatory conditions was analysed using genome-wide expression assays. Finally, a pre-clinical mouse model of folic acid-induced transition from acute kidney injury to CKD was used to analyse the preventive and therapeutic potential of these microbial metabolites in the development of CKD. Results: Faecal levels of propionate and butyrate in CKD patients gradually reduce as the disease progresses, and do so in close association with established clinical parameters for serum creatinine, blood urea nitrogen and the estimated glomerular filtration rate. Propionate and butyrate jointly downregulated the expression of 103 genes related to inflammatory processes and immune system activation triggered by TNF-α in tubular cells. In vivo, the administration of propionate and butyrate, either before or soon after injury, respectively prevented and slowed the progression of damage. This was indicated by a decrease in renal injury markers, the expression of pro-inflammatory and pro-fibrotic markers, and recovery of renal function over the long term. Conclusions: Propionate and butyrate levels are associated with a progressive loss of renal function in CKD patients. Early administration of these SCFAs prevents disease advancement in a pre-clinical model of acute renal damage, demonstrating their therapeutic potential independently of the gut microbiota.

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Strongyloides stercoralis infection reduces bacteria producing short-chain fatty acids and increases bacterial amino-acid biosynthesis in early CKD patients

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