Identification and characterization of the genome of a papillomavirus from skin lesions of four-toed hedgehogs (Atelerix albiventris).

The present study describes the clinical and pathological characteristics of skin lesions in two four-toed hedgehogs (Atelerix albiventris). We performed inverse PCR to identify the genome of papillomavirus (PV) in the skin lesions and subsequently sequenced the full genome of the virus, which was tentatively named Atelerix albiventris papillomavirus 1 (AalbPV1). The overall sequences of the viral genomes of both four-toed hedgehogs were identical. This study first identified the presence of a novel PV in Japanese four-toed hedgehogs and provided genetic information about this virus.

Endometrial Disease in Six Cats with Clinical and Histopathological Features Resembling Atypical Endometrial Hyperplasia in Humans.

In humans, atypical endometrial hyperplasia (AEH) is considered as a precancerous lesion of endometrial adenocarcinoma (EA), from which it must be distinguished. Precancerous lesions have not been reported in cats with EA. We now document the histopathological features of endometrial lesions in six cats, which histopathologically resembled human AEH and had a good prognosis following ovariohysterectomy. Grossly, one cat presented with papillomatous nodules and three cats had pyometra. Histopathologically, proliferation of endometrial epithelial cells without atypia was observed in all cases. In some regions of the endometrium, cells had increased atypia and were arranged in stratified layers, which formed irregular ducts and papillary structures. No invasive behaviour or vascular invasion was observed. On the basis of these findings, the cats were diagnosed with non-invasive or early-stage adenocarcinoma. Immunohistochemistry for oestrogen receptor and progesterone receptor revealed an inverse correlation with the severity of the endometrial lesions and degree of malignancy of tumour cells. Ki67 labelling revealed that mitotic activity increased as the lesion developed. All cats survived, with a median survival time of 385 days (range: 229-744 days). The distribution of the histopathological endometrial changes and the non-invasive behaviour in these feline cases resemble cases of AEH in humans.

Spatial and Temporal Variations in Pigment and Species Compositions of Snow Algae on Mt. Tateyama in Toyama Prefecture, Japan.

Snow algae are photosynthetic microbes that inhabit the melting snow surface in alpine and polar regions. We analyzed the pigment and species composition of colored snow collected on Mt. Tateyama in Japan during the melting seasons of 2015 and 2016. High-performance liquid chromatographic analyses of the pigments extracted from the colored snow showed that their composition varied within the study area and were classified into four types: Type A (astaxanthin-monoester dominant), Type B (medium astaxanthin-monoester content), Type C (abundant primary carotenoids and free-astaxanthin), and Type D (abundant primary carotenoids and astaxanthin diesters). Types A and B were most commonly observed in the study area, whereas Types C and D appeared only at specific sites. Analysis of the 18S ribosomal RNA (18S rRNA) gene revealed six major amplicon sequence variants (ASVs) of snow algae, belonging to the Sanguina, Chloromonas, and Chlainomonas groups. The relative abundance of the algal ASVs showed that Sanguina was dominant (>48%) in both Types A and B, suggesting that the difference in astaxanthin abundance between the two types was caused by the production of pigments in the algal cells. The algal community structures of Types C and D differed from those of Types A and B, indicating that the primary carotenoids and astaxanthin diesters were derived from certain algal species in these types. Therefore, astaxanthin-rich Sanguina algae mostly induced the red snow that appeared widely in this alpine area; however, they were partially dominated by Chloromonas or Chlainomonas algae, causing different pigment compositions.

Regulation of the development of asthmatic inflammation by in situ CD4(+)Foxp3 (+) T cells in a mouse model of late allergic asthma.

CD4(+)Foxp3(+)T cells (Tregs) mediate homeostatic peripheral tolerance by suppressing helper T2 cells in allergy. However, the regulation of asthmatic inflammation by local (in situ) Tregs in asthma remains unclear. BALB/c mice sensitized and challenged with ovalbumin (OVA) (asthma group) developed asthmatic inflammation with eosinophils and lymphocytes, but not mast cells. The number of Tregs in the circulation, pulmonary lymph nodes (pLNs), and thymi significantly decreased in the asthma group compared to the control group without OVA sensitization and challenge in the effector phase. The development of asthmatic inflammation is inversely related to decreased Tregs with reduced mRNA expression such as interleukin (IL)-4, transforming growth factor-ß1, and IL-10, but not interferon-γ, in pLNs. Moreover, M2 macrophages increased in the local site. The present study suggests that Tregs, at least in part, may regulate the development of asthmatic inflammation by cell-cell contact and regional cytokine productions.

Reovirus type-2-triggered autoimmune cholangitis in extrahepatic bile ducts of weanling DBA/1J mice.

