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    • A paper in 2017 continues to explain the quandary. "Many studies have shown higher density of the parasites in diseased inflammatory skin than in normal skin, but whether it is the cause or result of the inflammation remains unclear." [6]  A paper in 2018 may help to resolve this issue because for the first time it has been discovered that Demodex mites secrete bioactive molecules that reduced TLR2 expression in sebocytes. [7] So while the jury is still out on this subject, What do you think?  Which comes first, the demodex or the rosacea? Does it even matter? With your above statement I highlighted and giving my view on this topic which comes first, I am also stating the same thing that I think demodex came first well it is not experiment or evidence based but with the experience I have had. Human Permanent Ectoparasites; Recent Advances on Biology and Clinical Significance of Demodex Mites: Narrative Review Article With this journal which you quoted in your article , "Many studies have shown higher density of the parasites in diseased inflammatory skin than in normal skin, but whether it is the cause or result of the inflammation remains unclear." So I was elaborating this sentence that higher density might be the result of inflammation (inflammatory immune response) and then subsequently the cause of inflammation. So I explained this with the term “reciprocal correlation”. And let’s say if the higher density is the result of inflammation, so the altered cutaneous immune responses are the cause of persistent inflammation and that is what I was trying to state in my post but then I read the above journal in detail after your question and I found the confirmation of my  expression with these sentences of journal   “ Studies indicate increased number of D. folliculorum in immunocompromised patients”  and “It remains to be determined which kind of cellular immunity may foster mites’ proliferation” and my statement “the false immune response(altered immune response) might be the cause of increasing number of demodex”  state the same thing. Thank you for questions because what I was stating is experience based but after thoroughly reading the reference journals from your article I found the confirmation of the same thing.    
    • That is difficult to follow. In a paper by Powell, et al, it is stated that the mites "secrete bioactive molecules that reduced TLR2 expression in Sebocytes." The 'bioactive molecules' that the mites secrete keep the innate immune system from reacting to the mites when in normal numbers on normal skin, so my question is what causes the demodex to proliferate in greater numbers to what you say,  "cause inflammatory immune response and inflammatory immune response" ?   Could you better explain what you mean by "self-antigen presentation to immune cells rather than non-self which is false immune response? ?
    • In my view, normal skin also has demodex mites but less in number so they can't activate pro-inflammatory cytokines but when the number is more they activate it. so logically when the normal skin flora has demodex before rosacea has occured so demodex apparently came first and because demodex mites cause inflammatory immune response and inflammatory immune response is not just related to mites but self-antigen presentation to immune cells rather than non-self which is false immune response or we call it autoimmune response and attacks to healthy cells and so the false immune response might be the cause of increasing number of demodex .So demodex and rosacea have reciprocity with each other to increase its effects and outcomes.
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