Potential role of HPA axis and sympathetic nervous responses in depletion of B cells induced by H9N2 avian influenza virus infection.
Except severe pulmonary disease caused by influenza virus infection, an impaired immune system is also a clinic characteristic. However, the mechanism(s) of influenza virus infection-induced depletion of B cells was unknown. Here, we compared the effect of two variant virulence H9N2 virus infections...
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2012-01-01
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doaj-872c06570ae54a0f8a2a627bb71216622020-11-25T00:11:44ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-01712e5102910.1371/journal.pone.0051029Potential role of HPA axis and sympathetic nervous responses in depletion of B cells induced by H9N2 avian influenza virus infection.Wenbao QiJin TianChanghui ZhangJun HeZhangyong NingPeirong JiaoMing LiaoExcept severe pulmonary disease caused by influenza virus infection, an impaired immune system is also a clinic characteristic. However, the mechanism(s) of influenza virus infection-induced depletion of B cells was unknown. Here, we compared the effect of two variant virulence H9N2 virus infections on mouse B cells. Our study found that the infection with highly pathogenic virus (V) of led to depletion of spleen B cells and bone marrow (BM) early B cells, compared to lowly pathogenic virus (Ts). Moreover, high apoptosis and cell cycle arrest in spleen and BM were detected, suggesting important factors for the reduction of B cells in both organs. Further, this effect was not caused by virus replication in spleen and BM. Compared to Ts virus infection, V virus resulted in higher glucocorticoids (GCs) and lower leptin level in plasma. Intraperitoneal GCs receptor antagonist RU486 injection was sufficient to prevent the loss of spleen B cell and BM pro- and immature B cells, but similar result was not observed in leptin-treated mice. Depletion of spleen B cells and BM pro-B cells was also reversed by chemical sympathectomy mediated by the norepinephrine (NE) analog 6-hydroxydopamine (6-OHDA), but the treatment didn't affect the GCs level. This study demonstrated that depletion of B cells induced by H9N2 AIV was dependent on HPA axis and sympathetic response.http://europepmc.org/articles/PMC3519482?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Wenbao Qi Jin Tian Changhui Zhang Jun He Zhangyong Ning Peirong Jiao Ming Liao |
spellingShingle |
Wenbao Qi Jin Tian Changhui Zhang Jun He Zhangyong Ning Peirong Jiao Ming Liao Potential role of HPA axis and sympathetic nervous responses in depletion of B cells induced by H9N2 avian influenza virus infection. PLoS ONE |
author_facet |
Wenbao Qi Jin Tian Changhui Zhang Jun He Zhangyong Ning Peirong Jiao Ming Liao |
author_sort |
Wenbao Qi |
title |
Potential role of HPA axis and sympathetic nervous responses in depletion of B cells induced by H9N2 avian influenza virus infection. |
title_short |
Potential role of HPA axis and sympathetic nervous responses in depletion of B cells induced by H9N2 avian influenza virus infection. |
title_full |
Potential role of HPA axis and sympathetic nervous responses in depletion of B cells induced by H9N2 avian influenza virus infection. |
title_fullStr |
Potential role of HPA axis and sympathetic nervous responses in depletion of B cells induced by H9N2 avian influenza virus infection. |
title_full_unstemmed |
Potential role of HPA axis and sympathetic nervous responses in depletion of B cells induced by H9N2 avian influenza virus infection. |
title_sort |
potential role of hpa axis and sympathetic nervous responses in depletion of b cells induced by h9n2 avian influenza virus infection. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2012-01-01 |
description |
Except severe pulmonary disease caused by influenza virus infection, an impaired immune system is also a clinic characteristic. However, the mechanism(s) of influenza virus infection-induced depletion of B cells was unknown. Here, we compared the effect of two variant virulence H9N2 virus infections on mouse B cells. Our study found that the infection with highly pathogenic virus (V) of led to depletion of spleen B cells and bone marrow (BM) early B cells, compared to lowly pathogenic virus (Ts). Moreover, high apoptosis and cell cycle arrest in spleen and BM were detected, suggesting important factors for the reduction of B cells in both organs. Further, this effect was not caused by virus replication in spleen and BM. Compared to Ts virus infection, V virus resulted in higher glucocorticoids (GCs) and lower leptin level in plasma. Intraperitoneal GCs receptor antagonist RU486 injection was sufficient to prevent the loss of spleen B cell and BM pro- and immature B cells, but similar result was not observed in leptin-treated mice. Depletion of spleen B cells and BM pro-B cells was also reversed by chemical sympathectomy mediated by the norepinephrine (NE) analog 6-hydroxydopamine (6-OHDA), but the treatment didn't affect the GCs level. This study demonstrated that depletion of B cells induced by H9N2 AIV was dependent on HPA axis and sympathetic response. |
url |
http://europepmc.org/articles/PMC3519482?pdf=render |
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