Bee pollen and propolis improve neuroinflammation and dysbiosis induced by propionic acid, a short chain fatty acid in a rodent model of autism.


Journal

Lipids in health and disease
ISSN: 1476-511X
Titre abrégé: Lipids Health Dis
Pays: England
ID NLM: 101147696

Informations de publication

Date de publication:
16 Nov 2019
Historique:
received: 23 05 2019
accepted: 07 11 2019
entrez: 18 11 2019
pubmed: 18 11 2019
medline: 15 4 2020
Statut: epublish

Résumé

Neuroinflammation plays a major role in the pathogenesis of autism because the cytokine levels are typically disturbed in the brain in autistic patients. Prebiotics-rich diet maintains the healthy gut microbiota and hence can regulate the neuroinflammation indirectly. The study aimed to investigate the role of bee pollen and propolis in ameliorating neuroinflammation, including cytokine levels, in an animal model of autism. Hamsters were classified as four groups: Group I, control; Group II, autistic model/animals treated with 250 mg propionic acid (PPA)/kg body weight (BW)/day for 3 days; Group III, animals treated with bee pollen at a dose of 250 mg/kg BW/day for 4 weeks; and Group IV, animals treated with propolis at a dose of 250 mg/kg BW/day for 4 weeks. Neuroinflammatory responses were evaluated using the levels of interferon γ (IFN-γ), interleukin 1 alpha (IL-1α), IL-6, IL-10, IL-12 (p70), vascular endothelial growth factor (VEGF), and tumor necrosis factor α (TNFα). Significant decrease of IL-10 (P<0.026), VEGF (P<0.005), and TNFα(P<0.005) levels and increased IL-1α (P<0.032), IL-6(P<0.028), and IFN-γ (P<0.013) levels were observed between the four studied groups. The neurotoxic effects of PPA was clearly presented as much higher IL-6, as pro-inflammatory cytokine (P<0.05), concomitant with much lower IL-10, as anti-inflammatory cytokine(P<0.015) compared to controls. Both bee pollen and propolis were effective in ameliorating the neurotoxic effects of PPA demonstrating non-significant changes of IL-6 and IL-10 when compared to control healthy hamsters. Our findings indicate that both bee pollen and propolis protect against neuroinflammation in the rodent model of autism. However, further studies are needed to investigate the clinical benefits of prebiotics-rich diet in neurodevelopmental disorders, such as autism.

Sections du résumé

BACKGROUND BACKGROUND
Neuroinflammation plays a major role in the pathogenesis of autism because the cytokine levels are typically disturbed in the brain in autistic patients. Prebiotics-rich diet maintains the healthy gut microbiota and hence can regulate the neuroinflammation indirectly. The study aimed to investigate the role of bee pollen and propolis in ameliorating neuroinflammation, including cytokine levels, in an animal model of autism.
METHODS METHODS
Hamsters were classified as four groups: Group I, control; Group II, autistic model/animals treated with 250 mg propionic acid (PPA)/kg body weight (BW)/day for 3 days; Group III, animals treated with bee pollen at a dose of 250 mg/kg BW/day for 4 weeks; and Group IV, animals treated with propolis at a dose of 250 mg/kg BW/day for 4 weeks. Neuroinflammatory responses were evaluated using the levels of interferon γ (IFN-γ), interleukin 1 alpha (IL-1α), IL-6, IL-10, IL-12 (p70), vascular endothelial growth factor (VEGF), and tumor necrosis factor α (TNFα).
RESULTS RESULTS
Significant decrease of IL-10 (P<0.026), VEGF (P<0.005), and TNFα(P<0.005) levels and increased IL-1α (P<0.032), IL-6(P<0.028), and IFN-γ (P<0.013) levels were observed between the four studied groups. The neurotoxic effects of PPA was clearly presented as much higher IL-6, as pro-inflammatory cytokine (P<0.05), concomitant with much lower IL-10, as anti-inflammatory cytokine(P<0.015) compared to controls. Both bee pollen and propolis were effective in ameliorating the neurotoxic effects of PPA demonstrating non-significant changes of IL-6 and IL-10 when compared to control healthy hamsters.
CONCLUSIONS CONCLUSIONS
Our findings indicate that both bee pollen and propolis protect against neuroinflammation in the rodent model of autism. However, further studies are needed to investigate the clinical benefits of prebiotics-rich diet in neurodevelopmental disorders, such as autism.

