Hydrogen sulfide is a novel potential virulence factor of Mycoplasma pneumoniae: characterization of the unusual cysteine desulfurase/desulfhydrase HapE

Abstract

Mycoplasma pneumoniae is a human pathogen causing atypical pneumonia with a minimalized and highly streamlined genome. So far, hydrogen peroxide production, cytadherence, and the ADP-ribosylating CARDS toxin have been identified as pathogenicity determinants. We have studied haemolysis caused by M. pneumoniae, and discovered that hydrogen peroxide is responsible for the oxidation of heme, but not for lysis of erythrocytes. This feature could be attributed to hydrogen sulfide, a compound that has previously not been identified as virulence factor in lung pathogens. Indeed, we observed hydrogen sulfide production by M. pneumoniae. The search for a hydrogen sulfide-producing enzyme identified HapE, a protein with similarity to cysteine desulfurases. In contrast to typical cysteine desulfurases, HapE is a bifunctional enzyme: it has both the cysteine desulfurase activity to produce alanine and the cysteine desulfhydrase activity to produce pyruvate and hydrogen sulfide. Experiments with purified HapE showed that the enzymatic activity of the protein is responsible for haemolysis, demonstrating that HapE is a novel potential virulence factor of M. pneumoniae.

Virulence, antimicrobial resistance and phylogenetic analysis of zoonotic walking pneumonia Mycoplasma arginini in the one-humped camel (Camelus dromedarius)

“…The overlapping, but distinct effects of H 2 S, indicated that the bacteria possess a set of virulence determinants that synthesize and allow the bacteria getting efficient access to the host's resources. Großhennig et al (2016) shared results confirming H 2 S production and hemolysis were correlated in M.…”

“…This was the first time that correlation was recorded for M. arginini isolated from camels, where H 2 S was not previously identified as a virulence factor in lung pathogens in camels. This study also concluded that H 2 O 2 was the responsible agent for the oxidation of heme, but not for lysis of RBCs (Großhennig et al, 2016).…”

“…There were four assays used to demonstrate the phenotypic virulence potentiality of the 48 M. arginini isolates. This was conducted using the following: 1) the catalase enzyme activity was performed according to the procedure of Pritchard et al (2014); 2) the hemolytic and hemoxidative activity of M. arginini was determined by the method adopted by Großhennig et al (2016) using washed 2% sheep RBCs in PBS with or without supplements in a final volume of 1 ml; 3) the hydrogen sulfide (H 2 S) produced by the 48 M. arginini isolates was determined using lead acetate detection strips (Großhennig et al, 2016); and 4) biofilms grown on glass coverslips and in microtitre plates were quantified by measuring the absorbance (560 nm) of 100 ml of the solubilized crystal violet in a microtitre plate (McAuliffe et al, 2006).…”

Delayed Treatment with Sodium Hydrosulfide Improves Regional Blood Flow and Alleviates Cecal Ligation and Puncture (CLP)-Induced Septic Shock

“…First of all, did the NaHS infusion alter the progression of infection and was organ colonization affected by NaHS in the current study? Importantly, H 2 S can affect bacterial virulence and the sensitivity of bacteria to antibiotic treatment, at least in vitro (24,25) and H 2 S can also affect host immune function (26–28). It is, therefore, also conceivable that H 2 S (produced endogenously during sepsis, and/or when administered in the form of NaHS) may also have affected bacterial replication, organ invasion and/or the sensitivity of the bacteria to elimination by the immune system.…”

Association between genetic polymorphism of telomere-associated gene ACYP2 and the risk of HAPE among the Chinese Han population

“…[27] Simultaneously, some SNPs in ACYP2 have been identified to be associated with telomere length. [7,9,28,29] Subsequently, we performed a multivariate analysis adjusted for age and gender among HAPE patients and controls to investigate the association between ACYP2 genetic polymorphism and HAPE risk.…”