27 Apr 2018
Author
NellyP
Title

Chlamydia pneumoniae Hides inside Apoptotic Neutrophils to Silently Infect and Propagate in Macrophages

Body

http://www.plosone.org:80/article/info:doi/10.1371/journal.pone.0006020 Chlamydia pneumoniae Hides inside Apoptotic Neutrophils to Silently Infect and Propagate in Macrophages Jan Rupp1,2*, Lisa Pfleiderer3, Christiane Jugert1, Sonja Moeller1, Matthias Klinger4, Klaus Dalhoff2, Werner Solbach1, Steffen Stenger3, Tamas Laskay1, Ger van Zandbergen3* 1 Institute of Medical Microbiology and Hygiene, University of Luebeck, Luebeck, Germany, 2 Medical Clinic III, University hospital Schleswig-Holstein, Luebeck, Ger

Comments

Red

Oops, sorry Nelly.   Just posted the same article!   Very interesting...

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  Nelly and Red, you will live longer than me, I was also planning to post same article but you were faster.

  YILMAZ.

KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

 This article seems to be so important, because ıt make my mind confused about apoptosis. Whether apoptosis is good for us, or it's good for CPN? So do you think VitD3 and ALA help CPN by increasing apoptosis with viable cpn inside the apoptotic cells?

  YILMAZ

KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

Cpn doesn't want the cell to commit apoptosis while it's still growing and replicating inside the cell. Once its replication is finished, and all the RBs have transformed back into EBs, then it wants the cell to commit apoptosis.

Yes, I was surprised nobody seemed to be taking up on this one.

I too feel confused about what they seem to say re infected PMN apoptosis being gobbled up by macrophages which will result "in efficient propagation and immune protection within the human host" because it causes an increased TGF-ß production I too am confused, they seem to be looking at it as a positive aspect compared to direct infection of macrophages, characterized by an enhanced TNF-α response, which, they say, results in "persistent infection".

I would really like some feedback on this one.

I am a bit confused and I would like to understand what it might mean for us re treatment

Nelly (France-neuroLyme and ????)

 I will summarise what it means. When a macrophage is directly infected by CPN, evenif it can not kill CPN, it doesn't let CPN to multply, CPN turns to cryptic body resulting in permanent infection(that's just the same what protein synthesis inhibitors do).

 But if macrophage phagocytes an apoptptic PMN(with viable CPN in it), it doesn't see CPN and can not block it to multipy. Since macrophages are long living cells(a few months).This is auch a situation that even better than any CPN dreams. CPN can multiply again and again forminig thousands of EB as a result.

 Norman, as it's emphesized in the article CPN can not do the same in other cells. In PMNs, CPN can just delate apoptosis for a short time (from 48 hours to 66 hours in avarage) that means it gets only 18 hours extra. That's much shorter than a few months. So increasing apoptosis by using NF-kappa B inhibitors (such as ALA and VitD3) will probably give CPN more oppurtunity of being phagosited by an macrophage which is more than a dream as I said before.

   YILMAZ.

KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.