Pollens destroy respiratory epithelial cell anchors and drive alphaherpesvirus infection.

Pollens are well-known triggers of respiratory allergies and asthma. The pollen burden in today's ambient air is constantly increasing due to rising climate change and air pollution. How pollens interact with the respiratory mucosa remains largely unknown due to a lack of representative model systems. We here demonstrate how pollen proteases of Kentucky bluegrass, white birch and hazel selectively destroy integrity and anchorage of columnar respiratory epithelial cells, but not of basal cells, in both ex vivo respiratory mucosal explants and in vitro primary equine respiratory epithelial cells (EREC). In turn, this pollen protease-induced damage to respiratory epithelial cell anchorage resulted in increased infection by the host-specific and ancestral alphaherpesvirus equine herpesvirus type 1 (EHV1). Pollen proteases of all three plant species were characterized by zymography and those of white birch were fully identified for the first time as serine proteases of the subtilase family and meiotic prophase aminopeptidase 1 using mass spectrometry-based proteomics. Together, our findings demonstrate that pollen proteases selectively and irreversibly damage integrity and anchorage of columnar respiratory epithelial cells. In turn, alphaherpesviruses benefit from this partial loss-of-barrier function, resulting in increased infection of the respiratory epithelium.

Supplementing goat kids with coconut medium chain fatty acids in early life influences growth and rumen papillae development until 4 months after supplementation but effects on in vitro methane emissions and the rumen microbiota are transient.

The aim of this study was to investigate the methane (CH4) reducing potential of a combination of prenatal and/or postnatal treatment with coconut oil medium chain fatty acids (CO MCFA) in goat kids. The hypothesis is that influencing rumen function during early life has more chances for success than in the adult life, related to the resilience of the mature rumen microbiota. Forty-eight pregnant does were split into two experimental groups: treated does (D+) received 40 g/d of CO MCFA in a test compound feed, while control does (D-) received a control compound feed, during the last 3 wk of gestation. Twin kids from 10 does of each group were split up into a treated (K+) and nontreated (K-) group, resulting in four experimental groups: D+K+, D+K-, D-K+, and D-K-. The K+ kids received 1.8 mL/d of CO MCFA from birth until 2-wk postweaning (11 wk). Irrespective of treatment, the experimental rearing conditions resulted in absence of rumen protozoa at all sampling times, assessed by quantitative PCR (qPCR). In vitro incubations with rumen fluid at 4 wk old showed 82% lower CH4 production of inoculum from D+K+ kids compared to D-K- kids (P = 0.01). However, this was accompanied by lower total volatile fatty acids (tVFA) production (P = 0.006) and higher hydrogen accumulation (P = 0.008). QPCR targeting the mcrA and rrs genes confirmed a lower abundance of total methanogens (P < 0.02) and total eubacteria (P = 0.02) in D+K+ kids at 4 wk old. Methanogenic activity, as assessed by mcrA expression by RT-qPCR, was also lower in these kids. However, activity did not always reflect methanogen abundance. At 11 and 28 wk old, prenatal and postnatal effects on in vitro fermentation and rumen microbiota disappeared. Nevertheless, lower milk replacer intake in the first 4 wk resulted in reduced BW in K+ kids, persisting until 28 wk of age. Additionally, differences assigned to postnatal treatment were found in papillae density, width, and length in different areas of the rumen, recorded at 28 wk old. CONCLUSION: prenatal and postnatal supplementation with CO MCFA reduced in vitro CH4 emissions until 4 wk old by depressing methanogen abundance and activity but at the expense of rumen fermentation and eubacterial abundance. Unfortunately, daily gain of K+ kids was suppressed. Some rumen papillae characteristics differed at 28 wk old due to postnatal treatment which ended at 11 wk old, indicating rumen papillary development can be affected by the early-life nutritional circumstances.

Marginal dietary zinc concentration affects claw conformation measurements but not histological claw characteristics in weaned pigs.

The aim of the present study was to explore whether marginal dietary zinc (Zn) concentrations affect claw quality measurements in weaned pigs. Twenty-four weaned pigs were randomly assigned to two dietary treatment groups: (1) 42 mg Zn/kg diet from ingredients only (unsupplemented, marginal dietary Zn concentration below Zn requirements of 80 mg Zn/kg feed); and (2) 106 mg Zn/kg diet, where Zn was added as ZnO (common commercial dietary Zn concentration). Claw conformation characteristics were measured at the start (day 0, 4 weeks of age) and at the end (day 36) of the study, and the histological claw characteristics of horn wall and heel horn were examined on samples collected at 9 weeks of age. Non-supplemented pigs had narrower claw widths (P= 0.028) and lower toe heights (P= 0.010) at 9 weeks. The length of the dorsal border tended to be lower for the non-supplemented piglets (P= 0.092). Claw volume and claw horn size were lower (P= 0.003 and P < 0.001, respectively) for the non-supplemented pigs at 9 weeks of age. Horn growth and wear were lower for the non-supplemented pigs (P= 0.044 and P < 0.001, respectively), but net horn growth (horn growth minus wear) was not different (P= 0.406). No changes in the histological claw characteristics were observed. Differences in claw quality measurements were found between lateral and medial claw digits and between fore and hind claws. It was concluded that marginal dietary Zn concentration affected various claw quality measurements. Marginal dietary Zn concentrations may not be sufficient to maintain claw quality in pigs.