Serum and Fecal Markers of Intestinal Inflammation and Intestinal Barrier Permeability Are Elevated in Parkinson’s Disease
Parkinson’s disease (PD) is characterized by alpha-synuclein misfolding with subsequent intraneuronal amyloid formation and accumulation, low grade neuroinflammatory changes, and selective neurodegeneration. Available evidence suggests that the pathology usually begins in the gut and olfactory mucos...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2021-06-01
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| Series: | Frontiers in Neuroscience |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fnins.2021.689723/full |
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| author | Laura Dumitrescu Laura Dumitrescu Daciana Marta Adela Dănău Adela Dănău Antonia Lefter Antonia Lefter Delia Tulbă Delia Tulbă Liviu Cozma Liviu Cozma Emilia Manole Emilia Manole Mihaela Gherghiceanu Mihaela Gherghiceanu Laura Cristina Ceafalan Laura Cristina Ceafalan Bogdan Ovidiu Popescu Bogdan Ovidiu Popescu Bogdan Ovidiu Popescu |
| author_facet | Laura Dumitrescu Laura Dumitrescu Daciana Marta Adela Dănău Adela Dănău Antonia Lefter Antonia Lefter Delia Tulbă Delia Tulbă Liviu Cozma Liviu Cozma Emilia Manole Emilia Manole Mihaela Gherghiceanu Mihaela Gherghiceanu Laura Cristina Ceafalan Laura Cristina Ceafalan Bogdan Ovidiu Popescu Bogdan Ovidiu Popescu Bogdan Ovidiu Popescu |
| author_sort | Laura Dumitrescu |
| collection | DOAJ |
| description | Parkinson’s disease (PD) is characterized by alpha-synuclein misfolding with subsequent intraneuronal amyloid formation and accumulation, low grade neuroinflammatory changes, and selective neurodegeneration. Available evidence suggests that the pathology usually begins in the gut and olfactory mucosa, spreading to the brain via the vagus and olfactory nerves, by a prion-like mechanism. A causal relationship has not been established, but gut dysbiosis is prevalent in PD and may lead to intestinal inflammation and barrier dysfunction. Additionally, epidemiological data indicate a link between inflammatory bowel diseases and PD. Calprotectin and zonulin are markers of intestinal inflammation and barrier permeability, respectively. We evaluated their serum and fecal levels in 22 patients with sporadic PD and 16 unmatched healthy controls. Mean calprotectin was higher in PD, both in serum (14.26 mcg/ml ± 4.50 vs. 5.94 mcg/ml ± 3.80, p = 0.0125) and stool (164.54 mcg/g ± 54.19 vs. 56.19 mcg/g ± 35.88, p = 0.0048). Mean zonulin was also higher in PD serum (26.69 ng/ml ± 3.55 vs. 19.43 ng/ml ± 2.56, p = 0.0046) and stool (100.19 ng/ml ± 28.25 vs. 37.3 ng/ml ± 13.26, p = 0.0012). Calprotectin was above the upper reference limit in 19 PD serums and 6 controls (OR = 10.56, 95% CI = 2.17–51.42, p = 0.0025) and in 20 PD stool samples and 4 controls (OR = 30, 95% CI = 4.75–189.30, p = 0.000045). Increased zonulin was found only in the stool samples of 8 PD patients. Despite the small sample size, our findings are robust, complementing and supporting other recently published results. The relation between serum and fecal calprotectin and zonulin levels and sporadic PD warrants further investigation in larger cohorts. |
| first_indexed | 2024-12-22T00:30:53Z |
| format | Article |
| id | doaj.art-48fcf6245458499e8aaf8039ae9b28f7 |
| institution | Directory Open Access Journal |
| issn | 1662-453X |
| language | English |
| last_indexed | 2024-12-22T00:30:53Z |
| publishDate | 2021-06-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Neuroscience |
| spelling | doaj.art-48fcf6245458499e8aaf8039ae9b28f72022-12-21T18:44:56ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2021-06-011510.3389/fnins.2021.689723689723Serum and Fecal Markers of Intestinal Inflammation and Intestinal Barrier Permeability Are Elevated in Parkinson’s DiseaseLaura Dumitrescu0Laura Dumitrescu1Daciana Marta2Adela Dănău3Adela Dănău4Antonia Lefter5Antonia Lefter6Delia Tulbă7Delia Tulbă8Liviu Cozma9Liviu Cozma10Emilia Manole11Emilia Manole12Mihaela Gherghiceanu13Mihaela Gherghiceanu14Laura Cristina Ceafalan15Laura Cristina Ceafalan16Bogdan Ovidiu Popescu17Bogdan Ovidiu Popescu18Bogdan Ovidiu Popescu19Department of Clinical Neurosciences, Neurology Division at Colentina Clinical Hospital, Carol Davila University of Medicine and Pharmacy, Bucharest, RomaniaDepartment of Neurology, Colentina Clinical Hospital, Bucharest, RomaniaLaboratory of Cell Biology, Neurosciences and Experimental Myology, “Victor Babeş”, National Institute of Pathology, Bucharest, RomaniaDepartment of Clinical Neurosciences, Neurology Division at Colentina Clinical Hospital, Carol Davila University of Medicine and Pharmacy, Bucharest, RomaniaDepartment of Neurology, Colentina Clinical Hospital, Bucharest, RomaniaDepartment of Clinical Neurosciences, Neurology Division at Colentina Clinical Hospital, Carol Davila University of Medicine and Pharmacy, Bucharest, RomaniaDepartment of Neurology, Colentina Clinical Hospital, Bucharest, RomaniaDepartment of Clinical Neurosciences, Neurology Division at