Pharyngeal microflora disruption by antibiotics promotes airway hyperresponsiveness after respiratory syncytial virus infection.
Pharyngeal microflora disruption by antibiotics promotes airway hyperresponsiveness after respiratory syncytial virus infection.
复制标题
抗生素对咽部微生物群的破坏促进呼吸道合胞病毒感染后气道高反应性
DOI:
10.1371/journal.pone.0041104
复制
发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Liu E
中科院分区:
文献类型:
--
作者:
Ni K;Li S;Xia Q;Zang N;Deng Y;Xie X;Luo Z;Luo Y;Wang L;Fu Z;Liu E
Background Regulatory T cells (Treg cells), which are essential for regulation of immune response to respiratory syncytial virus (RSV) infection, are promoted by pharyngeal commensal pneumococcus. The effects of pharyngeal microflora disruption by antibiotics on airway responsiveness and relative immune responses after RSV infection have not been clarified. Methods Female BALB/c mice (aged 3 weeks) were infected with RSV and then treated with either oral antibiotics or oral double distilled water (ddH2O) from 1 d post infection (pi). Changes in pharyngeal microflora were analyzed after antibiotic treatment for 7 d and 14 d. At 8 d pi and 15 d pi, the inflammatory cells in bronchoalveolar lavage fluid (BALF) were investigated in combination with tests of pulmonary histopathology, airway hyperresponsiveness (AHR), pulmonary and splenic Treg cells responses. Pulmonary Foxp3 mRNA expression, IL-10 and TGF-β1 in BALF and lung homogenate were investigated at 15 d pi. Ovalbumin (OVA) challenge was used to induce AHR after RSV infection. Results The predominant pharyngeal commensal, Streptococcus, was cleared by antibiotic treatment for 7 d. Same change also existed after antibiotic treatment for 14 d. After RSV infection, AHR was promoted by antibiotic treatment at 15 d pi. Synchronous decreases of pulmonary Treg cells, Foxp3 mRNA and TGF-β1 were detected. Similar results were observed under OVA challenge. Conclusions After RSV infection, antibiotic treatment cleared pharyngeal commensal bacteria such as Streptococcus, which consequently, might induce AHR and decrease pulmonary Treg cells.
登录
查看更多内容
DOI:
10.1086/592714
发表时间:
2008-11-15
期刊:
The Journal of infectious diseases
影响因子:
--
作者:
Estripeaut D;Torres JP;Somers CS;Tagliabue C;Khokhar S;Bhoj VG;Grube SM;Wozniakowski A;Gomez AM;Ramilo O;Jafri HS;Mejias A
通讯作者:
Mejias A
DOI:
10.4049/jimmunol.1000423
发表时间:
2010-08-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Fulton RB;Meyerholz DK;Varga SM
通讯作者:
Varga SM
DOI:
10.1152/ajplung.00521.2007
发表时间:
2009-03-01
影响因子:
4.9
作者:
Burchell, Jennifer T.;Wikstrom, Matthew E.;Turner, Debra J.
通讯作者:
Turner, Debra J.
影响因子:
158.5
作者:
Bisgaard, Hans;Hermansen, Mette Northman;Pipper, Christian Bressen
通讯作者:
Pipper, Christian Bressen
影响因子:
2.8
作者:
de Gutierrez, RC;de Nader, OM;Nader-Macias, ME
通讯作者:
Nader-Macias, ME