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 T2 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.

In humans, horses, and rodents, an association between pulmonary fibrotic disorders and gammaherpesvirus infection has been suggested. In dogs, canine idiopathic pulmonary fibrosis (CIPF), a progressive fibrotic lung disease of unknown origin and poorly understood pathophysiology, has been reported to occur in West Highland white terriers (WHWTs). The present study investigated the potential association between CIPF and herpesvirus infection. A PCR assay, using a mixture of degenerate and deoxyinosine-substituted primers targeting highly conserved regions of the DNA polymerase gene (DPOL) of herpesviruses, was applied on both lung and blood samples from WHWTs affected with CIPF and controls. Herpesvirus DPOL sequence could not be amplified from any of 46 lung samples (28 affected WHWTs and 18 control dogs of various breeds) and 38 blood samples (19 CIPF WHWTs and 19 control age-matched WHWTs) included. An association between CIPF and herpesvirus infection is therefore unlikely. Investigation of other causes of the disease is warranted.

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.

Chemokine (C‐C motif) ligand 2 (CCL2) is a chemotactic cytokine recruiting monocytes, releasing growth factors and promoting adhesion in vascular endothelium. Elevated serum and urinary CCL2 levels and expression of its receptor (CCR2) have been associated with tumorigenesis in human urinary malignancies. CCL2 implication has not been investigated in canine urothelial carcinoma. The aim of this study was to evaluate CCL2 serum and urine levels (measured by ELISA) in dogs with urothelial carcinoma or non‐neoplastic urinary tract disease. CCL2 serum and urine levels were significantly higher in diseased dogs compared with healthy dogs (P < 0.001). Dogs with carcinoma had significantly higher serum and urine CCL2 levels (P = 0.001) than healthy dogs. Dogs with metastases showed significantly lower serum and urine CCL2 levels compared with the non‐metastasised tumour group (P = 0.007). CCL2 as a diagnostic marker for urothelial carcinoma held a sensitivity of 95.2% and a specificity of 38.2% in the urine. As a staging marker, sensitivity was 85.7% and specificity was 57.1% with a positive predictive value of 75.7% and a negative predictive value of 71.9%. Further investigation is needed to define the role of CCL2 as a prognostic marker in canine urothelial carcinoma.

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