MPO & NADPH Oxidase question

[Qester]

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Hello everyone,

I had a question regarding how bacteria are killed in both of the situations.

So in NADPH Ox deficiency you can't make super oxide. You can still use the Bacteria H2O2 to make HOCL to kill bacteria except for catalase +.

In MPO deficiency you can make H2O2, but cant make HOCL.

So my question is, is why does MPO usually present as asymptomatic? Shouldn't they still have the same problem with catalase positive organisms? What is the clinical difference between the two and why?

 

[Jabbed]

Superoxide is potent enough to kill most pathogens in the absence of MPO. Note that catalase degrades hydrogen peroxide, but not superoxide.

 

[Qester]

Superoxide is potent enough to kill most pathogens in the absence of MPO. Note that catalase degrades hydrogen peroxide, but not superoxide.

So the NADPH Ox pathway intermediate of superoxide free radical is bacteriocidal, while hydrogen peroxide on its own is not, thus an MPO deficiency is not as bad as an NADPH oxidase?

 

[Jabbed]

So the NADPH Ox pathway intermediate of superoxide free radical is bacteriocidal, while hydrogen peroxide on its own is not, thus an MPO deficiency is not as bad as an NADPH oxidase?

Oxygen → superoxide → hydrogen peroxide → hypochlorite.

All three products are bactericidal because they all generate free radicals and oxidative damage. As far as free radicals go, superoxide and hypochlorite are the most potent and hydrogen peroxide is less so.

Defect in CGD blocks oxygen → superoxide. Defect in MPO deficiency blocks hydrogen peroxide → hypochlorite. Bacterial catalase can breakdown hydrogen peroxide. Most bacteria produce hydrogen peroxide.

In CGD patients, catalase negative bacteria basically supply hydrogen peroxide for the formation of hypochlorite. In MPO deficiency, the macrophage is still able to produce superoxide (most important) and hydrogen peroxide (less important) in sufficient enough quantities to kill the pathogens. Having some hypochlorite would be sweet as it is strongly bactericidal, but it is just really not that necessary in most cases. As an aside, the only testable bug that I've seen in MPO deficiency is candida.

 

[Jabbed]

So the NADPH Ox pathway intermediate of superoxide free radical is bacteriocidal, while hydrogen peroxide on its own is not, thus an MPO deficiency is not as bad as an NADPH oxidase?

PS:Sorry for the long and redundant post given that you knew most of that information. Writing it all out was more for my benefit as a review.

 

[Qester]

Oxygen → superoxide → hydrogen peroxide → hypochlorite.

All three products are bactericidal because they all generate free radicals and oxidative damage. As far as free radicals go, superoxide and hypochlorite are the most potent and hydrogen peroxide is less so.

Defect in CGD blocks oxygen → superoxide. Defect in MPO deficiency blocks hydrogen peroxide → hypochlorite. Bacterial catalase can breakdown hydrogen peroxide. Most bacteria produce hydrogen peroxide.

In CGD patients, catalase negative bacteria basically supply hydrogen peroxide for the formation of hypochlorite. In MPO deficiency, the macrophage is still able to produce superoxide (most important) and hydrogen peroxide (less important) in sufficient enough quantities to kill the pathogens. Having some hypochlorite would be sweet as it is strongly bactericidal, but it is just really not that necessary in most cases. As an aside, the only testable bug that I've seen in MPO deficiency is candida.

Perfect thanks for the clarification. The resources I've been using had described hypochlorite as *the* killing radical. Then proceeded to describe how CGD is a normal presentation except for Cat+ which made sense. Then it went on to say that MPO is essentially asymptomatic except to Candida, yet it lacked *the* killing radical, which given that information would make me presume it to be disastrous.

Thanks for clarifying again!