Influence of immune status on the airborne colonization of piglets with methicillin-resistant staphylococcus aureus (MRSA) clonal complex (CC) 398

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Abstract

Colonized vertebrates including humans and pigs are to date the main reservoirs of livestock-associated Methicillin-resistant Staphylococcus aureus (LA-MRSA). Currently, the mechanisms underlying colonization of pigs are not fully understood.

We investigated the influence of piglet pre-immune status on airborne MRSA colonization. Three groups of MRSA-negative piglets were primed and exposed to airborne LA-MRSA (10 ⁴ colony forming units (cfu)/m ³) in an aerosol chamber for 24 h. One group was treated intramuscularly with dexamethasone (1 mg/kg body weight) to imitate weaning stress. The second group was exposed to bacterial endotoxin containing MRSA aerosol. Both conditions play a role in the development of multifactorial diseases and may promote MRSA colonization success. The third group served as control.

The piglets' MRSA status was monitored for 21 days via swab samples. At necropsy, specific tissues and organs were analyzed. Blood was collected to examine specific immunological parameters.

The duration of MRSA colonization was not extended in both treated groups compared to the control group, indicating the two immune-status influencing factors do not promote MRSA colonization. Blood sample analysis confirmed a mild dexamethasone-induced immune suppression and typical endotoxin-related changes in peripheral blood. Of note, the low-dose dexamethasone treatment showed a trend of increased MRSA clearance.

Most cited references 32

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Immune regulation by glucocorticoids

Derek Cain, JOHN CIDLOWSKI (2017)

In this Review, the authors discuss the effects of glucocorticoids on both innate and adaptive immunity. They explain the mechanistic basis of glucocorticoid-mediated immunosuppression and highlight the less well-appreciated roles of glucocorticoids in enhancing immune responses.

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Staphylococcus aureus Colonization: Modulation of Host Immune Response and Impact on Human Vaccine Design

Aisling F. Brown, John Leech, Thomas R. Rogers … (2014)

In apparent contrast to its invasive potential Staphylococcus aureus colonizes the anterior nares of 20–80% of the human population. The relationship between host and microbe appears particularly individualized and colonization status seems somehow predetermined. After decolonization, persistent carriers often become re-colonized with their prior S. aureus strain, whereas non-carriers resist experimental colonization. Efforts to identify factors facilitating colonization have thus far largely focused on the microorganism rather than on the human host. The host responds to S. aureus nasal colonization via local expression of anti-microbial peptides, lipids, and cytokines. Interplay with the co-existing microbiota also influences colonization and immune regulation. Transient or persistent S. aureus colonization induces specific systemic immune responses. Humoral responses are the most studied of these and little is known of cellular responses induced by colonization. Intriguingly, colonized patients who develop bacteremia may have a lower S. aureus-attributable mortality than their non-colonized counterparts. This could imply a staphylococcal-specific immune “priming” or immunomodulation occurring as a consequence of colonization and impacting on the outcome of infection. This has yet to be fully explored. An effective vaccine remains elusive. Anti-S. aureus vaccine strategies may need to drive both humoral and cellular immune responses to confer efficient protection. Understanding the influence of colonization on adaptive response is essential to intelligent vaccine design, and may determine the efficacy of vaccine-mediated immunity. Clinical trials should consider colonization status and the resulting impact of this on individual patient responses. We urgently need an increased appreciation of colonization and its modulation of host immunity.

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Glucocorticoids exert opposing effects on macrophage function dependent on their concentration.

Nora Müller, Christian Herold, Ji Hee Lim … (2007)

Glucocorticoids (GCs) are involved in the modulation of macrophage function and thereby control the host's immune responses to pathogens. However, neither the role of hormone concentration nor the differential contribution of the glucocorticoid (GR) and the mineralocorticoid receptors (MR) to these activities are known. Here we show that low levels of corticosterone enhance NO production as well as mRNA expression of pro-inflammatory cytokines, chemokines and enzymes required for mediator synthesis. In contrast, at high corticosterone concentrations macrophage function was strongly repressed. Importantly, inactivation of the GR by lentiviral delivery of siRNAs abrogated both the immunostimulatory and the immunosuppressive GC actions whereas inactivation of the MR had no effect. Furthermore, removal of endogenous GCs by adrenalectomy in vivo induced a preactivated state in macrophages that could be modulated by corticosterone. We conclude that GCs exert distinct effects on macrophage function dependent on their concentration, and that they primarily act through the GR despite concomitant expression of the MR.

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Author and article information

Journal

Journal ID (publisher-id): 1886

Title: European Journal of Microbiology and Immunology

Abbreviated Title: EuJMI

Publisher: Akadémiai Kiadó

ISSN (Electronic): 2062-8633

Publication date (Print): March 2020

Publication date (Electronic): March 2020

Volume: 10

Issue: 1

Pages: 1-10

Affiliations

[1 ] Institute for Animal Hygiene and Environmental Health, Centre for Infection medicine, Department for Veterinary Medicine, Freie Universitaet Berlin , Berlin, Germany

[2 ] Institute of Immunology, Centre for Infection medicine, Department for Veterinary Medicine, Freie Universitaet Berlin , Berlin, Germany

[3 ] Institute for Veterinary Epidemiology and Biostatistics, Freie Universitaet Berlin , Berlin, Germany

Author notes

[*]

Author for correspondence: Institute for Animal Hygiene and Environmental Health, Robert-von-Ostertag-Str. 7-13, 14163, Berlin; Kerstin.Rosen@ 123456fu-berlin.de ; tierhygiene@ 123456vetmed.fu-berlin.de ; Phone: +49 30 838 60908; Fax: +49 30 838 451863.

Article

DOI: 10.1556/1886.2019.00024

PMC ID: 7182117

SO-VID: 80a1babe-393c-461a-a8e1-438fce4d4622

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License ( https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes - if any - are indicated.

History

Date received : 11 November 2019

Date accepted : 14 December 2019

Page count

Pages: 10

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