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Serum amyloid A (SAA) proteins belong to a family of acute-phase reactants, playing an integral role in defending the organism from pathological damage. Despite a wealth of data on the regulation of SAA transcripts in teleosts, there is only limited information on these proteins’ abundance in fish. The aim of this study is to characterise SAA protein levels in salmonids using a newly developed antibody specific to salmonid SAA. The salmonid SAA antibody detected SAA and accurately discriminated between stimulated and control specimens from rainbow trout macrophage cell line (RTS-11) in vitro, as well as rainbow trout challenged with Aeromonas salmonicida- or flagellin-stimulated Atlantic salmon in vivo. The presence of SAA protein was analysed in RTS-11 cell line supernatants, liver, and spleen samples using ELISA, immunoblotting, and immunohistochemistry. This study is the first to characterise SAA protein levels in salmonids in vivo and in vitro. The newly developed salmonid SAA antibody was able to discriminate between stimulated and unstimulated specimens, showing that it can be used to study the acute-phase response in salmonids with the potential to be further developed into assays to monitor and evaluate health in wild and farmed fish.

Tumour-associated neutrophils (TANs) can support tumour growth by suppressing cytotoxic lymphocytes. AT-RvD1 is an eicosanoid that can antagonise neutrophil trafficking instigated by ALX/FPR2 ligands such as serum amyloid A (SAA). We aimed to establish whether SAA and ALOX5 expression associates with TANs and investigate the immunomodulatory actions of AT-RvD1 in vivo. MPO-positive neutrophils were quantified in tumour blocks from lung adenocarcinoma (n = 48) and control tissue (n = 20) by IHC. Tumour expression of SAA and ALOX5 were analysed by RTqPCR and an oncogenic KrasG12D lung adenocarcinoma mouse model was used to investigate the in vivo efficacy of AT-RvD1 treatment. ALOX5 expression was markedly reduced in lung adenocarcinoma tumours. The SAA/ALOX5 ratio strongly correlated with TANs and was significantly increased in tumours harbouring an oncogenic KRAS mutation. AT-RvD1 treatment reduced tumour growth in KrasG12D mice, which was accompanied by suppressed cellular proliferation within parenchymal lesions. In addition, AT-RvD1 significantly reduced the neutrophil to lymphocyte ratio (NLR), an established prognostic marker of poor survival in adenocarcinoma. This study identifies a novel molecular signature whereby elevated levels of SAA relative to ALOX5 favour accumulation of TANs. Furthermore, the ALOX5/5-LO enzymatic product, AT-RvD1, markedly reduced the NLR and suppressed tumour growth in KrasG12D mice.

Alcoholic liver disease (ALD) is the major cause of chronic liver disease and a global health concern. ALD pathogenesis is initiated with liver steatosis, and ALD can progress to steatohepatitis, fibrosis, cirrhosis and even hepatocellular carcinoma. Salvianic acid A (SAA) is a phenolic acid component of Danshen, a Chinese herbal medicine with possible hepatoprotective properties. The purpose of this study was to investigate the effect of SAA on chronic alcoholic liver injury and its molecular mechanism. We found that SAA significantly inhibited alcohol‐induced liver injury and ameliorated ethanol‐induced hepatic inflammation. These protective effects of SAA were likely carried out through its suppression of the BRD4/HMGB1 signalling pathway, because SAA treatment largely diminished alcohol‐induced BRD4 expression and HMGB1 nuclear translocation and release. Importantly, BRD4 knockdown prevented ethanol‐induced HMGB1 release and inflammatory cytokine production in AML‐12 cells. Similarly, alcohol‐induced pro‐inflammatory cytokines were blocked by HMGB1 siRNA. Collectively, our results reveal that activation of the BRD4/HMGB1 pathway is involved in ALD pathogenesis. Therefore, manipulation of the BRD4/HMGB1 pathway through strategies such as SAA treatment holds great therapeutic potential for chronic alcoholic liver disease therapy.

(1) Background: Horses infected by a tick-borne encephalitis virus (TBEV) can develop clinically apparent infections. In humans, vaccination is the most effective preventive measure, while a vaccine is not available for horses. The objective of this study was to describe the immune response in horses after a TBEV vaccination with a human vaccine. (2) Materials and Methods: Seven healthy horses were randomised to a treatment or a control group in a stratified fashion based on TBEV–IgG concentrations on day −4. The treatment group (n = 4) was intramuscularly vaccinated using an inactivated human TBEV vaccine on days 0 and 28; the control group (n = 3) did not receive an injection. A clinical examination and blood sampling were performed on day –4, 0, 2, 4, 6, 8, 10, 14, 28, 30, 32, 34, 36, 38, 43, 56, 84, and 373. A linear mixed model analysis was used to compare IgG and IgM concentrations, neutralising antibody (nAb) titres, leucocyte count, serum amyloid A (SAA), and fibrinogen and globulin concentrations between the groups and time points. (3) Results: The clinical examination was normal in all horses at all time points. There were no significant changes in SAA, globulin, and fibrinogen concentrations and leucocyte count between the groups or time points (all p > 0.05). There was no significant increase in IgG, IgM, or nAb titres in the control group over time (all p > 0.05). In the vaccination group, there was a significant increase in IgG concentration and nAb titres after the second vaccination (p < 0.0001). There was no significant increase in IgM antibodies after the TBEV vaccination (all p > 0.05). One horse in the vaccination group had an IgM concentration above the laboratory reference on day 10. (4) Conclusions: The human TBEV vaccine did not have side effects when used in healthy horses in this study. A significant rise in TBEV-specific IgG antibodies and nAbs after the second vaccination was observed. However, IgG and nAb titres have been shown to decrease within 1 year after vaccination. The results of this study indicate that a vaccination with a human vaccine only induces a mild rise in IgM antibodies and only in previously naive horses. With no significant changes to inflammatory parameters in the vaccinated horses, it remains unclear whether vaccination with the human vaccine leads to protective immunity.

