Phytomodulatory potentials of Aloe vera against Salmonella OmpR-mediated inflammation.
Mediators released during inflammatory response play an essential role in eliminating microbes or microbial products. However, the uncontrolled release of cytotoxic substances characterized by extensive inflammation may adversely affect normal tissues. Under such conditions it is important to manage the hyperinflammation in order to change the clinical manifestations of the disease. Accordingly, the present study was designed to evaluate the modulation of Salmonella OmpR mediated inflammation by Aloe vera, a plant known to contain antiinflammatory ingredients. It was observed that outer-membrane proteins (OMPs) extracted from the wild type strain of S. typhimurium caused inflammation of greater magnitude compared with the OMPs extracted from its mutant construct as evident from the oedema test as well as the hyperalgesic (flicking) response of the animals under experimental conditions. However, Aloe vera applied topically, administered intraperitoneally or in combination modulated the inflammatory response. The maximum effect was observed with the combined formulation indicating modulation at local as well as systemic levels. The results reveal that this modulation could be due to the potential of Aloe vera to decrease peroxidative damage via a decrease in the levels of monokines (TNF-alpha, IL-1 and IL-6) and an increase in the level of superoxide dismutase (SOD). Moreover, the presence of SOD in Aloe vera itself might be responsible for enhancing its levels in the macrophages. On the other hand, no significant change in the catalase activity was observed by Aloe vera treatment. The use of Aloe vera, therefore, seems to have a promising role in the modulation of Salmonella OmpR mediated inflammation.
Rishi
Praveen
P
Department of Microbiology, Panjab University, Chandigarh 160014, India. rishipraveen@yahoo.com
Rampuria
Anjali
A
Tewari
Rupinder
R
Koul
Ashwani
A
D000287:Administration, Topical; D000504:Aloe / Q000737:chemistry*; D000818:Animals; D001425:Bacterial Outer Membrane Proteins / Q000494:pharmacology; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D004487:Edema / Q000139:chemically induced / Q000188:drug therapy / Q000473:pathology; D006614:Hindlimb; D006930:Hyperalgesia / Q000188:drug therapy / Q000503:physiopathology; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D018836:Inflammation Mediators / Q000494:pharmacology*; D007274:Injections, Intraperitoneal; D015227:Lipid Peroxidation / Q000187:drug effects; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D015846:Monokines / Q000378:metabolism; D010146:Pain / Q000188:drug therapy; D010936:Plant Extracts / Q000494:pharmacology*; D012486:Salmonella typhimurium / Q000737:chemistry / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
D001425:Bacterial Outer Membrane Proteins; D018836:Inflammation Mediators; D015846:Monokines; D010936:Plant Extracts; D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase