Rotavirus intestinal infection induces an oral mucosa cytokine response

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Abstract

Introduction

Salivary glands are known immune effector sites and considered to be part of the whole mucosal immune system. The aim of the present study was to assess the salivary immune response to rotavirus (RV) infection through the analysis of the cytokine immune profile in saliva.

Material and methods

A prospective comparative study of serial saliva samples from 27 RV-infected patients (sampled upon admission to the hospital during acute phase and at convalescence—i.e. at least three months after recovery) and 36 healthy controls was performed. Concentrations of 11 salivary cytokines (IFN-γ, IFN-α ₂, IL-1β, IL-6, IL-8, IL-10, IL-15, IL12 _p70, TNF-α, IFN-λ ₁, IL-22) were determined. Cytokine levels were compared between healthy controls acute infection and convalescence. The correlation between clinical data and salivary cytokine profile in infected children was assessed.

Results

The salivary cytokine profile changes significantly in response to acute RV infection. In RV-infected patients, IL-22 levels were increased in the acute phase with respect to convalescence ( P-value < 0.001). Comparisons between infected and control group showed significant differences in salivary IFN-α ₂, IL-1β, IL-6, IL-8, IL-10 and IL-22. Although acute-phase levels of IL-12, IL-10, IL-6 and IFN-γ showed nominal association with Vesikari’s severity, this trend did not reach statistical significance after multiple test adjustment.

Conclusions

RV infection induces a host salivary immune response, indicating that immune mucosal response to RV infection is not confined to the intestinal mucosa. Our data point to a whole mucosal implication in the RV infection as a result of the integrative mucosal immune response, and suggest the salivary gland as effector site for RV infection.

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The Class 2 alpha-helical cytokines consist of interleukin-10 (IL-10), IL-19, IL-20, IL-22, IL-24 (Mda-7), and IL-26, interferons (IFN-alpha, -beta, -epsilon, -kappa, -omega, -delta, -tau, and -gamma) and interferon-like molecules (limitin, IL-28A, IL-28B, and IL-29). The interaction of these cytokines with their specific receptor molecules initiates a broad and varied array of signals that induce cellular antiviral states, modulate inflammatory responses, inhibit or stimulate cell growth, produce or inhibit apoptosis, and affect many immune mechanisms. The information derived from crystal structures and molecular evolution has led to progress in the analysis of the molecular mechanisms initiating their biological activities. These cytokines have significant roles in a variety of pathophysiological processes as well as in regulation of the immune system. Further investigation of these critical intercellular signaling molecules will provide important information to enable these proteins to be used more extensively in therapy for a variety of diseases.

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Author and article information

Contributors

José Gómez-Rial:

ORCID: http://orcid.org/0000-0002-3173-8484

Role: ConceptualizationRole: Data curationRole: InvestigationRole: SupervisionRole: Writing – original draftRole: Writing – review & editing

María José Curras-Tuala: Role: InvestigationRole: MethodologyRole: Visualization

Irene Rivero-Calle: Role: ConceptualizationRole: MethodologyRole: Resources

Carmen Rodríguez-Tenreiro: Role: Project administration

Lorenzo Redondo-Collazo: Role: ResourcesRole: Visualization

Alberto Gómez-Carballa: Role: InvestigationRole: MethodologyRole: Software

Jacobo Pardo-Seco: Role: Data curationRole: Software

Antonio Salas: Role: ConceptualizationRole: Formal analysisRole: MethodologyRole: ResourcesRole: ValidationRole: Writing – review & editing

Federico Martinón-Torres: Role: Formal analysisRole: ResourcesRole: SupervisionRole: ValidationRole: Writing – review & editing

Miren Iturriza-Gómara: Role: Editor

Journal

Journal ID (nlm-ta): PLoS One

Journal ID (iso-abbrev): PLoS ONE

Journal ID (publisher-id): plos

Journal ID (pmc): plosone

Title: PLoS ONE

Publisher: Public Library of Science (San Francisco, CA USA )

ISSN (Electronic): 1932-6203

Publication date (Electronic): 5 April 2018

Publication date Collection: 2018

Volume: 13

Issue: 4

Electronic Location Identifier: e0195314

Affiliations

[1 ] Grupo de Investigación en Genética, Vacunas, Infecciones y Pediatría (GENVIP), Hospital Clínico Universitario de Santiago de Compostela, Galicia, Spain

[2 ] Laboratorio de Inmunología, Servicio de Análisis Clínicos, Hospital Clínico Universitario de Santiago de Compostela, Galicia, Spain

[3 ] Translational Pediatrics and Infectious Diseases, Department of Pediatrics, Hospital Clínico Universitario de Santiago de Compostela, Galicia, Spain

[4 ] GenPoB Research Group, Instituto de Investigaciones Sanitarias (IDIS), Hospital Clínico Universitario de Santiago de Compostela, Galicia, Spain

[5 ] Unidade de Xenética, Departamento de Anatomía Patolóxica e Ciencias Forenses, Instituto de Ciencias Forenses, Facultade de Medicina, Universidade de Santiago de Compostela, Galicia, Spain

University of Liverpool, UNITED KINGDOM

Author notes

Competing Interests: The authors also declare that no competing interests exist. Funding received from Merck Sharp and Dohme does not alter our adherence to PLOS ONE policies on sharing data and materials.

* E-mail: jose.gomez.rial@ 123456sergas.es

Author information

José Gómez-Rial http://orcid.org/0000-0002-3173-8484

Article

Publisher ID: PONE-D-17-33435

DOI: 10.1371/journal.pone.0195314

PMC ID: 5886481

PubMed ID: 29621276

SO-VID: 01429e0d-e0ea-4a97-b885-8ef4c3a0de37

License:

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

History

Date received : 15 September 2017

Date accepted : 20 March 2018

Page count

Figures: 2, Tables: 4, Pages: 11