Urodynamic and morphometric characteristics of the lower urogenital tract of male Beagle littermates from four months to two years of age.

OBJECTIVE: To describe functional and anatomic changes of the lower urogenital tract of healthy male dogs during the sexually immature period and up to 2 years of age by urodynamic and morphometric assessment. ANIMALS: 6 sexually intact male Beagle littermates. PROCEDURES: Dogs underwent electromyography-coupled urodynamic tests, CT-assisted retrograde urethrography, prostatic washes, and blood sampling monthly from 4 through 12 months of age and then at 3-month intervals. Urodynamic and morphometric variables and serum canine prostate-specific esterase concentrations were analyzed by statistical methods. RESULTS: Integrated pressure of the urethra was significantly increased beginning at 8 months of age, compared with earlier time points. Urethral pressure peak amplitudes varied among anatomic regions. During bladder filling, few electromyographic signals were concurrent with urethral pressure peaks; these were most commonly detected in the penile portion of the urethra. Urethral length and prostate gland volume were significantly greater from 7 to 24 months of age than at younger ages. Urethral length was approximately 26 to 27 cm after 9 months, and prostate gland volume was approximately 11 to 12 cm3 after 11 months of age. Serum canine prostate-specific esterase concentrations correlated with prostate gland volume. Urinary bladder threshold volume was significantly increased at 6 months of age, compared with that at 4 months, with a maximum of 197.7 mL at 24 months. CONCLUSIONS AND CLINICAL RELEVANCE: Urethral resistance was acquired at approximately 8 months of age, when growth of the lower urinary tract was incomplete. Electromyographic and integrated pressure measurement results and the distribution and amplitude of urethral pressure peaks highlighted the potential role of the prostate gland and possibly the bulbocavernosus muscles in control of continence.

A gammaherpesvirus licenses CD8 T cells to protect the host from pneumovirus-induced immunopathologies.

Human respiratory syncytial virus (RSV) is a pneumovirus that causes severe infections in infants worldwide. Despite intensive research, safe and effective vaccines against RSV have remained elusive. The main reason is that RSV infection of children previously immunized with formalin-inactivated-RSV vaccines has been associated with exacerbated pathology, a phenomenon called RSV vaccine-enhanced respiratory disease. In parallel, despite the high RSV prevalence, only a minor proportion of children develop severe diseases. Interestingly, variation in the immune responses against RSV or following RSV vaccination could be linked with differences of exposure to microbes during childhood. Gammaherpesviruses (γHVs), such as the Epstein-Barr virus, are persistent viruses that deeply influence the immune system of their host and could therefore affect the development of pneumovirus-induced immunopathologies for the long term. Here, we showed that a previous ɣHV infection protects against both pneumovirus vaccine-enhanced disease and pneumovirus primary infection and that CD8 T cells are essential for this protection. These observations shed a new light on the understanding of pneumovirus-induced diseases and open new perspectives for the development of vaccine strategies.

Author Correction: A gammaherpesvirus provides protection against allergic asthma by inducing the replacement of resident alveolar macrophages with regulatory monocytes.

In the version of this article initially published, the accession code for the RNA-seq data set deposited in the NCBI public repository Sequence Read Archive was missing from the 'Data availability' subsection of the Methods section. The accession code is SRP125477.

A gammaherpesvirus provides protection against allergic asthma by inducing the replacement of resident alveolar macrophages with regulatory monocytes.

The hygiene hypothesis postulates that the recent increase in allergic diseases such as asthma and hay fever observed in Western countries is linked to reduced exposure to childhood infections. Here we investigated how infection with a gammaherpesvirus affected the subsequent development of allergic asthma. We found that murid herpesvirus 4 (MuHV-4) inhibited the development of house dust mite (HDM)-induced experimental asthma by modulating lung innate immune cells. Specifically, infection with MuHV-4 caused the replacement of resident alveolar macrophages (AMs) by monocytes with regulatory functions. Monocyte-derived AMs blocked the ability of dendritic cells to trigger a HDM-specific response by the TH2 subset of helper T cells. Our results indicate that replacement of embryonic AMs by regulatory monocytes is a major mechanism underlying the long-term training of lung immunity after infection.