$H_2S$ is the end product of sulfur related respirations (like sulfate respiration, sulfur respiration, etc...).
By aerob (oxygen) respiration the oxygen in $O_2$ has 0 oxidation number, by $CO_2$ the oxygen has -2 oxidation number, so it was reduced while the carbon was oxidized.
By the thiosulfate respiration of Salmonella enterica the following reaction happens by the reduction of thiosulfate: $S_2O_3^{2-} +2H^+ + 2e^- \to HS^- + HSO_3^{-}$. In this case the sulfur in $S_2O_3^{2-}$ has +2 oxidation number while the sulfur in $HS^-$ has -2 oxidation number, so the sulfur was reduced, it was an electron acceptor, just like oxygen by aerob respiration.
So in the case of Salmonella enterica $H_2S$ production is a byproduct of anaerob respiration. It makes growth faster.
Sulfate-reducing bacteria are those bacteria that can obtain energy by
oxidizing organic compounds or molecular hydrogen (H2) while reducing
sulfate (SO2- 4) to hydrogen sulfide (H2S).1 In a sense, these
organisms "breathe" sulfate rather than oxygen in a form of anaerobic
respiration.
Salmonella typhimurium produces H2S from thiosulfate or sulfite.
S. enterica uses gut inflammation to enhance its sulfur related respiration to outgrow the resident microbes in the intestinal lumen (microbiota). The inflammation creates tetrathionate $S_4O_6^{2-}$ in which the sulfur has an average oxidation number of +2.5. This tetrathionate is reduced by the tetrathionate reductase into thiosulfate with sulfur having +2 oxidation number. So sulfur related respiration helps to make growth faster in order to colonize the gut.
Here we show that reactive oxygen species generated during
inflammation react with endogenous, luminal sulphur compounds
(thiosulphate) to form a new respiratory electron acceptor,
tetrathionate. The genes conferring the ability to use tetrathionate
as an electron acceptor produce a growth advantage for S. Typhimurium
over the competing microbiota in the lumen of the inflamed gut. We
conclude that S. Typhimurium virulence factors induce host-driven
production of a new electron acceptor that allows the pathogen to use
respiration to compete with fermenting gut microbes. Thus the ability
to trigger intestinal inflammation is crucial for the biology of this
diarrhoeal pathogen.
Since $H_2S$ is a gasotransmitter in the human body, there can be other mechanisms which help S. enterica.
- in small amounts $H_2S$ has anti-inflammatory and anti-apoptotic effects
- in large amounts $H_2S$ has pro-inflammatory and pro-apoptotic effects
So S. enterica can probably cause inflammation due to killing cells with a fast release of $H_2S$ or prevent inflammation and keep infected cells alive with a slow release of $H_2S$. I found many evidence of the pro-inflammatory theory. By the anti-apoptotic theory I wasn't so lucky, I found only a single review about anti-apoptotic strategies of intracellular pathogens, but it did not mention $H_2S$ production as a possible mechanism. So it might not be true, further studies needed...
In the digestive system, H2S exerts potent anti-inflammatory actions,
regulates blood flow and smooth muscle tone, modulates epithelial
secretion and promotes healing of ulcers [4, 5].
Hydrogen sulfide (H2S) is the most recent endogenous gasotransmitter
that has been reported to serve many physiological and pathological
functions in different tissues. Studies over the past decade have
revealed that H2S can be synthesized through numerous pathways and its
bioavailability regulated through its conversion into different
biochemical forms. H2S exerts its biological effects in various
manners including redox regulation of protein and small molecular
weight thiols, polysulfides, thiosulfate/sulfite, iron-sulfur cluster
proteins, and anti-oxidant properties that affect multiple cellular
and molecular responses.
Understanding precise pathophysiological signaling mechanisms and the
metabolism of H2S is a topic of active research. Unraveling H2S
interactions within different tissues, with other biochemical
molecules and various signaling mediators is becoming ever more
complex.
These results demonstrate that H2S donors can down-regulate adhesion
molecule and proinflammatory cytokine expression, therefore
identifying H2S, its synthesis enzymes, and molecular targets (e.g.,
KATP channels) as potential targets for novel anti-inflammatory
therapies.
