title: Pharyngeal microflora disruption by antibiotics promotes airway hyperresponsiveness after respiratory syncytial virus infection.
abstract: 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 (ddH(2)O) 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.
authors: Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Chongqing Medical University, Chongqing, China.
authors: Ke
authors: K
authors: Ni
authors: Simin
authors: S
authors: Li
authors: Qiuling
authors: Q
authors: Xia
authors: Na
authors: N
authors: Zang
authors: Yu
authors: Y
authors: Deng
authors: Xiaohong
authors: X
authors: Xie
authors: Zhengxiu
authors: Z
authors: Luo
authors: Yan
authors: Y
authors: Luo
authors: Lijia
authors: L
authors: Wang
authors: Zhou
authors: Z
authors: Fu
authors: Enmei
authors: E
authors: Liu
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000009:adverse effects* / Q000627:therapeutic use*; D002438:Cefoperazone / Q000009:adverse effects / Q000627:therapeutic use; D005260:Female; D051858:Forkhead Transcription Factors / Q000235:genetics; D005786:Gene Expression Regulation / Q000187:drug effects / Q000276:immunology; D006967:Hypersensitivity / Q000209:etiology* / Q000276:immunology / Q000382:microbiology; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D054892:Metagenome / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D010614:Pharynx / Q000187:drug effects* / Q000382:microbiology*; D018357:Respiratory Syncytial Virus Infections / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: D000900:Anti-Bacterial Agents; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D053773:Transforming Growth Factor beta1; D002438:Cefoperazone