U n i t C d I m m u nolog ie-M icro bio log ie, B-5000 Namur, BelgiumIsolation of Brucella spp. in marine mammals has been reported during the past several years. A Brucella strain from the spleen and liver of a minke whale (Balaenoptera acutorostrata) was isolated. Conventional typing methods indicated that this isolate was related to the genus Brucella but did not match the profiles of any known Brucella species or biovar. Successful PCR amplification of the Brucella rrs-rrl spacer sequence and of the insertion sequence IS6501 also indicated that the minke whale strain was related to the genus Brucella. In addition, the rrs gene of this strain shared a very high degree of nucleotide identity (>98%) with published Brucella spp. rrs sequences. However, RFLP studies using an IS6501-specif ic probe showed a unique profile for this strain in comparison with the profiles of the six known Brucella species. Moreover, analysis of the omp2 locus by PCR-RFLP, by Southern hybridization using omp2a-and omp2b-specif ic probes, and b y DNA sequencing showed that the minke whale isolate possesses two copies of the omp2b gene instead of one omp2a and one omp2b gene copy or two copies of the omp2a gene described in the six known Brucella species. Thus, molecular typing methods showed that this isolate is clearly distinct from all other known Brucella species and strains. The specific molecular features of this minke whale Brucella isolate raise questions about the lineage between the Brucella strains isolated from marine mammals and the Brucella species isolated from terrestrial mammals.
Several reports suggest that activated airway smooth muscle (ASM) cells are capable of generating various proinflammatory mediators, including cytokines and chemokines. However, little is known about the mechanism involved in this process. In this regard, we have examined the expression and the role of the high affinity IgE receptor (FcεRI) by ASM cells. Human ASM cells were found to constitutively express transcripts coding for α, β, and γ subunits of FcεRI. Flow cytometry and Western blot analysis confirmed the expression of FcεRI α-chain protein. Interestingly, FcεRI α-chain immunoreactivity was also demonstrated in smooth muscle within bronchial biopsies of asthmatic subjects. Cross-linking of FcεRI induced mobilization of free calcium in ASM cells, one of the critical signals to trigger smooth muscle contraction. Furthermore, cultured ASM cells released IL-4, IL-13, IL-5, and eotaxin but not IFN-γ, when sensitized with IgE followed by anti-IgE Ab cross-linking. The addition of anti-FcεRI α-chain Abs directed against IgE binding site inhibited this release. Taken together, these results suggest a potential new and important mechanism by which ASM cells may participate in airway inflammation and bronchoconstriction associated with allergic asthma.
Asthma is characterized by an increase in airway smooth muscle mass and a decreased distance between the smooth muscle layer and the epithelium. Furthermore, there is evidence to indicate that airway smooth muscle cells (ASMC) express a wide variety of receptors involved in the immune response. The aims of this study were to examine the expression of CCR3 on ASMC, to compare this expression between asthmatic and nonasthmatic subjects, and to determine the implications of CCR3 expression in the migration of ASMC. We first demonstrated that ASMC constitutively express CCR3 at both mRNA and protein levels. Interestingly, TNF-α increases ASMC surface expression of CCR3 from 33 to 74%. Furthermore, using FACS analysis, we found that ASMC CCR3 is expressed to a greater degree in asthmatic vs control subjects (95 vs 75%). Functionality of the receptor was demonstrated by calcium assay; the addition of CCR3 ligand eotaxin to ASMC resulted in an increase in intracellular calcium production. Interestingly, ASMC was seen to demonstrate a positive chemotactic response to eotaxin. Indeed, ASMC significantly migrated toward 100 ng/ml eotaxin (2.2-fold increase, compared with control). In conclusion, the expression of CCR3 by ASMC is increased in asthmatics, and our data show that a CCR3 ligand such as eotaxin induces migration of ASMC in vitro. These results may suggest that eotaxin could be involved in the increased smooth muscle mass observed in asthmatics through the activation of CCR3.
BackgroundBovine respiratory disease (BRD) is 1 of the 2 most important causes of morbidity and mortality in dairy calves. Surprisingly, field data are scant concerning the prevalence of respiratory pathogens involved in BRD in preweaned dairy calves, especially in small herds.ObjectivesTo identify the main respiratory pathogens isolated from calves in Québec dairy herds with a high incidence of BRD, and to determine if there is an association between the presence of these pathogens and clinical signs of pneumonia, lung consolidation, or average daily gain.AnimalsCross‐sectional study using a convenience sample of 95 preweaned dairy calves from 11 dairy herds.MethodsAt enrollment, calves were weighed, clinically examined, swabbed (nasal and nasopharyngeal), and lung ultrasonography was performed. One month later, all calves were reweighed.ResultsTwenty‐two calves had clinical BRD and 49 had ultrasonographic evidence of lung consolidation. Pasteurella multocida, Mannheimia haemolytica, and Histophilus somni were isolated in 54, 17, and 12 calves, respectively. Mycoplasma bovis was identified by PCR testing or culture in 19 calves, and 78 calves were found to be positive for Mycoplasma spp. Bovine coronavirus was detected in 38 calves and bovine respiratory syncytial virus in 1. Only the presence of M. bovis was associated with higher odds of clinical signs, lung consolidation, and lower average daily gain.Conclusions and Clinical ImportanceResults suggested that nasopharyngeal carriage of M. bovis was detrimental to health and growth of dairy calves in small herds with a high incidence of BRD.
Clinical mastitis is an important disease in dairies. Its treatment is mainly based on the use of antimicrobial drugs. Numerous non-antimicrobial drugs and treatment strategies have already been reported for clinical mastitis treatment, but data on their efficacy have never been collated in a systematic way. The objective of this systematic review was to identify treatments other than conventional antimicrobials for the treatment of clinical mastitis in lactating dairy cows. A systematic review was performed with studies written in English or French selected from CAB Abstracts, PubMed, and Web of Science from January 1970 to June 2014. Controlled clinical trials, observational studies, and experimental challenges were retained. Lactating dairy cows with clinical mastitis were the participant of interest. All treatments other than conventional antimicrobials for clinical mastitis during lactation were retained. Only studies comparing the treatment under investigation to a negative or positive control, or both, were included. Outcomes evaluated were clinical and bacteriological cure rates and milk production. Selection of the study, data extraction, and assessment of risk of bias was performed by 3 reviewers. Assessment of risk of bias was evaluated using the Cochrane Collaboration tool for systematic review of interventions. A total of 2,451 manuscripts were first identified and 39 manuscripts corresponding to 41 studies were included. Among these, 22 were clinical trials, 18 were experimental studies, and 1 was an observational study. The treatments evaluated were conventional anti-inflammatory drugs (n = 14), oxytocin with or without frequent milk out (n = 5), biologics (n = 9), homeopathy (n = 5), botanicals (n = 4), probiotics (n = 2), and other alternative products (n = 2). All trials had at least one unclear or high risk of bias. Most trials (n = 13) did not observe significant differences in clinical or bacteriological cure rates in comparison with negative or positive controls. Few studies evaluated the effect of treatment on milk yield. In general, the power of the different studies was very low, thus precluding conclusions on noninferiority or nonsuperiority of the treatments investigated. No evidence-based recommendations could be given for the use of an alternative or non-antimicrobial conventional treatment for clinical mastitis. However, probiotics and oxytocin with or without frequent milk out should not be recommended. We concluded that homeopathic treatments are not efficient for management of clinical mastitis.
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