Strongyloides stercoralis infection induces gut dysbiosis in chronic kidney disease patients.
Journal
PLoS neglected tropical diseases
ISSN: 1935-2735
Titre abrégé: PLoS Negl Trop Dis
Pays: United States
ID NLM: 101291488
Informations de publication
Date de publication:
09 2022
09 2022
Historique:
received:
07
03
2022
accepted:
09
08
2022
revised:
16
09
2022
pubmed:
7
9
2022
medline:
21
9
2022
entrez:
6
9
2022
Statut:
epublish
Résumé
Strongyloides stercoralis infection typically causes severe symptoms in immunocompromised patients. This infection can also alter the gut microbiota and is often found in areas where chronic kidney disease (CKD) is common. However, the relationship between S. stercoralis and the gut microbiome in chronic kidney disease (CKD) is not understood fully. Recent studies have shown that gut dysbiosis plays an important role in the progression of CKD. Hence, this study aims to investigate the association of S. stercoralis infection and gut microbiome in CKD patients. Among 838 volunteers from Khon Kaen Province, northeastern Thailand, 40 subjects with CKD were enrolled and divided into two groups (S. stercoralis-infected and -uninfected) matched for age, sex and biochemical parameters. Next-generation technology was used to amplify and sequence the V3-V4 region of the 16S rRNA gene to provide a profile of the gut microbiota. Results revealed that members of the S. stercoralis-infected group had lower gut microbial diversity than was seen in the uninfected group. Interestingly, there was significantly greater representation of some pathogenic bacteria in the S. stercoralis-infected CKD group, including Escherichia-Shigella (P = 0.013), Rothia (P = 0.013) and Aggregatibacter (P = 0.03). There was also a trend towards increased Actinomyces, Streptococcus and Haemophilus (P > 0.05) in this group. On the other hand, the S. stercoralis-infected CKD group had significantly lower representation of SCFA-producing bacteria such as Anaerostipes (P = 0.01), Coprococcus_1 (0.043) and a non-significant decrease of Akkermansia, Eubacterium rectale and Eubacterium hallii (P > 0.05) relative to the uninfected group. Interesting, the genera Escherichia-Shigella and Anaerostipes exhibited opposing trends, which were significantly related to sex, age, infection status and CKD stages. The genus Escherichia-Shigella was significantly more abundant in CKD patients over the age of 65 years and infected with S. stercoralis. A correlation analysis showed inverse moderate correlation between the abundance of the genus of Escherichia-Shigella and the level of estimated glomerular filtration rate (eGFR). Conclusion, the results suggest that S. stercoralis infection induced gut dysbiosis in the CKD patients, which might be involved in CKD progression.
Sections du résumé
BACKGROUND
Strongyloides stercoralis infection typically causes severe symptoms in immunocompromised patients. This infection can also alter the gut microbiota and is often found in areas where chronic kidney disease (CKD) is common. However, the relationship between S. stercoralis and the gut microbiome in chronic kidney disease (CKD) is not understood fully. Recent studies have shown that gut dysbiosis plays an important role in the progression of CKD. Hence, this study aims to investigate the association of S. stercoralis infection and gut microbiome in CKD patients.
METHODOLOGY/PRINCIPAL FINDINGS
Among 838 volunteers from Khon Kaen Province, northeastern Thailand, 40 subjects with CKD were enrolled and divided into two groups (S. stercoralis-infected and -uninfected) matched for age, sex and biochemical parameters. Next-generation technology was used to amplify and sequence the V3-V4 region of the 16S rRNA gene to provide a profile of the gut microbiota. Results revealed that members of the S. stercoralis-infected group had lower gut microbial diversity than was seen in the uninfected group. Interestingly, there was significantly greater representation of some pathogenic bacteria in the S. stercoralis-infected CKD group, including Escherichia-Shigella (P = 0.013), Rothia (P = 0.013) and Aggregatibacter (P = 0.03). There was also a trend towards increased Actinomyces, Streptococcus and Haemophilus (P > 0.05) in this group. On the other hand, the S. stercoralis-infected CKD group had significantly lower representation of SCFA-producing bacteria such as Anaerostipes (P = 0.01), Coprococcus_1 (0.043) and a non-significant decrease of Akkermansia, Eubacterium rectale and Eubacterium hallii (P > 0.05) relative to the uninfected group. Interesting, the genera Escherichia-Shigella and Anaerostipes exhibited opposing trends, which were significantly related to sex, age, infection status and CKD stages. The genus Escherichia-Shigella was significantly more abundant in CKD patients over the age of 65 years and infected with S. stercoralis. A correlation analysis showed inverse moderate correlation between the abundance of the genus of Escherichia-Shigella and the level of estimated glomerular filtration rate (eGFR).
CONCLUSIONS/SIGNIFICANCE
Conclusion, the results suggest that S. stercoralis infection induced gut dysbiosis in the CKD patients, which might be involved in CKD progression.