Colentina Clinical Hospital, Carol Davila University of Medicine and Pharmacy, Bucharest, RomaniaDepartment of Neurology, Colentina Clinical Hospital, Bucharest, RomaniaDepartment of Clinical Neurosciences, Neurology Division at Colentina Clinical Hospital, Carol Davila University of Medicine and Pharmacy, Bucharest, RomaniaDepartment of Neurology, Colentina Clinical Hospital, Bucharest, RomaniaLaboratory of Cell Biology, Neurosciences and Experimental Myology, “Victor Babeş”, National Institute of Pathology, Bucharest, RomaniaPathology Department, Colentina Clinical Hospital, Bucharest, RomaniaLaboratory of Cell Biology, Neurosciences and Experimental Myology, “Victor Babeş”, National Institute of Pathology, Bucharest, RomaniaDepartment of Cellular and Molecular Biology and Histology, Carol Davila University of Medicine and Pharmacy, Bucharest, RomaniaLaboratory of Cell Biology, Neurosciences and Experimental Myology, “Victor Babeş”, National Institute of Pathology, Bucharest, RomaniaDepartment of Cellular and Molecular Biology and Histology, Carol Davila University of Medicine and Pharmacy, Bucharest, RomaniaDepartment of Clinical Neurosciences, Neurology Division at Colentina Clinical Hospital, Carol Davila University of Medicine and Pharmacy, Bucharest, RomaniaDepartment of Neurology, Colentina Clinical Hospital, Bucharest, RomaniaLaboratory of Cell Biology, Neurosciences and Experimental Myology, “Victor Babeş”, National Institute of Pathology, Bucharest, RomaniaParkinson’s disease (PD) is characterized by alpha-synuclein misfolding with subsequent intraneuronal amyloid formation and accumulation, low grade neuroinflammatory changes, and selective neurodegeneration. Available evidence suggests that the pathology usually begins in the gut and olfactory mucosa, spreading to the brain via the vagus and olfactory nerves, by a prion-like mechanism. A causal relationship has not been established, but gut dysbiosis is prevalent in PD and may lead to intestinal inflammation and barrier dysfunction. Additionally, epidemiological data indicate a link between inflammatory bowel diseases and PD. Calprotectin and zonulin are markers of intestinal inflammation and barrier permeability, respectively. We evaluated their serum and fecal levels in 22 patients with sporadic PD and 16 unmatched healthy controls. Mean calprotectin was higher in PD, both in serum (14.26 mcg/ml ± 4.50 vs. 5.94 mcg/ml ± 3.80, p = 0.0125) and stool (164.54 mcg/g ± 54.19 vs. 56.19 mcg/g ± 35.88, p = 0.0048). Mean zonulin was also higher in PD serum (26.69 ng/ml ± 3.55 vs. 19.43 ng/ml ± 2.56, p = 0.0046) and stool (100.19 ng/ml ± 28.25 vs. 37.3 ng/ml ± 13.26, p = 0.0012). Calprotectin was above the upper reference limit in 19 PD serums and 6 controls (OR = 10.56, 95% CI = 2.17–51.42, p = 0.0025) and in 20 PD stool samples and 4 controls (OR = 30, 95% CI = 4.75–189.30, p = 0.000045). Increased zonulin was found only in the stool samples of 8 PD patients. Despite the small sample size, our findings are robust, complementing and supporting other recently published results. The relation between serum and fecal calprotectin and zonulin levels and sporadic PD warrants further investigation in larger cohorts.https://www.frontiersin.org/articles/10.3389/fnins.2021.689723/fullcalprotectinParkinson’s diseaseintestinal inflammationintestinal barrier permeabilityzonulin |
| spellingShingle | Laura Dumitrescu Laura Dumitrescu Daciana Marta Adela Dănău Adela Dănău Antonia Lefter Antonia Lefter Delia Tulbă Delia Tulbă Liviu Cozma Liviu Cozma Emilia Manole Emilia Manole Mihaela Gherghiceanu Mihaela Gherghiceanu Laura Cristina Ceafalan Laura Cristina Ceafalan Bogdan Ovidiu Popescu Bogdan Ovidiu Popescu Bogdan Ovidiu Popescu Serum and Fecal Markers of Intestinal Inflammation and Intestinal Barrier Permeability Are Elevated in Parkinson’s Disease Frontiers in Neuroscience calprotectin Parkinson’s disease intestinal inflammation intestinal barrier permeability zonulin |
| title | Serum and Fecal Markers of Intestinal Inflammation and Intestinal Barrier Permeability Are Elevated in Parkinson’s Disease |
| title_full | Serum and Fecal Markers of Intestinal Inflammation and Intestinal Barrier Permeability Are Elevated in Parkinson’s Disease |
| title_fullStr | Serum and Fecal Markers of Intestinal Inflammation and Intestinal Barrier Permeability Are Elevated in Parkinson’s Disease |
| title_full_unstemmed | Serum and Fecal Markers of Intestinal Inflammation and Intestinal Barrier Permeability Are Elevated in Parkinson’s Disease |
| title_short | Serum and Fecal Markers of Intestinal Inflammation and Intestinal Barrier Permeability Are Elevated in Parkinson’s Disease |
| title_sort | serum and fecal markers of intestinal inflammation and intestinal barrier permeability are elevated in parkinson s disease |
| topic | calprotectin Parkinson’s disease intestinal inflammation intestinal barrier permeability zonulin |
| url | https://www.frontiersin.org/articles/10.3389/fnins.2021.689723/full |
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