Host hydrogen rather than that produced by the pathogen is important for Salmonella enterica serovar Typhimurium virulence.
[typhoid]
Salmonella enterica serovar Typhimurium utilizes molecular hydrogen as a substrate in various respiratory pathways, via H2-uptake enzymes termed Hya, Hyb, and Hyd. A different hydrogenase, the hydrogen evolving Hyc enzyme removes excess reductant during fermentative growth. Virulence phenotypes conferred by mutations in hyc genes, either alone or in combination with mutations in the H2-uptake enzyme genes are addressed. Anaerobically grown single ΔhycB or ΔhycC deletion strains were more sensitive to acid than the wild-type, but the Δhyc strains were like the virulent parent strain for both mouse morbidity/mortality and in organ burden numbers. Even fecal recovery numbers for both mutant strains at several time points prior to the animals succumbing to salmonellosis were like the parent. Neither hydrogen uptake nor evolution of the gas was detected in a hydrogenase quadruple mutant strain containing deletions in hya, hyb, hyd and hyc genes. As previously described, a strain lacking all H2 uptake ability was severely attenuated in its virulence characteristics, and the quadruple mutant strain had the same (greatly-attenuated) phenotype. While H2 levels were greatly reduced in ceca of mice treated with antibiotics, both ΔhycB or ΔhycC strains were still like the parent in ability to cause typhoid salmonellosis. It seems that H2 produced by the pathogen (through FHL and Hyc) is insignificant in terms of providing respiratory reductant to facilitate either organ colonization or contribute to gut growth leading to pathogenesis.
