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      The Role of Infection in Acute Exacerbation of Idiopathic Pulmonary Fibrosis

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          Abstract

          Background

          Acute exacerbation of IPF (AE-IPF) is associated with high mortality. We studied changes in pathogen involvement during AE-IPF and explored a possible role of infection in AE-IPF.

          Objectives

          Our purpose is to investigate the role of infection in AE-IPF.

          Methods

          Overall, we recruited 170 IPF patients (48 AE-IPF, 122 stable) and 70 controls at Shanghai Pulmonary Hospital. Specific IgM against microbial pathogens and pathogens in sputum were assessed. RNA sequences of pathogens in nasopharyngeal swab of IPF patients were detected by PathChip. A panel of serum parameters reflecting immune function were assessed.

          Results

          Antiviral/bacterial IgM was higher in IPF vs. controls and in AE-IPF vs. stable IPF. Thirty-eight different bacterial strains were detected in IPF patient sputum. Bacteria-positive results were found in 9/48 (18.8%) of AE-IPF and in 26/122 (21.3%) stable IPF. Fifty-seven different viruses were detected in nasopharyngeal swabs of IPF patients. Virus-positive nasopharyngeal swabs were found in 18/30 (60%) of tested AE-IPF and in 13/30 (43.3%) of stable IPF. AE-IPF showed increased inflammatory cytokines (IL-6, IFN- γ, MIG, IL-17, and IL-9) vs. stable IPF and controls. Mortality of AE-IPF in one year (39.5%) was higher compared to stable IPF (28.7%) .Conclusions. IPF patients had different colonization with pathogens in sputum and nasopharyngeal swabs; they also displayed abnormally activated immune response, which was exacerbated during AE-IPF.

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          Most cited references28

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          Critical role of IL-17RA in immunopathology of influenza infection.

          Christopher Crowe, Kong Chen, Derek A. Pociask … (2009)
          Acute lung injury due to influenza infection is associated with high mortality, an increase in neutrophils in the airspace, and increases in tissue myeloperoxidase (MPO). Because IL-17A and IL-17F, ligands for IL-17 receptor antagonist (IL-17RA), have been shown to mediate neutrophil migration into the lung in response to LPS or Gram-negative bacterial pneumonia, we hypothesized that IL-17RA signaling was critical for acute lung injury in response to pulmonary influenza infection. IL-17RA was critical for weight loss and both neutrophil migration and increases in tissue myeloperoxidase (MPO) after influenza infection. However, IL-17RA was dispensable for the recruitment of CD8(+) T cells specific for influenza hemagglutinin or nucleocapsid protein. Consistent with this, IL-17RA was not required for viral clearance. However, in the setting of influenza infection, IL-17RA(-/-) mice showed significantly reduced levels of oxidized phospholipids, which have previously been shown to be an important mediator in several models of acute lung injury, including influenza infection and gastric acid aspiration. Taken together, these data support targeting IL-17 or IL-17RA in acute lung injury due to acute viral infection.
          Article 0 comments Cited 152 times – based on 0 reviews     Review now
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            IL-9 induces differentiation of TH17 cells and enhances function of FoxP3+ natural regulatory T cells.

            Wassim Elyaman, Elizabeth Bradshaw, Catherine Uyttenhove … (2009)
            The development of T helper (T(H))17 and regulatory T (T(reg)) cells is reciprocally regulated by cytokines. Transforming growth factor (TGF)-beta alone induces FoxP3(+) T(reg) cells, but together with IL-6 or IL-21 induces T(H)17 cells. Here we demonstrate that IL-9 is a key molecule that affects differentiation of T(H)17 cells and T(reg) function. IL-9 predominantly produced by T(H)17 cells, synergizes with TGF-beta1 to differentiate naïve CD4(+) T cells into T(H)17 cells, while IL-9 secretion by T(H)17 cells is regulated by IL-23. Interestingly, IL-9 enhances the suppressive functions of FoxP3(+) CD4(+) T(reg) cells in vitro, and absence of IL-9 signaling weakens the suppressive activity of nT(regs) in vivo, leading to an increase in effector cells and worsening of experimental autoimmune encephalomyelitis. The mechanism of IL-9 effects on T(H)17 and T(regs) is through activation of STAT3 and STAT5 signaling. Our findings highlight a role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.
            Article 0 comments Cited 150 times – based on 0 reviews     Review now
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              Interleukin-17 in host defence against bacterial, mycobacterial and fungal pathogens.

              Sing Way, M Kate Curtis (2009)
              The mammalian immune system is intricately regulated, allowing for potent pathogen-specific immunity to be rapidly activated in response to infection with a broad and diverse array of potential pathogens. As a result of their ability to differentiate into distinct effector lineages, CD4 T cells significantly contribute to pathogen-specific adaptive immune responses. Through the production of effector cytokines, CD4 T helper (Th) cells orchestrate the precise mobilization of specific immune cells to eradicate infection. The protective effects of the newly identified lineage of Th17 cells against pathogens like Klebsiella pneumoniae, Citrobacter rodentium and Candida albicans indicate the capacity of Th17 cells to confer protection against extracellular bacterial and fungal pathogens, filling a critical void in host immunity not covered by the classically described Th1 lineage that activates immunity to intracellular pathogens or the Th2 lineage that is important in protection against mucosal parasitic pathogens. Host defence by Th17 cells extends beyond protection against extracellular bacterial and fungal pathogens, as demonstrated in infections against intracellular bacteria like Listeria monocytogenes and Salmonella enterica, as well as Mycobacterium tuberculosis. Herein, we summarize both experimental data from mouse infection models and epidemiological studies in humans that demonstrate the protective effects of interleukin-17 and Th17 CD4 T cells in immunity to bacterial, mycobacterial and fungal pathogens.
              Article 0 comments Cited 141 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Hui-Ping Li:
                ORCID: http://orcid.org/0000-0002-6998-9828
                Journal
                Journal ID (nlm-ta): Mediators Inflamm
                Journal ID (iso-abbrev): Mediators Inflamm
                Journal ID (publisher-id): MI
                Title: Mediators of Inflammation
                Publisher: Hindawi
                ISSN (Print): 0962-9351
                ISSN (Electronic): 1466-1861
                Publication date Collection: 2019
                Publication date (Electronic): 3 January 2019
                Volume: 2019
                Electronic Location Identifier: 5160694
                Affiliations
                1Department of Respiratory Medicine, Shanghai Pulmonary Hospital, Tongji University, School of Medicine, Shanghai, China
                2School of Medicine, Suzhou University, Suzhou, China
                3McMaster University Hamilton, Department of Medicine and Pathology/Molecular Medicine, ON, Canada
                Author notes

                Guest Editor: Bishi Fu

                Author information
                http://orcid.org/0000-0002-6998-9828
                Article
                DOI: 10.1155/2019/5160694
                PMC ID: 6335849
                PubMed ID: 30718973
                SO-VID: c52bde63-51f4-4368-80c1-099a0ec10cee
                Copyright © Copyright © 2019 Dong Weng et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 27 June 2018
                Date revision received : 3 October 2018
                Date accepted : 5 November 2018
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81730002
                Award ID: 81670055
                Award ID: 81670056
                Award ID: 91442103
                Award ID: 81500052
                Award ID: 81570057
                Funded by: Ministry of Science and Technology of the People's Republic of China
                Award ID: 2016YFC1100200
                Award ID: 2016YFC1100204
                Funded by: Shanghai Hospital Development Center
                Award ID: 16CR3054A
                Funded by: Fundamental Research Funds for the Central Universities
                Award ID: 22120180020
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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