Identifiants

pubmed: 31733650
doi: 10.1186/s12944-019-1150-0
pii: 10.1186/s12944-019-1150-0
pmc: PMC6858724
doi:

Substances chimiques

Cytokines 0
Propionates 0
Propolis 9009-62-5
propionic acid JHU490RVYR

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

200

Subventions

Organisme : This research project was supported by the Deanship of Scientific Research, Princess Nora Bint Abdulrahman University, The authors thank the Deanship of Scientific Research and RSSU at King Saud University for the technical support.
ID : Grant number ----

Commentaires et corrections

Type : ErratumIn

Références

Kern JK, Geier DA, Sykes LK, Geier MR. Relevance of neuroinflammation and encephalitis in autism. Front Cell Neurosci. 2016;9:519. https://doi.org/10.3389/fncel.2015.00519 .
doi: 10.3389/fncel.2015.00519 pubmed: 26834565 pmcid: 4717322
Hrabovska SV, Salyha YT. Animal models of autism spectrum disorders and behavioral techniques of their examination. Neurophysiology. 2016;48:380–8. https://doi.org/10.1007/s11062-017-9613-2 .
doi: 10.1007/s11062-017-9613-2
Cryan JF, Holmes A. The ascent of mouse: advances in modelling human depression and anxiety. Nat Rev Drug Discov. 2005;4(9):775–90.
doi: 10.1038/nrd1825
Jan G, Belzacq AS, Haouzi D, Rouault A, Métivier D, Kroemer G, et al. Propionibacteria induce apoptosis of colorectal carcinoma cells via short-chain fatty acids acting on mitochondria. Cell Death Differ. 2002;9:179–88.
doi: 10.1038/sj.cdd.4400935
Al-Lahham SH, Peppelenbosch MP, Rolfson H, Vonk RJ, Venema K. Biological effects of propionic acid in humans; metabolism, potential applications and underlying mechanisms. Biochim Biophys Acta. 1801;2010:1175–83.
Borgstrom MK, Edwardsson S, Svensater G, Twetman S. Acid formation in sucrose exposed dental plaque in relation to caries incidence in schoolchildren. Clin Oral Investig. 2000;4:9–12.
doi: 10.1007/s007840050106
Karuri AR, Dobrowsky E, Tannock IF. Selective cellular acidification and toxicity of weak organic acids in an acidic microenvironment. Br J Cancer. 1993;68:1080–7.
doi: 10.1038/bjc.1993.485
El-Ansary AK, Ben Bacha A, Kotb M. Etiology of autistic features: the persisting neurotoxic effects of propionic acid. J Neuroinflammation. 2012;9:74. https://doi.org/10.1186/1742-2094-9-74 .
doi: 10.1186/1742-2094-9-74 pubmed: 22531301 pmcid: 3425128
Mirza R, Sharma B. Selective modulator of peroxisome proliferator-activated receptor-α protectspropionic acid induced autism-like phenotypes in rats. Life Sci. 2018. https://doi.org/10.1016/j.lfs.2018.10.045 .
doi: 10.1016/j.lfs.2018.10.045
Stackebrandt E, Rainey FA. Phylogenetic relationships. In: Rood JI, McClane BA, Songer JG, Titball RW. The clostridia, molecular biology and pathogenesis. Academic Press. 1997; 3–19.
Song Y, Liu C, Finegold SM. Real-time PCR quantification of clostridia in feces of autistic children. Appl Environ Microbiol. 2004;70:6459–65.
doi: 10.1128/AEM.70.11.6459-6465.2004
Finegold SM, Dowd SE, Gontcharova V, Liu C, Henley KE, Wolcott RD, et al. Pyrosequencing study of fecal microflora of autistic and control children. Anaerobe. 2010;16:444–53.
doi: 10.1016/j.anaerobe.2010.06.008
Masi A, Glozier N, Dale R, Guastella AJ. The immune system, cytokines, and biomarkers in autism spectrum disorder. Neurosci Bull. 2017;33:194–204. https://doi.org/10.1007/s12264-017-0103-8 .
doi: 10.1007/s12264-017-0103-8 pubmed: 28238116 pmcid: 5360854
Filiano AJ, Gadani SP, Kipnis J. Interactions of innate and adaptive immunity in brain development and function. Brain Res. 1617;2015:18–27.
Dantzer R. Cytokine, sickness behavior, and depression. Immunol Allergy Clin N Am. 2009;29:247–64.
doi: 10.1016/j.iac.2009.02.002
Li QQ, Wang K, Marcucci MC, Helena CA, Sawaya F, Hu L, et al. Nutrient-rich bee pollen: A treasure trove of active natural metabolites. J Funct Foods. 2018;19:472–84.
doi: 10.1016/j.jff.2018.09.008
Allan SM, Tyrrell PJ, Rothwell NJ. Interleukin-1 and neuronal injury. Nat Rev Immunol. 2005;5:629–40.
doi: 10.1038/nri1664
Aleksandrova NP, Danilova GA, Aleksandrov VG. Cyclooxygenase pathway in modulation of the ventilatory response to hypercapnia by interleukin-1β in rats. Respir Physiol Neurobiol. 2015;209:85–90.
doi: 10.1016/j.resp.2014.12.006
El-Ansary A, Al-Ayadhi L. GABAergic/glutamatergic imbalance relative to excessive neuroinflammation in autism spectrum disorders. J Neuroinflammation. 2014;11:189.
doi: 10.1186/s12974-014-0189-0
Strle K, Zhou JH, Shen WH, Broussard SR, Johnson RW, Freund GG, et al. Interleukin-10 in the brain. Crit Rev Immunol. 2001;21:427–49. https://doi.org/10.1615/CritRevImmunol.v21.i5.20 .
doi: 10.1615/CritRevImmunol.v21.i5.20 pubmed: 11942558
Osborn DA, Sinn JK. Prebiotics in infants for prevention of allergic disease and food hypersensitivity. Cochrane Database Syst Rev. 2007;4:CD006475.
Kleessen B, Sykura B, Zunft HJ, Blaut M. Effects of inulin and lactose on fecal microflora, microbial activity, and bowel habit in elderly constipated persons. Am J Clin Nutr. 1997;65:1397–402.
doi: 10.1093/ajcn/65.5.1397
Taha EKA. Chemical composition and amounts of mineral elements in honeybee-collected pollen in relation to botanical origin. J Apic Sci. 2015;59:75–81.
Ares AM, Valverde S, Bernal JL, Nozal MJ, Bernal J. Extraction and determination of bioactive compounds from bee pollen. J Pharm Biomed Anal. 2018;147:110–24.
doi: 10.1016/j.jpba.2017.08.009
Hegazi AG. Role of cytokines in Apitherapy. J Clin Cell Immunol. 2015;6:5.
doi: 10.4172/2155-9899.1000299
Silva JC, Rodrigues S, Feás X, Estevinho LM. Antimicrobial activity, phenolic profile and role in the inflammation of própolis. Food Chem Toxicol. 2012;50:1790–5.
doi: 10.1016/j.fct.2012.02.097
Rothwell N. Interleukin-1 and neuronal injury: mechanisms, modification, and therapeutic potential. Brain Behav Immun. 2003;17:152–7.
doi: 10.1016/S0889-1591(02)00098-3
Roquetto AR, Monteiro NES, Moura CS, Toreti VC, de Pace F, Santos AD, et al. Green propolis modulates gut microbiota, reduces endotoxemia and expression of TLR4 pathway in mice fed a high-fat diet. Food Res Int. 2015;76:796–803.
doi: 10.1016/j.foodres.2015.07.026
DeGrandi-Hoffman G, Gage SL, Corby-Harris V, Carroll M, Chambers M, Graham H, Watkins deJong E, Hidalgo G, Calle S, Azzouz-Olden F, Meador C, Snyder L, Ziolkowski N. Connecting the nutrient composition of seasonal pollens with changing nutritional needs of honey bee (Apis mellifera L.) colonies. J Insect Physiol. 2018 Aug - Sep;109:114–124.
doi: 10.1016/j.jinsphys.2018.07.002
Cartmell T, Ball C, Bristow AF, Mitchell D, Poole S. Endogenous interleukin-10 is required for the defervescence of fever evoked by local lipopolysaccharide-induced and Staphylococcus aureus-induced inflammation in rats. J Physiol. 2003;549:653–64.
doi: 10.1113/jphysiol.2002.037291
Conti B, Tabarean I, Andrei C, Bartfai T. Cytokines and fever. Front Biosci. 2004;9:1433–49.
doi: 10.2741/1341
Galic MA, Riazi K, Pittman QJ. Cytokines and brain excitability. Front Neuroendocrinol. 2012;33:116–25.
doi: 10.1016/j.yfrne.2011.12.002
Denisow B, Denisow-Pietrzyk M. Biological and therapeutic properties of bee pollen: a review. J Sci Food Agric. 2016;96(13):4303.
doi: 10.1002/jsfa.7729
Parandin R, Daroogari S. Anti-inflammatory and Antinociceptive activities of the Ethanolic extract of Propolis in male mice and rats. Zahedan J Res Med Sci. 2019;21(2):e84150.