Background Leptospirosis is a neglected but widespread zoonotic disease throughout the world. Most mammals are hosts of Leptospira spp., including domestic cats, species in which no consensus has been reached on the clinical presentation or diagnosis of the disease. The study of acute-phase proteins (APPs) and biomarkers of oxidative status would contribute to knowledge about the disease in cats. This report evaluated four APPs: Serum amyloid A-SAA, Haptoglobin–Hp, albumin and Paraoxonase 1-PON1 and the antioxidant response through Total Antioxidant Capacity-TAC, in 32 free-roaming cats. Cats were classified as seroreactive for anti-leptospiral antibodies (group 1, n  = 8), infected with Leptospira spp (group 2, n  = 5) and leptospires-free cats (group 3, n  = 19). Results SAA differences were observed between groups 1 and 2 ( p -value = 0.01) and between groups 2 and 3 ( p -value = 0.0001). Hp concentration differences were only detected between groups 2 and 3 ( p -value = 0.001). Albumin concentrations only differed between groups 1 and 3 ( p -value = 0.017) and 2 and 3 ( p -value < 0.005). Cats in groups 1 ( p -value < 0.005) and 2 ( p -value < 0.005) had lower PON1 concentrations than group 3. No statistically significant differences between pairs of groups were detected for TAC concentrations. The principal component analysis (PCA) retained two principal components, (PC1 and PC2), explaining 60.1% of the observed variability of the inflammatory proteins and the antioxidant TAC. Conclusions Increases in Serum SAA, Hp, and decreases in PON1 activity may indicate an active inflammatory state in infected cats (currently or recently infected).

ABSTRACT Background Bordetella bronchiseptica is an essential bacterial pathogen characterized by chronic respiratory disease in dogs known as Kennel cough. The presence of causative antibodies in animals can also be detected by lipopolysaccharide antigen‐based enzyme linked immunosorbent assay (ELISA). In recent years, it has been determined that there is a significant relationship between acute phase proteins and diseases, and disease follow‐up can be done within the framework of this relationship. Methods In this study, blood sera from 150 dogs in an animal shelter in Van province were evaluated for B. bronchiseptica by the homemade ELISA method, and their correlations with serum amyloid A (SAA) were investigated. Blood serum samples were analysed for antibodies against B. bronchiseptica using a homemade ELISA method. Positive animals were also molecularly confirmed using nasal swabs by PCR. A commercial ELISA kit determined SAA levels in blood sera. Results Eighteen (12%) of the analysed blood serum samples were found positive by the homemade ELISA method. SAA concentrations in the positive blood sera were elevated from 12.7 to ≤38.98 mg/L. SAA concentrations in blood sera serologically positive for B. bronchiseptica were statistically significant. Conclusions In this study, in which the relationship between SAA concentration and B. bronchiseptica was investigated for the first time in Turkey, it was concluded that SAA concentration analysis may help diagnose and monitor the disease. In addition, the presence and prevalence of this critical and zoonotic agent causing chronic respiratory tract disease in dogs in Van province was revealed for the first time in this study. A study in Van, Turkey examined Bordetella bronchiseptica in shelter dogs using ELISA and PCR. Overall, 12% of blood samples tested positive. Serum amyloid A (SAA) levels were significantly elevated in positive cases, suggesting SAA could be a useful diagnostic marker for this chronic respiratory disease‐causing bacterial pathogen.

