Protective effects of camel milk against pathogenicity induced by Escherichia coli and Staphylococcus aureus in Wistar rats.
The aim of the present study was to investigate the protective effects of camel milk on hepatic pathogenicity induced by experimental infection with Escherichia (E. coli) and Staphylococcus aureus (S. aureus) in Wistar rats. The rats were divided into six groups: The control and camel milk groups received water and camel milk, respectively; two groups received camel milk for 2 weeks prior to intraperitoneal injection of either E. coli or S. aureus; and two groups were injected intraperitoneally with E. coli and S. aureus, respectively. All animals were maintained under observation for 7 days prior to biochemical and gene expression analyses. The rats treated with camel milk alone exhibited no changes in expression levels of glutamic‑pyruvate transaminase (GPT) or glutamic‑oxaloacetic transaminase (GOT), compared with the water‑treated group. The E. coli‑ and S. aureus‑injected rats exhibited a significant increase in oxidative stress, and prior treatment with camel milk normalized the observed changes in the expression levels of GPT, GOT and malondialdehyde (MDA). Treatment with camel milk decreased the total bacterial count in liver tissue samples obtained from the rats injected with E. coli and S. aureus. Camel milk administration increased the expression levels of glutathione‑S‑transferase and superoxide dismutase, which were downregulated following E. coli and S. aureus injection. In addition, camel milk downregulated the increased expression of interleukin‑6 and apoptosis‑associated genes. Of note, administration of camel milk alone increased the expression levels of the B cell lymphoma 2‑associated X protein and survivin anti‑apoptotic genes, and supplementation prior to the injection of E. coli and S. aureus induced further upregulation, In conclusion, camel milk exerted protective effects against E. coli and S. aureus pathogenicity, by modulating the extent of lipid peroxidation, together with the antioxidant defense system, immune cytokines, apoptosis and the expression of anti-apoptotic genes in the liver of Wistar rats.
Medical Laboratory Department, Faculty of Applied Medical Sciences, Turabah, Taif University, Taif 21944, Saudi Arabia.
Mohamed Mohamed
MM
Soliman
Department of Medical Microbiology, Faculty of Applied Medical Sciences, Turabah, Taif University, Taif 21974, Saudi Arabia.
Magdy Yassin
MY
Hassan
Department of Medical Microbiology, Faculty of Applied Medical Sciences, Turabah, Taif University, Taif 21974, Saudi Arabia.
Salama Abdel-Hafiz
SA
Mostafa
Department of Biochemistry, Faculty of Veterinary Medicine, Benha University, Benha, Qalyubia 13511, Egypt.
Hussein Abdel-Maksoud
HA
Ali
Department of Medical Biotechnology, Faculty of Applied Medical Sciences, Turabah, Taif University, Taif 21974, Saudi Arabia.
Osama Moseilhy
OM
Saleh
D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001219:Aspartate Aminotransferases / Q000378:metabolism; D002162:Camelus; D004926:Escherichia coli / Q000472:pathogenicity*; D008099:Liver / Q000187:drug effects / Q000382:microbiology; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D008892:Milk; D018384:Oxidative Stress; D020011:Protective Agents / Q000627:therapeutic use*; D017208:Rats, Wistar; D013211:Staphylococcus aureus / Q000472:pathogenicity*; D000077022:Survivin; D051028:bcl-2-Associated X Protein / Q000378:metabolism
D000900:Anti-Bacterial Agents; C516989:Birc5 protein, rat; D008869:Microtubule-Associated Proteins; D020011:Protective Agents; D000077022:Survivin; D051028:bcl-2-Associated X Protein; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase