One of the first things you need to determine (imo) is where the H2S is coming from. Is it released by s.aureus during fermentation/growth on the tissue? or is its release mediated by the immunesystem/woundhealing process. In the latter case, since LPS and LTA are both recognized by TLRs..my guess is that LTA would also induce H2S release. But i would not be surprised if the H2S is mainly released by s. aureus.

Dank Jeroen,

Thanks very much. I definitely need to read up on TLRs.

H2S is used by S.aureus as part of its defense against oxidation

(https://www.researchgate.net/publication/51808281_H2S_a_universal_defense_against_antibiotics_in_bacteria ).

To answer your question, both H2S scenarios you suggest are correct.

A) Staph makes its H2S from the growth on its host, i.e. from the host's cysteine and homocysteine I believe (and perhaps other sources too).

B) However, my original question really involves the host making even more H2S. We make H2S as a response to stress through two enzymes (CBS, CSE). On page 570 of the following article "Roles of nitric oxide, carbon monoxide, and hydrogen sulfide in the regulation of the hypothalamic–pituitary–adrenal axis" (see http://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2010.06606.x/abstract) I read that LPS upregulates our gene expression for one of these enzymes (CSE).

Given that H2S is so prevalent in certain Staph infections (burn wounds, sepsis, etc.) I am assuming that LTA, like LPS, also upregulates our endogenous H2S production. This is the assumption I am trying to confirm for sure.

Which is more significant, A) Staph-made-H2S, or B) Staph-induced-host-made-H2S, I can not answer at this stage.

Many Thanks

Derek

(BTW, I hope the 300th year anniversary celebrations of the Treaty of Utrecht went well this year.)

Article H2S: A Universal Defense Against Antibiotics in Bacteria