Thus, all of the above findings demonstrate that H2S induces
cytoprotection by an anti-apoptotic pathway.
A short course of H2S infusion was associated with reduction of lung
and kidney injury. Prolonged infusion did not enhance protection.
Systemically, infusion of H2S increased both the pro-inflammatory
response during endotoxemia, as demonstrated by increased TNF-α
levels, as well as the anti-inflammatory response, as demonstrated by
increased IL-10 levels. In LPS-stimulated whole blood of healthy
volunteers, co-incubation with H2S had solely anti-inflammatory
effects, resulting in decreased TNF-α levels and increased IL-10
levels. Co-incubation with a neutralizing IL-10 antibody partly
abrogated the decrease in TNF-α levels. In conclusion, a short course
of H2S infusion reduced organ injury during endotoxemia, at least in
part via upregulation of IL-10.
H2S causes apoptosis in HPSCs by activating the mitochondrial pathway.
It is suggested that H2S might be one of the factors modifying the
pathogenesis of pulpitis by causing loss of viability of HPSCs through
apoptosis.
The level ofendogenous H2S was increasing along with the infection
occurrence and the gradient of infection aggravate. We can presume
that endogenous H2S participated in inflammatory reaction of abdominal
infection and could be one of the serology index which concerned with
the gradient of infection.
The evidences showed that H2S has an obvious effect on colon smooth
muscle contraction, and can increase the intestinal movements in slow
transmit constipation. Our experiment states that H2S has
anti-inflammation effect in prophase of acute peritoneal cavity
infection.
H2S is believed to have two contradicting roles in inflammation. It
acts as both pro- and anti-inflammatory molecule(9). Li et al.
reported that the physiological concentration of H2S has
anti-inflammatory effects, while higher concentrations of H2S can
produce pro-inflammatory effects(10). The H2S inflammatory role was
also studied in different systems. In the gastrointestinal tract, the
H2S regulating role functions by activating KATP channels in order to
promote the inflammation response(57). The similar H2S function was
observed in pancreas(7), but the actual mechanisms are largely
unknown. In conclusion, H2S pathway is a possible route for targeting
the inflammation treatment. However, much work needs to be done for
understanding the mechanisms of the contradictory roles of H2S in
inflammation.
Developing evidence suggests that dysbiosis (abnormal microbial
composition or function) can contribute to if not cause chronic
intestinal inflammation. 5,7 This inflammation can be caused either by
an abnormal composition of entericbacteria with an elevated ratio of
aggressive vs protective species, defective production of short-chain
fatty acids and other protective microbial products, or enhanced
production of hydrogen sulfide and nitrates that block butyrate
metabolism and disrupt the mucosal barrier.
These results showed that physiological concentrations of H2S can
induce apoptosis of PDL cells and HGFs in periodontitis, suggesting
that H2S may play an important role in periodontal tissue damage in
periodontal diseases.
We have shown that inactivation of H2S producing enzymes
(cystathionine beta-synthase, cystathionine gamma lyase, or
3-mercaptopyruvate sulfurtransferase) and NO-synthase in several Gram
(+) and Gram (−) bacteria render them highly sensitive to different
classes of antibiotics (Gusarov et al., Science 325 (2009) 1380–1384;
Shatalin et al. Science 334 (2011) 986–990). We also presented
evidence that Bacillus anthracis-derived NO is critical at the early
stage of infection (Shatalin et al. PNAS 105 (2008) 1009–1013). Here
we show that: (1) cbs/cse and nos mutations change Bacilli global gene
transcription profile; (2) apore formation process in cbs/cse and nos
mutants of B. anthracis is affected; (3) virulence of cbs/cse and nos
mutants of B. anthracis is diminished. These results demonstrate that
bacterial H2S and NO are an important virulence factors, and that
enzymes generated these gases may serve as an attractive target for
antimicrobial therapy.
Btw. there is non-hydrogen sulfide producing S. enterica too, which can probably (no study about this yet) cause salmonellosis. So using thiosulfate as electron acceptor and producing $H_2S$ might not be essential by the infection. (There are other non-sulfur electron acceptors e.g. nitrate, fumarate, etc... for the case of anaerob metabolism.)
Overall hydrogen-sulfide and other gasotransmitters are important virulence factors of many pathogens.
