Polymicrobial sepsis and non-specific immunization induce adaptive immunosuppression to a similar degree.

Sepsis is frequently complicated by a state of profound immunosuppression, in its extreme form known as immunoparalysis. We have studied the role of the adaptive immune system in the murine acute peritonitis model. To read out adaptive immunosuppression, we primed post-septic and control animals by...

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Main Authors: Katrin Schmoeckel, Daniel M Mrochen, Jochen Hühn, Christian Pötschke, Barbara M Bröker
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2018-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC5802895?pdf=render
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spelling doaj-98f2ffda4dad4792a88861662477cf472020-11-25T02:47:26ZengPublic Library of Science (PLoS)PLoS ONE1932-62032018-01-01132e019219710.1371/journal.pone.0192197Polymicrobial sepsis and non-specific immunization induce adaptive immunosuppression to a similar degree.Katrin SchmoeckelDaniel M MrochenJochen HühnChristian PötschkeBarbara M BrökerSepsis is frequently complicated by a state of profound immunosuppression, in its extreme form known as immunoparalysis. We have studied the role of the adaptive immune system in the murine acute peritonitis model. To read out adaptive immunosuppression, we primed post-septic and control animals by immunization with the model antigen TNP-ovalbumin in alum, and measured the specific antibody-responses via ELISA and ELISpot assay as well as T-cell responses in a proliferation assay after restimulation. Specific antibody titers, antibody affinity and plasma cell counts in the bone marrow were reduced in post-septic animals. The antigen-induced splenic proliferation was also impaired. The adaptive immunosuppression was positively correlated with an overwhelming general antibody response to the septic insult. Remarkably, antigen "overload" by non-specific immunization induced a similar degree of adaptive immunosuppression in the absence of sepsis. In both settings, depletion of regulatory T cells before priming reversed some parameters of the immunosuppression. In conclusion, our data show that adaptive immunosuppression occurs independent of profound systemic inflammation and life-threatening illness.http://europepmc.org/articles/PMC5802895?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Katrin Schmoeckel
Daniel M Mrochen
Jochen Hühn
Christian Pötschke
Barbara M Bröker
spellingShingle Katrin Schmoeckel
Daniel M Mrochen
Jochen Hühn
Christian Pötschke
Barbara M Bröker
Polymicrobial sepsis and non-specific immunization induce adaptive immunosuppression to a similar degree.
PLoS ONE
author_facet Katrin Schmoeckel
Daniel M Mrochen
Jochen Hühn
Christian Pötschke
Barbara M Bröker
author_sort Katrin Schmoeckel
title Polymicrobial sepsis and non-specific immunization induce adaptive immunosuppression to a similar degree.
title_short Polymicrobial sepsis and non-specific immunization induce adaptive immunosuppression to a similar degree.
title_full Polymicrobial sepsis and non-specific immunization induce adaptive immunosuppression to a similar degree.
title_fullStr Polymicrobial sepsis and non-specific immunization induce adaptive immunosuppression to a similar degree.
title_full_unstemmed Polymicrobial sepsis and non-specific immunization induce adaptive immunosuppression to a similar degree.
title_sort polymicrobial sepsis and non-specific immunization induce adaptive immunosuppression to a similar degree.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2018-01-01
description Sepsis is frequently complicated by a state of profound immunosuppression, in its extreme form known as immunoparalysis. We have studied the role of the adaptive immune system in the murine acute peritonitis model. To read out adaptive immunosuppression, we primed post-septic and control animals by immunization with the model antigen TNP-ovalbumin in alum, and measured the specific antibody-responses via ELISA and ELISpot assay as well as T-cell responses in a proliferation assay after restimulation. Specific antibody titers, antibody affinity and plasma cell counts in the bone marrow were reduced in post-septic animals. The antigen-induced splenic proliferation was also impaired. The adaptive immunosuppression was positively correlated with an overwhelming general antibody response to the septic insult. Remarkably, antigen "overload" by non-specific immunization induced a similar degree of adaptive immunosuppression in the absence of sepsis. In both settings, depletion of regulatory T cells before priming reversed some parameters of the immunosuppression. In conclusion, our data show that adaptive immunosuppression occurs independent of profound systemic inflammation and life-threatening illness.
url http://europepmc.org/articles/PMC5802895?pdf=render
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