showed that mice temporarily impaired in their anti-inflammatory response suffered substantial survival costs, but only when in advanced age. To our knowledge, reproductive costs of failure of the anti-inflammatory network have never been investigated yet, in spite of germ line being particularly sensitive to infection and free radical species released during the oxidative burst . 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 around the blockade of the IL-10. Conclusions Our results provide evidence that immune regulation confers protection against the risk of inflammation-induced infertility during contamination. They also suggest that disruption of the effectors involved in the regulation of the inflammatory response can have serious fitness consequences even under moderate inflammatory insult and benign environmental conditions. Introduction Ecological immunology has emerged as a discipline in the late 90th with the fundament that anti-parasite defenses cannot confer maximal protection because of the costs associated with immunity , . Early studies focused CCT251545 on i) the metabolic costs of immune maintenance and activation C; ii) the life history consequences of immune activation C. Even though not all studies converged towards measurable costs of immunity , , an overall picture emerged consistent with the view that the expression of immune defenses is usually constrained by the associated costs , . This early work mostly neglected the costs that are induced by a misdirected or an overreacting immune response (but see , ). Both antigen-specific and antigen non-specific immune responses can be erroneously directed against the host cells and tissue potentially generating devastating damage . Immune disorders are among the most prevalent human diseases and again involve both antigen-specific and antigen non-specific mechanisms. Autoimmunity and immunopathology have understandably drawn considerable attention from biomedical scientists, but we still largely ignore how they can shape the evolution of immune defenses and parasite exploitation strategies C. This gap on our knowledge around the fitness consequences of immunopathology has started to be filled with studied conducted on laboratory and free-ranging animals C. Inflammation is one of the most important components of immune protection. Upon entering in contact with GRS pathogen antigens, cells of the inflammatory response release signaling molecules (pro-inflammatory cytokines) which amplify the response by recruiting other macrophages and granulocytes to the contamination site. These cytokines can therefore be seen as a turn on signal. As long as effector cells do produce these signaling molecules the inflammatory process continues. To prevent inflammatory damage, another set of signaling molecules have the function of turning the signal off. These regulatory, anti-inflammatory cytokines play therefore an essential role to maintain organism homeostasis during the contamination, and studies on humans and mice have shown the involvement of poor immune regulation in several inflammatory diseases . Aging is accompanied by profound changes in the functioning of the immune system C. The number of na? ve T lymphocytes declines with age making elderly less able to respond to novel antigens , . Senescent immune profiles are usually also characterized by an increase of inflammatory markers , , whose cause might be an impaired regulation . Recently, a few papers have resolved the fitness consequences of impaired immune regulation of the inflammatory response using a phenotypic manipulation that blocks the receptors of one of the principal anti-inflammatory cytokines (IL-10). These studies have shown that disrupting the anti-inflammatory response exacerbates the cost of contamination in mice infected with parasites . Similarly, using bacterial lipopolysaccharide as a proxy of bacterial infection, Belloni et al.  showed that mice temporarily impaired in their anti-inflammatory response suffered substantial survival costs, but CCT251545 only when in advanced age. To our knowledge, reproductive costs of failure of the anti-inflammatory CCT251545 network have never been investigated yet, in spite of germ line being particularly sensitive to contamination and free radical species released during the oxidative burst . Infection and inflammation can.