Acute murine-betacoronavirus infection impairs testicular steroidogenesis and the quality of sperm production.

Although several testicular alterations promoted by coronavirus infection have been demonstrated, the extent, causes, and players of testicular pathogenesis are not totally understood. The present study aimed to investigate the short-term effects on male fertility of intranasally administered murine hepatitis virus strain 3 (MHV-3), a member of the genus Betacoronavirus, which causes a severe systemic acute infection. This mouse model might be used as a in vivo prototype for investigating the impact of betacoronavirus on the endocrine and exocrine testicular functions with the advantage to be performed in a biosafety level 2 condition. Herein, we performed virological, histopathological, and molecular studies regarding the testicular spermatogenesis and the spermatic quality analyses in an MHV-3-infected C57BL/6 mice. The main outcomes showed that MHV-3 infects mouse testis and induces a testicular inflammatory state, impairing the steroidogenic pathway. The infection led to several alterations in the testicular parenchyma, such as: seminiferous epithelium sloughing, retention of residual bodies, germ cell apoptosis, alterations in intercellular junction proteins, and worse spermatogenic parameters. Moreover, the levels of plasmatic testosterone as well as the quality of sperm production reduced. Therefore, the present data suggest that the viral/inflammatory impairment of the steroidogenic pathway and the consequent imbalance of androgen levels is critical in testicular pathology, disturbing the SC barrier function and the germ cell differentiation. Our study is important for comprehending the effects of beta coronavirus infections on testis function in order to develop treatments that could prevent virus-mediated male infertility.

Commensal microbiota is fundamental for the development of inflammatory pain.

The ability of an individual to sense pain is fundamental for its capacity to adapt to its environment and to avoid damage. The sensation of pain can be enhanced by acute or chronic inflammation. In the present study, we have investigated whether inflammatory pain, as measured by hypernociceptive responses, was modified in the absence of the microbiota. To this end, we evaluated mechanical nociceptive responses induced by a range of inflammatory stimuli in germ-free and conventional mice. Our experiments show that inflammatory hypernociception induced by carrageenan, lipopolysaccharide, TNF-alpha, IL-1beta, and the chemokine CXCL1 was reduced in germ-free mice. In contrast, hypernociception induced by prostaglandins and dopamine was similar in germ-free or conventional mice. Reduction of hypernociception induced by carrageenan was associated with reduced tissue inflammation and could be reversed by reposition of the microbiota or systemic administration of lipopolysaccharide. Significantly, decreased hypernociception in germ-free mice was accompanied by enhanced IL-10 expression upon stimulation and could be reversed by treatment with an anti-IL-10 antibody. Therefore, these results show that contact with commensal microbiota is necessary for mice to develop inflammatory hypernociception. These findings implicate an important role of the interaction between the commensal microbiota and the host in favoring adaptation to environmental stresses, including those that cause pain.

The effect of nitrous oxide on the inhibition of somatosensory evoked potentials by sevoflurane in children.

Inhalational anaesthetics inhibit somatosensory evoked potentials. The present study examined the effect of nitrous oxide in anaesthetic mixture with sevoflurane on the somatosensory evoked potential in children. Forty-five patients aged between 6 months and 6 years undergoing club foot surgery were studied to verify the influence of sevoflurane alone (21 patients) and sevoflurane with nitrous oxide (24 patients) on the somatosensory evoked potential. Fractional inspired concentration of nitrous oxide and fractional end-tidal (alveolar) sevoflurane were measured to estimate the multiples and submultiples of the minimal alveolar concentration (age corrected). The somatosensory evoked potential signals were obtained by stimulation of the median nerve. Nitrous oxide (FI = 0.63 +/- 2.5) with sevoflurane caused more reduction in the amplitude of somatosensory evoked potential waves and a greater increase in the latency of somatosensory evoked potential waves in comparison with sevoflurane alone. The results show that it is possible to obtain the inhibition of somatosensory evoked potential with smaller concentrations of sevoflurane, when it is used with nitrous oxide.