Occurrence and analysis of aflatoxin M1 in milk produced by Indian dairy species

A total of 600 samples of milk from different species [buffalo (150), cow (150), goat (150), and sheep (150)] were analyzed for aflatoxin M1 (AFM₁) contamination using high-performance liquid chromatography and enzyme-linked immunosorbent assay (ELISA) methods. AFM₁ contamination was found in buffalo (38.6%), cow (45.3%), goat (33.3%), and sheep (36.6%) milk. The mean value of AFM₁ was 0.026?µg?L^?1 in buffalo, 0.018?µg?L^?1 in cow, 0.014?µg?L^?1 in goat, and 0.017?µg?L^?1 in sheep milk. In all types of milks, the level of AFM₁ concentration was higher in milk obtained from urban and semi-urban areas, whereas it was found minimal in milk from rural areas. The results of the analysis of AFM₁ level by the ELISA analysis (ng?L^?1) was observed in 46.5% of all samples. The amount of AFM₁ in 16% buffalo, 44% cow, 10% goat, and 12% sheep milk samples was above the maximum tolerance limit accepted by the European Union.     

Clinical associations between IL-17 family cytokines and periodontitis and potential differential roles for IL-17A and IL-17E in periodontal immunity

Objective

IL-17A is implicated in periodontitis pathogenesis. The roles of IL-17B–IL-17F and IL-17A/F are unknown. This study aimed to determine clinical associations between IL-17 family cytokines and periodontitis and to investigate the biological roles of IL-17A and IL-17E using in vitro model systems.

Materials and methods

Samples from 97 patients with periodontitis and 77 healthy volunteers were used in the study. Serum, saliva and gingival crevicular fluid (GCF) levels of IL-17 family cytokines were measured by ELISA. Oral keratinocytes were stimulated with a P. gingivalis biofilm, or IL-17A, in the presence and absence of IL-17E and the expression of IL-8 and CXCL5 were investigated by ELISA and real-time-PCR. NF-κB phosphorylation in similar experiments was also measured using a cell-based ELISA.

Results

Serum, saliva and GCF IL-17A levels were higher in periodontitis patients and correlated positively with clinical parameters of attachment loss, pocket depth and bleeding on probing. Serum IL-17E levels were lower in periodontitis patients and the serum IL-17A:IL-17E ratio correlated positively with clinical parameters. In vitro, IL-17E inhibited Porphyromonas gingivalis and IL-17A induced expression of chemokines by reducing phosphorylation of the NF-κB p65 subunit.

Conclusions

Serum IL-17A:IL-17E may be a marker of disease severity. IL-17E may have opposing roles to IL-17A in periodontitis pathogenesis. IL-17E can negatively regulate IL-17A and periodontal pathogen induced expression of chemokines by oral keratinocytes.     

Is Interleukin‐17 Involved in the Interaction Between Polycystic Ovary Syndrome and Gingival Inflammation?

Background: Polycystic ovarian syndrome (PCOS) is a hormonal disorder of females of reproductive age that impacts their oral and systemic health. The aim of this study is to evaluate interleukin‐17A (IL‐17A), IL‐17F, IL‐17A/F, and IL‐17E (IL‐25) levels in gingival crevicular fluid (GCF), saliva, and serum of non‐obese females with PCOS and with either a clinically healthy periodontium or gingivitis. Methods: Thirty‐one females with PCOS, 30 females with PCOS and gingivitis, and 12 systemically and periodontally healthy females participated in the study. Clinical periodontal measurements, body mass index, and Ferriman‐Gallwey score (FGS) (a measure of hirsutism in females) were recorded. Circulating levels of sex hormones, cortisol, and insulin were also determined. Levels of IL‐17 cytokines were measured by enzyme‐linked immunosorbent assay. Results: The general linear model multivariate analysis, adjusting for age or plaque index, showed that the two groups with PCOS had higher concentrations of IL‐17A, IL‐17F, and IL‐17A/F in serum and higher levels of IL‐17A and IL‐17F in GCF and saliva but lower serum IL‐17E than systemically healthy females. Levels of IL‐17E were lowest in females with PCOS and gingivitis who also had the highest FGS. Serum IL‐17A and IL‐17F levels correlated positively with FGS and periodontal probing depth (all ρ >0.33; P <0.005). Serum IL‐17E showed the reverse relationship and also correlated negatively with IL‐17A (ρ >?0.28; P <0.05). Conclusions: IL‐17 levels are altered in non‐obese females with PCOS and may influence gingival inflammation. Additional studies are warranted to clarify the relationship between PCOS and gingivitis.     

Gingival Crevicular Fluid,Serum Levels of Receptor Activator of Nuclear Factor‐κB Ligand,Osteoprotegerin, and Interleukin‐17 in Patients With Rheumatoid Arthritis and Osteoporosis and With Periodontal Disease

Background: This study is performed to evaluate gingival crevicular fluid (GCF) and serum levels of soluble receptor activator of nuclear factor‐κB ligand (sRANKL), interleukin (IL)‐17A, IL‐17E, IL‐17F, IL‐17A/F, and osteoprotegerin (OPG) in women with rheumatoid arthritis (RA), osteoporosis (OPR), and those who are systemically healthy (SH), all with periodontal disease. Methods: GCF and serum samples were obtained before any periodontal intervention from 17 women with RA, 19 with OPR, and 13 who were SH with periodontitis. Full‐mouth clinical periodontal measurements were recorded. sRANKL, OPG, and IL‐17 levels were determined by enzyme‐linked immunosorbent assay. Results: Clinical periodontal measurements were similar in the three study groups. Although the total amounts of GCF albumin, OPG, IL‐17A, and IL‐17A/F were similar in the study groups, there were statistically significant differences in GCF concentrations of sRANKL, OPG, IL‐17A, IL‐17E, IL‐17F, and IL‐17A/F. The sRANKL/OPG ratios were significantly higher in the RA group than in the OPR and SH groups (P <0.05). Serum sRANKL, sRANKL/OPG, and IL‐17A/IL‐17E ratios were significantly higher, whereas OPG concentrations were significantly lower in the RA group compared to other groups (P <0.05). Serum IL‐17A concentrations were significantly higher in the RA and OPR groups than in the SH group (P <0.05). Conclusion: Increased inflammatory mediator levels in patients with RA, despite the long‐term use of various anti‐inflammatory drugs, suggest that these patients may have a propensity to overproduce these inflammatory mediators.