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Background Comparison of clinical findings, chest radiographs (CXR), lung ultrasound (LUS) findings, and C‐reactive protein (CRP) concentrations at admission and serial follow‐up in dogs with aspiration pneumonia (AP) is lacking. Hypothesis Lung ultrasound lesions in dogs with AP are similar to those described in humans with community‐acquired pneumonia (comAP); the severity of CXR and LUS lesions are similar; normalization of CRP concentration precedes resolution of imaging abnormalities and more closely reflects the clinical improvement of dogs. Animals Seventeen dogs with AP. Methods Prospective observational study. Clinical examination, CXR, LUS, and CRP measurements performed at admission (n = 17), 2 weeks (n = 13), and 1 month after diagnosis (n = 6). All dogs received antimicrobial therapy. Lung ultrasound and CXR canine aspiration scoring systems used to compare abnormalities. Results B‐lines and shred signs with or without bronchograms were identified on LUS in 14 of 17 and 16 of 17, at admission. Chest radiographs and LUS scores differed significantly using both canine AP scoring systems at each time point (18 regions per dog, P < .001). Clinical and CRP normalization occurred in all dogs during follow up. Shred signs disappeared on LUS in all but 1 of 6 dogs at 1 month follow‐up, while B‐lines and CXR abnormalities persisted in 4 of 6 and all dogs, respectively. Conclusion and Clinical Importance Lung ultrasound findings resemble those of humans with comAP and differ from CXR findings. Shred signs and high CRP concentrations better reflect clinical findings during serial evaluation of dogs.

Background Evidence regarding optimal treatment duration in dogs with aspiration pneumonia (AP) and the role of thoracic radiographs (TXR) and lung ultrasonography (LUS) in the long‐term follow‐up of affected dogs is lacking. C‐reactive protein (CRP) is a reliable acute phase protein to monitor bacterial pneumonia in dogs. Hypothesis Investigate the safety of antimicrobial discontinuation based on clinical improvement and serum CRP normalization, as well as the usefulness of TXR and LUS for follow‐up. Animals Dogs diagnosed with AP and treated with antimicrobials. Methods Prospective observational study. Antimicrobials were discontinued based on clinical improvement and serum CRP normalization after 1, 3, or 5 weeks. At each consultation, a quality‐of‐life questionnaire, physical examination, serum CRP, TXR, and LUS were assessed. Short‐ (2 weeks) and long‐term (>1 month) follow‐ups after treatment discontinuation were performed to monitor for possible relapses. Results Seventeen dogs were included. Antimicrobials were discontinued after 1 week in 12 dogs (70.6%) and 3 weeks in the remaining 5 dogs (29.4%). Short‐term relapse was not observed in any dog and long‐term relapse was diagnosed in 3 dogs. Thoracic radiographs and LUS were useful for diagnosis, but did not add additional information during follow‐up, because image normalization lagged behind clinical improvement and serum CRP normalization. Conclusion and Clinical Importance Dogs with AP can be safely and effectively treated using a short‐term antimicrobial regimen discontinued after clinical improvement and serum CRP normalization. Imaging might still be useful for complicated cases with a less favorable response to treatment.

3 In the authors' experience, this border tends to vary with species, breed, respiratory effort and underlying lung lesions. 3 It is also the authors' experience that it can be difficult to determine the caudal extent of the lung margin on a lateral radiograph, particularly given this border changes during the respiratory cycle. [...]it is interesting to note that as VetBLUE increases the sites assessed from a single intercostal space to multiple intercostal spaces, it more closely aligns with earlier studies published by Dr Armenise 6 and the protocol used in the current study. An abstract in dogs suggests LUS protocols that examine larger lung surface area can detect pathology otherwise missed with protocols that scan less lung surface area, although this is a small study and prospective veterinary studies are needed to know how many sites need to be scanned to maximize sensitivity and specificity at finding underlying pleural and lung pathology. 8 The duration of time to perform lung ultrasound will likely need to be balanced against the speed with which a diagnosis needs to be made.