Auteurs

Kawther Aabed (K)

Biology Department, College of Science, Princess Nourah Bint Abdulrahman University, Riyadh, Saudi Arabia.

Ramesa Shafi Bhat (RS)

Biochemistry Department, College of Sciences, King Saud University, Riyadh, Saudi Arabia.

Abeer Al-Dbass (A)

Biochemistry Department, College of Sciences, King Saud University, Riyadh, Saudi Arabia.

Nadine Moubayed (N)

Biology Department, College of Sciences, King Saud University, Riyadh, Saudi Arabia.

Norah Algahtani (N)

Central laboratory, Female Centre for Scientific and Medical Studies, King Saud University, Riyadh, Saudi Arabia.

Nada M Merghani (NM)

Central laboratory, Female Centre for Scientific and Medical Studies, King Saud University, Riyadh, Saudi Arabia.

Azizah Alanazi (A)

Department of Cell Biology, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.

Naima Zayed (N)

Therapeutic Chemistry Department, National Research Centre, Dokki, Cairo, Egypt.

Afaf El-Ansary (A)

Central laboratory, Female Centre for Scientific and Medical Studies, King Saud University, Riyadh, Saudi Arabia. afafkelansary@gmail.com.
Therapeutic Chemistry Department, National Research Centre, Dokki, Cairo, Egypt. afafkelansary@gmail.com.

Articles similaires

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male
Humans Meals Time Factors Female Adult

Classifications MeSH