BACKGROUND: Reovirus is a proposed cause of infantile biliary atresia. However, mechanistic insight regarding Reo-2 as a potential cholangiotropic virus is lacking. Furthermore, it is unknown whether Reo-2 infection can induce autoimmune-mediated bile duct injury. METHODS: Lesions of bile ducts in newborn DBA/1J mice infected with Reo-2 were analyzed immunopathologically. RESULTS: Damage to biliary epithelia occurs after Reo-2 infection. In addition, nonsuppurative cholangitis with fibrosis in extrahepatic (especially septal) bile ducts developed following complete viral clearance from the liver. At the inflamed ducts, major histocompatibility complex class I expressing((+)) and FAS(+) cholangiocytes were associated with FAS ligand(+) lymphocytes and tumor necrosis factor-α(+) mononuclear cells (macrophages and lymphocytes). These cholangiocytes were apoptotic and necrotic. Moreover, affected ducts were infiltrated by CD3(+), CD4(+), CD8(+), IFN-γ(+), and FAS(+) lymphocytes. Analysis of blood from Reo-2-infected mice revealed that they developed anticholangiocyte cytoplasm antibodies and had high serum IFN-γ concentration. Notably, there was no increase in Foxp3(+) lymphocytes at inflamed ducts, lymph nodes, and thymi. CONCLUSION: Reo-2 infection induced T-helper cell type 1-dependent injury to bile ducts in weanling mice. The lesions observed in mice may be analogous to those associated with human infantile biliary atresia, which are caused by an autoimmune-mediated process.

Complex carcinoma of the mammary gland in a free-living Japanese raccoon dog (Nyctereutes procyonoides viverrinus).

A complex carcinoma of the mammary gland was diagnosed in a free-living old female Japanese raccoon dog (Nyctereutes procyonoides viverrinus). Invasion into lymphatic vessels and metastasis in the inguinal lymph node were observed. This is the first report of complex carcinoma of the mammary gland in a raccoon dog.

Reovirus type-2 infection in newborn DBA/1J mice reduces the development of late allergic asthma.

The aim of the present study was to determine whether or not the development of a helper T (Th) 1 response induced by Reovirus type-2 (Reo-2) infection would protect against the development of Th2-mediated late allergic asthma. This hypothesis was examined by infecting one day old neonatal DB A/1J mice with Reo-2 in an ovalbumin (OVA)-induced late asthma model. Compared with the controls (either infected or uninfected mice with or without OVA sensitization and/or OVA challenge), Reo-2 infection lessened the magnitude of the subsequent allergic Th2-mediated late asthma. In infected mice with allergic late asthma, there was decreased infiltration of interleukin (IL)-4(+), IL-5(+), IL-13(+) and very late antigen (VLA)-4(+) lymphocytes, and eotaxin-2(+) and VLA-4(+) eosinophils, in both bronchial and bronchiolar lesions. Also the expression of vascular cell adhesion molecule (VCAM)-1 and eotaxin-2 on vascular endothelial cells was reduced. Moreover, the systemic production of IL-4, IL-5, tumour necrosis factor-α and OVA-specific IgE was reduced, whereas systemic IFN-γ production was increased. In addition, there was no increase in IFN-α production. Thus the present study suggests that systemic Reo-2 infection at birth may reduce the development of subsequent late allergic asthma by the induction of a Th1 response. Therefore the potential suppressive mechanism(s) that might be induced by Reo-2 infection in newborn mice and their effects on the development of late allergic asthma are discussed.

Eosinophilic venulitis in the small intestines in a mouse model of late asthma.

The allergen-unchallenged enteric lesions in late allergic asthma are largely unknown. To clarify this point, BALB/c mice were sensitized by ovalbumin (OVA)/aluminum adjuvant intraperitoneally two times (on days 0 and 10) and then challenged with OVA intranasally on day 14 (asthma group). Four days after the challenge, small intestinal lesions were examined. By this treatment, diarrhea was not observed in the asthma group. Compared to the controls with or without OVA sensitization and/or OVA challenge, the asthma group developed eosinophilic venulitis without an increase in mucosal mast cells in small intestines, whereas intestinal epithelial cells were relatively intact. A few numbers of interleukin (IL)-4(+) and IL-5(+) lymphoid cells were recognized in intestines in the asthma group, but not in the controls. Expression of vascular cell adhesion molecule-1 on venular endothelium and eotaxin-2(+) eosinophils, but not epithelial cells, in intestines were detected in the asthma group, but not in the controls. Total IgE, OVA-specific IgE and eotaxin, and IL-5, but not interferon-γ, were produced systemically in the asthma group compared to the controls. The present study suggests that eosinophilic venulitis without mast cells in the intestine may be induced by the systemic, but not by local, helper T 2-type responses. In addition, eosinophilic venulitis in small intestines may be subclinical enteric lesions.