+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Increased concentrations of soluble B7-H3 and interleukin 36 in bronchoalveolar lavage fluid of Children with Mycoplasma pneumoniae pneumonia


      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.



          The purpose of this study is to explore the correlations of interleukin 36 (IL-36) and Soluble B7-H3 (sB7-H3) levels in bronchoalveolar lavage fluid (BALF) with clinical characteristics and laboratory findings.


          A total of 35 children with M. pneumnoiae pneumonia (MPP) and 15 control subjects were enrolled. BALF concentrations of sB7-H3 and IL-36 were detected using enzyme-linked immunosorbent assays and clinical profiles of children with MPP were obtained.


          Children with MPP had significantly higher levels of sB7-H3 and IL-36 compared to control subjects (both P < 0.05). Meanwhile, children with pleural effusion had significantly higher levels of sB7-H3 and IL-36 compared to children without pleural effusion (both P < 0.05). BALF concentration of sB7-H3 was strongly associated with concentration of IL-36 ( r = 0.796, P < 0.0001) and sB7-H3 was correlated with duration of fever ( r = 0.427, P = 0.11) and length of stay ( r = 0.345, P = 0.043). Both concentrations of sB7-H3 and IL-36 were significantly decreased in convalescent phase after treatment (both P < 0.05).


          Both soluble B7-H3 and IL-36 may play an important role in pathogenesis of M. pneumoniae infection and sB7-H3 could be useful as a prognostic predictor or biomarker of MPP.

          Electronic supplementary material

          The online version of this article (doi:10.1186/s12879-016-1555-6) contains supplementary material, which is available to authorized users.

          Related collections

          Most cited references27

          • Record: found
          • Abstract: found
          • Article: not found

          Mycoplasma pneumoniae and its role as a human pathogen.

          Mycoplasma pneumoniae is a unique bacterium that does not always receive the attention it merits considering the number of illnesses it causes and the degree of morbidity associated with it in both children and adults. Serious infections requiring hospitalization, while rare, occur in both adults and children and may involve multiple organ systems. The severity of disease appears to be related to the degree to which the host immune response reacts to the infection. Extrapulmonary complications involving all of the major organ systems can occur in association with M. pneumoniae infection as a result of direct invasion and/or autoimmune response. The extrapulmonary manifestations are sometimes of greater severity and clinical importance than the primary respiratory infection. Evidence for this organism's contributory role in chronic lung conditions such as asthma is accumulating. Effective management of M. pneumoniae infections can usually be achieved with macrolides, tetracyclines, or fluoroquinolones. As more is learned about the pathogenesis and immune response elicited by M. pneumoniae, improvement in methods for diagnosis and prevention of disease due to this organism may occur.
            • Record: found
            • Abstract: found
            • Article: not found

            IL-36R ligands are potent regulators of dendritic and T cells.

            IL-36α (IL-1F6), IL-36β (IL-1F8), and IL-36γ (IL-1F9) are members of the IL-1 family of cytokines. These cytokines bind to IL-36R (IL-1Rrp2) and IL-1RAcP, activating similar intracellular signals as IL-1, whereas IL-36Ra (IL-1F5) acts as an IL-36R antagonist (IL-36Ra). In this study, we show that both murine bone marrow-derived dendritic cells (BMDCs) and CD4(+) T lymphocytes constitutively express IL-36R and respond to IL-36α, IL-36β, and IL-36γ. IL-36 induced the production of proinflammatory cytokines, including IL-12, IL-1β, IL-6, TNF-α, and IL-23 by BMDCs with a more potent stimulatory effect than that of other IL-1 cytokines. In addition, IL-36β enhanced the expression of CD80, CD86, and MHC class II by BMDCs. IL-36 also induced the production of IFN-γ, IL-4, and IL-17 by CD4(+) T cells and cultured splenocytes. These stimulatory effects were antagonized by IL-36Ra when used in 100- to 1000-fold molar excess. The immunization of mice with IL-36β significantly and specifically promoted Th1 responses. Our data thus indicate a critical role of IL-36R ligands in the interface between innate and adaptive immunity, leading to the stimulation of T helper responses.
              • Record: found
              • Abstract: found
              • Article: not found

              Regulation and function of interleukin-36 cytokines in homeostasis and pathological conditions.

              IL-36α, IL-36β, and IL-36γ are members of the IL-1 family of cytokines that signal through a common receptor composed of IL-36R and IL-1R/AcP to activate NF-κB and MAPKs, such as p38 and JNK, and promote inflammatory responses. IL-36Ra is a natural antagonist of the 3 IL-36 agonists that binds to IL-36R and inhibits binding of the agonistic ligands. These cytokines are expressed predominantly by epithelial cells and act on a number of cells, including immune cells, epithelial cells, and fibroblasts. Processing of the N terminus is required for full agonist or antagonist activity for all IL-36 members. The role of IL-36 has been demonstrated extensively in the skin, where it can act on keratinocytes and immune cells to induce a robust inflammatory response and is implicated strongly through functional and genetic evidence in the pathology of psoriatic disorders. Emerging data also suggest a role for this cytokine family in pulmonary physiology and pathology. Although much has been learned about the biochemistry of IL-36 and its role in various tissues, it is clear that we are at an early stage in our understanding of the full biology of these cytokines.

                Author and article information

                +86-512-67788302 , +86 512 67786204 , szdxjiwei@163.com
                BMC Infect Dis
                BMC Infect. Dis
                BMC Infectious Diseases
                BioMed Central (London )
                17 May 2016
                17 May 2016
                : 16
                : 212
                [ ]Department of Respiratory Disease, Children’s Hospital of Soochow University, Soochow University, Suzhou, China
                [ ]General surgery department, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
                [ ]Clinical Immunology Laboratory, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
                © Chen et al. 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                : 20 November 2015
                : 10 May 2016
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81401296
                Award ID: 81570016
                Award Recipient :
                Funded by: Suzhou Science and Technology Projects
                Award ID: SYS201350
                Award Recipient :
                Funded by: Suzhou Science and Technology Projects
                Award ID: SYS201435
                Award Recipient :
                Funded by: Science and Technology Projects of Suzhou sanitary bureau
                Award ID: lczx201409
                Award Recipient :
                Funded by: Science and Technology Projects of Jiangsu Provincial Commission of Health and Family Planning
                Award ID: Q201403
                Award Recipient :
                Funded by: Science and Technology Projects of Chinese Traditional Medicine Bureau of Jiangsu Province
                Award ID: YB2015176
                Award Recipient :
                Research Article
                Custom metadata
                © The Author(s) 2016

                Infectious disease & Microbiology
                mycoplasma pneumoniae pneumonia,b7-h3,interleukin 36,children,bronchoalveolar lavage fluid


                Comment on this article