Background Intestinal Peyer’s patches (PPs) form unique niches for bacteria-immune cell interactions that direct host immunity and shape the microbiome. Here we investigate how peroral administration of probiotic bacterium Limosilactobacillus reuteri R2LC affects B lymphocytes and IgA induction in the PPs, as well as the downstream consequences on intestinal microbiota and susceptibility to inflammation. Results The B cells of PPs were separated by size to circumvent activation-dependent cell identification biases due to dynamic expression of markers, which resulted in two phenotypically, transcriptionally, and spatially distinct subsets: small IgD + /GL7 − /S1PR1 + / Bcl6 , CCR6 -expressing pre-germinal center (GC)-like B cells with innate-like functions located subepithelially, and large GL7 + /S1PR1 − /Ki67 + / Bcl6 , CD69- expressing B cells with strong metabolic activity found in the GC. Peroral L. reuteri administration expanded both B cell subsets and enhanced the innate-like properties of pre-GC-like B cells while retaining them in the sub-epithelial compartment by increased sphingosine-1-phosphate/S1PR1 signaling. Furthermore, L. reuteri promoted GC-like B cell differentiation, which involved expansion of the GC area and autocrine TGFβ-1 activation. Consequently, PD-1-T follicular helper cell-dependent IgA induction and production was increased by L. reuteri , which shifted the intestinal microbiome and protected against dextran-sulfate-sodium induced colitis and dysbiosis. Conclusions The Peyer’s patches sense, enhance and transmit probiotic signals by increasing the numbers and effector functions of distinct B cell subsets, resulting in increased IgA production, altered intestinal microbiota, and protection against inflammation. 3CbyP5PufHSWXKDo4r3t6t Video abstract

Adaptive immune responses regulate the development of atherosclerosis, with a detrimental effect of type 1 but a protective role of type 2 immune responses. Immunization of Apolipoprotein E‐deficient (ApoE−/−) mice with Freund's adjuvant inhibits the development of atherosclerosis. However, the underlying mechanisms are not fully understood. Thymic stromal lymphopoietin (TSLP) is an IL7‐like cytokine with essential impact on type 2 immune responses (Th2). Thymic stromal lymphopoietin is strongly expressed in epithelial cells of the skin, but also in various immune cells following appropriate stimulation. In this study, we investigated whether TSLP may be crucial for the anti‐atherogenic effect of Freund's adjuvant. Subcutaneous injection of complete Freund's adjuvant (CFA) rapidly led to the expression of TSLP and IL1β at the site of injection. In male mice, CFA‐induced TSLP occurred in immigrated monocytes—and not epithelial cells—and was dependent on NLRP3 inflammasome activation and IL1β‐signalling. In females, CFA‐induced TSLP was independent of IL1β and upon ovariectomy. CFA/OVA led to a more pronounced imbalance of the T cell response in TSLPR−/− mice, with increased INFγ/IL4 ratio compared with wild‐type controls. To test whether TSLP contributes to the anti‐atherogenic effects of Freund's adjuvant, we treated ApoE−/− and ApoE−/−/TSLPR−/− mice with either CFA/IFA or PBS. ApoE−/− mice showed less atherogenesis upon CFA/IFA compared with PBS injections. ApoE−/−/TSLPR−/− mice had no attenuation of atherogenesis upon CFA/IFA treatment. Freund's adjuvant executes significant immune‐modulating effects via TSLP induction. TSLP‐TSLPR signalling is critical for CFA/IFA‐mediated attenuation of atherosclerosis.

BackgroundHereditary spastic paraplegia (HSP) is a group of clinically and genetically heterogeneous neurodegenerative disorders characterised by progressive spasticity and weakness in the lower limbs. Mutations in PLP1 on the X chromosome cause spastic paraplegia type 2 (SPG2) or the allelic Pelizaeus–Merzbacher Disease (PMD). The PLP1 protein is a major myelin protein involved in stabilisation and maintenance of the myelin sheath. The function of the protein has been studied in the rumpshaker mouse, which is a model of SPG2/PMD.ObjectiveTo characterise the phenotype of patients with the ‘rumpshaker mutation.’PatientsA family with HSP caused by the ‘rumpshaker mutation.’ResultsThe patients showed nystagmus during infancy and had early onset of HSP. They had normal cognition, and cerebral MRI showed relatively unspecific white matter abnormalities on T2 sequences without clear progression. Urinary urgency was reported among the female carriers. MRS of both patients showed increased myo-inositol in the white matter, while decreased N-acetylaspartate was found exclusively in the oldest patient. All evoked potential examinations were compatible with severe central demyelination, while no signs of peripheral demyelination or axonal degeneration were found. 18F-FDG-PET scans were normal.ConclusionThe phenotypes of the patients reported here are the mildest described to be caused by the rumpshaker mutation and represent the mildest form among the spectrum of PLP1 related disorders. No definite symptoms in the female carriers could be ascribed to the mutation. These data suggest the pathology to be an underlying dysmyelinating disorder in combination with a central axonal degeneration.