Objective To clarify the effects on and the mechanism of salvianic acid A sodium (SAAS) in the recovery of motor function after spinal cord injury. Methods In vivo and in vitro experiments were carried out in this research to determine the effects of SAAS on tissue damage, neuron survival, microglia polarization, and inflammation after spinal cord injury (SCI). Differentially expressed genes treated with SAAS were screened by transcriptome sequencing, and the molecular mechanism was investigated simultaneously. Results The results revealed that SAAS could promote type M2 polarization of microglia and reduce the proportion of type M1. In this way, it reduced the secretion and expression of inflammatory factors. Compared with Lipopolysaccharides(LPS), 345 genes were upregulated and 407 genes were downregulated in the LPS + SAAS treatment group. In the SAAS group, expression levels of Ndufa12, IL‐6, TNF‐α, and Vdac1 were significantly reduced, while a marked elevation was found in MIP2. In addition, results found in an animal model showed that SAAS could obviously facilitate motor function recovery of mice after spinal cord injury, and it had a good protective effect on spinal cord tissue and neuron cells. Conclusion As a result, the present study clarified both the protective effect of SAAS on neurons after spinal cord injury and the anti‐inflammatory effect of microglia, which is expected to serve as a theoretical basis for clinical treatment. Salvianic acid A sodium can improve the recovery of motor function in rats with spinal cord injury. Its mechanism may be to protect neurons and promote type M2 polarization of microglia by regulating the MIP2/Vdac1 /Ndufa12 signaling axis.

Objective: The aim of this study was to explore the value of serum amyloid A protein (SAA) and neutrophil-to-lymphocyte ratio (NLR) testing in the diagnosis and treatment of children with influenza A. Methods: Specimens were collected from 85 children with influenza A, 85 children with a bacterial infection, and 86 healthy children. The levels of SAA and C-reactive protein (CRP) were measured, and routine blood tests were performed. Results: The levels of SAA and CRP in the bacterial infection group were significantly higher than those in the influenza A group, and the levels in the influenza A group were higher than those in the healthy children. The NLR level in the influenza A group was not different from that in the bacterial infection group, but the NLR levels in the influenza A group and the bacterial infection group were higher than that in the healthy controls. The number of white blood cell (WBC) in the influenza A group was not different from that in healthy children, while the WBC counts in the control and bacterial infection groups were higher than that in the influenza A group. The distribution width of red blood cells in the bacterial infection group was higher than that in healthy controls. The receiver operating characteristic curve analysis showed that the area under the curve for the diagnoses of influenza A for SAA, NLR, and CRP was 0.806, 0.768, and 0.699, respectively. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of SAA/NLR (SAA and NLR in the series) were 68.24%/76.47% (57.65%), 84.88%/72.09% (96.76%), 81.69%/73.03% (96.08%), 73.00%/75.61% (70.00%), and 76.61%/74.27% (77.78%), respectively. Conclusion: In the early diagnosis of children with influenza A, the values of SAA and NLR are high. Thus, they could be used for monitoring and efficacy evaluation during the course of the disease.

Aleutian disease (AD) is a chronic disease of mink caused by the Aleutian Mink Disease Virus (AMDV) that results in dysfunction of the immune system. The prevalence of asymptomatic AMDV infections suggests a necessity to explore their effects on the cellular mechanisms of non-specific immunity in farmed mink. The study evaluated the phagocytic activity and oxygen metabolism of peripheral blood granulocytes and monocytes in mink with chronic subclinical AMDV infection. Moreover, the intensity of inflammatory processes was assessed based on the serum amyloid A (SAA) concentration. The analyses involved 24 brown mink females aged 12–24 months. The experimental group (group I) consisted of mink with chronic subclinical AMDV infections, and the control group (group II) included healthy animals. The statistical analysis was performed using the Mann-Whitney U rank test. Phagocytic activity of granulocytes and monocytes was carried out using flow cytometry, and SAA concentration was determined with enzyme-linked immunosorbent assay (ELISA). Compared with the control group, there was a significant decrease in the phagocytic activity and oxygen metabolism of granulocytes and monocytes in the AMDV-infected mink (p < 0.05). Additionally, it was found that the mean SAA value was significantly higher in the group infected with AMDV than in the control group (p < 0.05). The obtained data indicate that monitoring the serum SAA levels in mink with asymptomatic inflammation may help assess the health of mink and detect asymptomatic inflammation caused by AMDV infection.

Background and aim: Urocortin 1 (UCN) and adrenomedullin (AM) are two recently discovered neuropeptides that, due to their distribution and binding to receptors in immune cells, have emerged as potential endogenous anti-inflammatory factors. Crohn’s disease is a chronic debilitating disease characterised by a Th1 driven severe inflammation of the gastrointestinal tract. This study investigated the therapeutic effect of UCN and AM in a murine model of colitis. Methods and results: Treatment with UCN or AM ameliorated significantly the clinical and histopathological severity of the inflammatory colitis, abrogating body weight loss, diarrhoea, and inflammation, and increased the survival rate of colitic mice. The therapeutic effect was associated with downregulation of both inflammatory and Th1 driven autoimmune responses, including regulation of a wide spectrum of inflammatory mediators. In addition, partial involvement of interleukin 10 secreting regulatory cells in this therapeutic effect was demonstrated. Importantly, UCN or AM treatments were therapeutically effective in established colitis and avoided recurrence of the disease. Conclusions: This work identifies UCN and AM as two potent anti-inflammatory factors with the capacity to deactivate the intestinal inflammatory response and restore mucosal immune tolerance at multiple levels. Consequently, both peptides represent novel multistep therapeutic approaches for the treatment of Crohn’s disease and other Th1 mediated inflammatory diseases.