The effect of type-1 fimbrial immunization on gut pathophysiological response in rats infected with Salmonella enterica subsp. enterica serovar Typhimurium.
The pathophysiological mechanism of Salmonella enterica subsp. enterica serovar Typhimurium (Salmonella typhimurium) induced gastroenteritis is controlled by interplay of various cell signaling events. Adherence of this organism through type-1 fimbriae is known to be a vital prerequisite for the establishment of infection. In the present investigation male albino Wistar rats were immunized with purified type-1 fimbriae and challenged intragastrically with S. typhimurium. Electrolyte transport and level of different second messengers were studied in four different groups of animals. Transepithelial fluxes of Na+ and Cl- revealed absorption in immunized-challenged group as observed in case of control and immunized group while secretion was observed in infected group. Ca2+ and 3-0-methyl-D-glucose fluxes did not show any change. Significant increase in the level of intracellular Ca2+, cAMP, membrane form of protein kinase C, prostaglandins, NADPH oxidase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, total oxygen free radicals, reactive nitrogen intermediates, citrulline and lipid peroxidation was found in the infected group. However, in the immunized-challenged group, the values of all the parameters were found to be same as that of control as well as immunized groups. Na+, K(+)-ATPase and calmodulin levels were found to be unaltered in all the groups of animals. Thus, the immunization with type-1 fimbriae has been found to be quite effective leading to the prevention of multiple physiologic derangements in isolated ileal cells suggesting the protective role of the fimbriae.
Verma
Amrisha
A
Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Basu
Sulagna
S
Ghosh
Sujata
S
Majumdar
S
S
Ganguly
N K
NK
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002147:Calmodulin / Q000378:metabolism; D002712:Chlorides / Q000378:metabolism; D002956:Citrulline / Q000378:metabolism; D010861:Fimbriae, Bacterial / Q000276:immunology*; D005609:Free Radicals / Q000378:metabolism; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D007114:Immunization; D007410:Intestinal Diseases / Q000378:metabolism / Q000503:physiopathology*; D015227:Lipid Peroxidation; D008297:Male; D019255:NADPH Oxidases / Q000378:metabolism; D010734:Phosphogluconate Dehydrogenase / Q000378:metabolism; D011453:Prostaglandins / Q000378:metabolism; D011493:Protein Kinase C / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012481:Salmonella Infections, Animal / Q000378:metabolism / Q000503:physiopathology*; D012486:Salmonella typhimurium / Q000472:pathogenicity*; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D002147:Calmodulin; D002712:Chlorides; D005609:Free Radicals; D011453:Prostaglandins; D002956:Citrulline; D012964:Sodium; D010734:Phosphogluconate Dehydrogenase; D005954:Glucosephosphate Dehydrogenase; D019255:NADPH Oxidases; D011493:Protein Kinase C; D000254:Sodium-Potassium-Exchanging ATPase; D002118:Calcium