Identifiants
pubmed: 36067216
doi: 10.1371/journal.pntd.0010302
pii: PNTD-D-22-00290
pmc: PMC9481163
doi:
Substances chimiques
RNA, Ribosomal, 16S
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0010302Déclaration de conflit d'intérêts
The authors have declared that no competing interest exist.
Références
PLoS One. 2014 Jun 12;9(6):e99006
pubmed: 24922509
Front Microbiol. 2018 May 14;9:843
pubmed: 29867790
Int J Mol Sci. 2020 Mar 14;21(6):
pubmed: 32183306
JAMA. 2007 Nov 7;298(17):2038-47
pubmed: 17986697
Am J Kidney Dis. 2014 May;63(5):713-35
pubmed: 24647050
Infect Dis Clin North Am. 2019 Mar;33(1):135-151
pubmed: 30712758
Nephron. 1996;74(2):349-55
pubmed: 8893154
Sci Rep. 2018 Oct 23;8(1):15651
pubmed: 30353019
Genome Announc. 2015 Apr 02;3(2):
pubmed: 25838483
PLoS One. 2010 Mar 24;5(3):e9836
pubmed: 20352091
Genome Res. 2011 Mar;21(3):494-504
pubmed: 21212162
J Clin Microbiol. 2014 Sep;52(9):3184-9
pubmed: 24951810
Nat Methods. 2013 Oct;10(10):996-8
pubmed: 23955772
Appl Environ Microbiol. 2006 Jul;72(7):5069-72
pubmed: 16820507
Transl Res. 2017 Jan;179:24-37
pubmed: 27187743
Appl Environ Microbiol. 2007 Aug;73(16):5261-7
pubmed: 17586664
Int J Mol Sci. 2021 Feb 21;22(4):
pubmed: 33669932
Nutrients. 2020 Jul 25;12(8):
pubmed: 32722370
Clin Sci (Lond). 2019 Sep 10;133(17):1857-1870
pubmed: 31467135
Clin J Am Soc Nephrol. 2016 Mar 7;11(3):379-85
pubmed: 26712810
Medicine (Baltimore). 2016 May;95(19):e3638
pubmed: 27175679
Nucleic Acids Res. 2013 Jan;41(Database issue):D590-6
pubmed: 23193283
Syst Appl Microbiol. 2002 Apr;25(1):46-51
pubmed: 12086188
Bioinformatics. 2011 Nov 1;27(21):2957-63
pubmed: 21903629
Kidney Int. 2013 Feb;83(2):308-15
pubmed: 22992469
PLoS One. 2016 Nov 2;11(11):e0165798
pubmed: 27806126
Acta Trop. 2020 Mar;203:105291
pubmed: 31816322
Circ J. 2018 Dec 25;83(1):182-192
pubmed: 30487369
Am J Nephrol. 2014;39(3):230-237
pubmed: 24643131
Am J Trop Med Hyg. 2018 Dec;99(6):1583-1586
pubmed: 30277207
Nat Rev Microbiol. 2021 Jan;19(1):55-71
pubmed: 32887946
Am J Physiol Renal Physiol. 2018 Sep 1;315(3):F487-F502
pubmed: 29693447
NPJ Biofilms Microbiomes. 2021 Mar 3;7(1):20
pubmed: 33658514
J Ren Nutr. 2014 Mar;24(2):110-5
pubmed: 24447438
Nephrology (Carlton). 2012 Nov;17(8):733-8
pubmed: 22817644
Sci Rep. 2018 Oct 18;8(1):15406
pubmed: 30337607
Genome Biol. 2011 Jun 24;12(6):R60
pubmed: 21702898
Metabolites. 2022 Mar 31;12(4):
pubmed: 35448495
Nat Methods. 2013 Jan;10(1):57-9
pubmed: 23202435
High Throughput. 2020 Mar 27;9(2):
pubmed: 32230716
J Am Soc Nephrol. 2014 Apr;25(4):657-70
pubmed: 24231662
Nat Rev Nephrol. 2017 Jun;13(6):344-358
pubmed: 28435157
Front Immunol. 2019 Mar 11;10:277
pubmed: 30915065
J Ren Nutr. 2002 Jan;12(1):17-31
pubmed: 11823990
Acta Trop. 2019 Feb;190:284-287
pubmed: 30521805
Nat Methods. 2010 May;7(5):335-6
pubmed: 20383131
Metabolites. 2020 Apr 04;10(4):
pubmed: 32260384
BMC Public Health. 2020 Aug 27;20(1):1299
pubmed: 32854662
Nucleic Acids Res. 2004 Mar 19;32(5):1792-7
pubmed: 15034147
J Clin Med. 2017 Sep 19;6(9):
pubmed: 28925931
mSphere. 2018 Mar 7;3(2):
pubmed: 29564397
Bioinformatics. 2011 Aug 15;27(16):2194-200
pubmed: 21700674