Potential role for alternatively activated macrophages in the secondary bacterial infection during recovery from influenza.
Potential role for alternatively activated macrophages in the secondary bacterial infection during recovery from influenza.
复制标题
DOI:
10.1016/j.imlet.2011.10.009
复制
发表时间:
2012-01-30
影响因子:
4.4
通讯作者:
Cross, Alan S.
中科院分区:
文献类型:
--
作者:
Chen, Wilbur H.;Toapanta, Franklin R.;Shirey, Kari Ann;Zhang, Lei;Giannelou, Angeliki;Page, Carly;Frieman, Matthew B.;Vogel, Stefanie N.;Cross, Alan S.
Secondary bacterial infections are a common complication of influenza. Innate immune host defenses appear to be impaired following influenza, leading to susceptibility to subsequent bacterial infections. Alternatively activated macrophages (AAM) in the lungs may play a critical role in eliciting the hypersusceptibility to secondary bacterial pneumonia. C57BL6 mice were challenged with sublethal doses of the mouse-adapted A/PR/8/34 (PR8) influenza virus or saline and allowed to recover. At complete recovery (day 14), mice were re-challenged with sublethal doses of Streptococcus pneumoniae serotype 3 (Sp3). PR8-recovered mice developed a rapidly fatal pulmonary infection to a 100-fold sublethal pneumococcal challenge, whereas PR8-naive mice demonstrated no mortality or illness. The cytokines which induce AAM (IL-4 and IL-13) and the expression of genes associated with AAM (Arginase-1, FIZZ1, and YM1) were elevated after PR8 infection. Flow cytometry suggests that alveolar macrophages demonstrate the AAM-phenotype, as indicated by MGL-1 and MHCII expression, in response to PR8 infection. Recovery from PR8 was associated with blunted cytokine responses to TLR ligands. The mechanisms of immune regulation during recovery from influenza are being elucidated. We provide evidence that pulmonary AAM are induced during influenza infection and may contribute to the elicitation of hypersusceptibility to a secondary bacterial infection.
登录
查看更多内容
DOI:
10.1086/591708
发表时间:
2008-10-01
期刊:
The Journal of infectious diseases
影响因子:
--
作者:
Morens DM;Taubenberger JK;Fauci AS
通讯作者:
Fauci AS
影响因子:
6.4
作者:
Peltola, VT;Murti, KG;McCullers, JA
通讯作者:
McCullers, JA
DOI:
10.1084/jem.176.1.287
发表时间:
1992-07-01
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Stein M;Keshav S;Harris N;Gordon S
通讯作者:
Gordon S
影响因子:
6.4
作者:
McCullers, JA;Bartmess, KC
通讯作者:
Bartmess, KC
影响因子:
15.3
作者:
Didierlaurent, Arnaud;Goulding, John;Patel, Seema;Snelgrove, Robert;Low, Lionel;Bebien, Magali;Lawrence, Toby;van Rijt, Leonie S.;Lambrecht, Bart N.;Sirard, Jean-Claude;Hussell, Tracy
通讯作者:
Hussell, Tracy