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

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Abstract

Background

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.

Methods

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.

Results

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).

Conclusion

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.

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Most cited references 27

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Mycoplasma pneumoniae and its role as a human pathogen.

Ken B Waites, Deborah F. Talkington (2004)

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.

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

Christopher Sims, Praxedis Martin, Carlos Ronchi … (2011)

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.

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IL-1F5, -F6, -F8, and -F9: a novel IL-1 family signaling system that is active in psoriasis and promotes keratinocyte antimicrobial peptide expression.

Candace Loyd, Xianying Xing, Frank Wang … (2011)

IL-1F6, IL-1F8, and IL-1F9 and the IL-1R6(RP2) receptor antagonist IL-1F5 constitute a novel IL-1 signaling system that is poorly characterized in skin. To further characterize these cytokines in healthy and inflamed skin, we studied their expression in healthy control, uninvolved psoriasis, and psoriasis plaque skin using quantitative RT-PCR and immunohistochemistry. Expression of IL-1F5, -1F6, -1F8, and -1F9 were increased 2 to 3 orders of magnitude in psoriasis plaque versus uninvolved psoriasis skin, which was supported immunohistologically. Moreover, treatment of psoriasis with etanercept led to significantly decreased IL-1F5, -1F6, -1F8, and -1F9 mRNAs, concomitant with clinical improvement. Similarly increased expression of IL-1F5, -1F6, -1F8, and -1F9 was seen in the involved skin of two mouse models of psoriasis. Suggestive of their importance in inflamed epithelia, IL-1α and TNF-α induced IL-1F5, -1F6, -1F8, and -1F9 transcript expression by normal human keratinocytes. Microarray analysis revealed that these cytokines induce the expression of antimicrobial peptides and matrix metalloproteinases by reconstituted human epidermis. In particular, IL-1F8 increased mRNA expression of human β-defensin (HBD)-2, HBD-3, and CAMP and protein secretion of HBD-2 and HBD-3. Collectively, our data suggest important roles for these novel cytokines in inflammatory skin diseases and identify these peptides as potential targets for antipsoriatic therapies.

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Author and article information

Contributors

Wei Ji: +86-512-67788302 , +86 512 67786204 , szdxjiwei@163.com

Yongdong Yan: yyd3060@163.com

Journal

Journal ID (nlm-ta): BMC Infect Dis

Journal ID (iso-abbrev): BMC Infect. Dis

Title: BMC Infectious Diseases

Publisher: BioMed Central (London )

ISSN (Electronic): 1471-2334

Publication date (Electronic): 17 May 2016

Publication date PMC-release: 17 May 2016

Publication date Collection: 2016

Volume: 16

Electronic Location Identifier: 212

Affiliations

[ ]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

Article

Publisher ID: 1555

DOI: 10.1186/s12879-016-1555-6

PMC ID: 4869194

PubMed ID: 27188891

SO-VID: 4f26e859-53f0-4121-b389-4cf9bda9060a

License:

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.

History

Date received : 20 November 2015

Date accepted : 10 May 2016

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;

Award ID: 81401296

Award ID: 81570016

Award Recipient : Zhengrong Chen Wei Ji

Funded by: Suzhou Science and Technology Projects

Award ID: SYS201350

Award Recipient : Zhengrong Chen

Funded by: Suzhou Science and Technology Projects

Award ID: SYS201435

Award Recipient : Yongdong Yan

Funded by: Science and Technology Projects of Suzhou sanitary bureau

Award ID: lczx201409

Award Recipient : Yongdong Yan

Funded by: Science and Technology Projects of Jiangsu Provincial Commission of Health and Family Planning

Award ID: Q201403

Award Recipient : Zhengrong Chen

Funded by: Science and Technology Projects of Chinese Traditional Medicine Bureau of Jiangsu Province

Award ID: YB2015176

Award Recipient : Zhengrong Chen

Custom metadata

ScienceOpen disciplines: Infectious disease & Microbiology

Keywords: mycoplasma pneumoniae pneumonia,b7-h3,interleukin 36,children,bronchoalveolar lavage fluid

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ScienceOpen disciplines: Infectious disease & Microbiology

Keywords: mycoplasma pneumoniae pneumonia, b7-h3, interleukin 36, children, bronchoalveolar lavage fluid

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

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Most cited references 27

Mycoplasma pneumoniae and its role as a human pathogen.

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

IL-1F5, -F6, -F8, and -F9: a novel IL-1 family signaling system that is active in psoriasis and promotes keratinocyte antimicrobial peptide expression.

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