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Disrupting immune regulation incurs transient costs in male reproductive function.

Authors
  • Belloni, Virginia1
  • Sorci, Gabriele2
  • Paccagnini, Eugenio3
  • Guerreiro, Romain2
  • Bellenger, Jérôme4
  • Faivre, Bruno2
  • 1 Biogéosciences, CNRS UMR 6282, Université de Bourgogne, Dijon, France ; Department Tropical Medicine, University of Tulane, New Orleans, Louisiana, United States of America. , (France)
  • 2 Biogéosciences, CNRS UMR 6282, Université de Bourgogne, Dijon, France. , (France)
  • 3 Dipartimento di Biologia Evolutiva, Universita' di Siena, Siena, Italia.
  • 4 Lipides Nutrition Cancer, INSERM UMR 866, Université de Bourgogne, Dijon, France. , (France)
Type
Published Article
Journal
PLoS ONE
Publisher
Public Library of Science
Publication Date
Jan 01, 2014
Volume
9
Issue
1
Identifiers
DOI: 10.1371/journal.pone.0084606
PMID: 24400103
Source
Medline
Language
English
License
Unknown

Abstract

Immune protection against pathogenic organisms has been shown to incur costs. Previous studies investigating the cost of immunity have mostly focused on the metabolic requirements of immune maintenance and activation. In addition to these metabolic costs, the immune system can induce damage to the host if the immune response is mis-targeted or over-expressed. Given its non-specific nature, an over-expressed inflammatory response is often associated with substantial damage for the host. Here, we investigated the cost of an over-expressed inflammatory response in the reproductive function of male mice. We experimentally blocked the receptors of an anti-inflammatory cytokine (IL-10) in male mice exposed to a mild inflammatory challenge, with each treatment having an appropriate control group. The experiment was conducted on two age classes, young (3 month old) and old (15 month old) mice, to assess any age-related difference in the cost of a disrupted immune regulation. We found that the concomitant exposure to an inflammatory insult and the blockade of IL-10 induced a reduction in testis mass, compared to the three other groups. The frequency of abnormal sperm morphology was also higher in the group of mice exposed to the inflammatory challenge but did not depend on the blockade of the IL-10. Our results provide evidence that immune regulation confers protection against the risk of inflammation-induced infertility during infection. They also suggest that disruption of the effectors involved in the regulation of the inflammatory response can have serious fitness consequences even under mild inflammatory insult and benign environmental conditions.

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