scholarly journals B7-H3 blockade decreases macrophage inflammatory response and alleviates clinical symptoms of arthritis

Author(s):  
Jie Yang ◽  
Xiong Jian ◽  
Yundi Guo ◽  
Li Gu ◽  
Pingping Wu ◽  
...  
2013 ◽  
Vol 4 (4) ◽  
pp. 18-22
Author(s):  
Natalia Anatolievna Barhatova

In article include results of analyses specials clinical and laboratories manifestations the local and general forms of infection on the soft tissues at the children in different age. Were revealed the most significant factors of risk development general form of infection in the children´s age. Also were determined clinical specials of systemic inflammatory response syndrome in dependent of the character inflammatory reaction of soft tissues, time of hospitalization and time of surgical intervention. Were revealed the most typical combinations symptoms of systemic inflammatory response syndrome on the child in different age. It´s allow improve early clinical diagnostic of sepsis on the child and shorten time of start equivalent therapy of general forms of infection.


2021 ◽  
Vol 10 (3) ◽  
pp. 2402-2413

Currently, a novel coronavirus disease 2019 (COVID 19) caused by SARS-CoV-2 has emerged worldwide. This chronic viral infection causes an acute respiratory distress syndrome (ARDS) which its pathophysiology is not yet well elucidated. However, ARDS has shown that ARDS causes diffuse alveolar damages induced by an excessive inflammatory response and a lack of anti-inflammatory response to the virus. Furthermore, these pathophysiological characteristics are associated with multiorgan failure and can increase the mortality rate. The difference in immune system response against COVID-19 is not well known. However, variability in innate immune system receptors between patients infected with SARS-CoV-2 as a function of aging and sex can explain this difference. Thus, innate immune memory or trained immunity mediated by epigenetic mechanisms is also involved in the variability response against COVID-19. The action of an adaptative immune response, in particular, antigen presentation via HLA is also a key element in this variability. Finally, each viral strain's capacity in evading the action of the immune response has also been suggested as an important mechanism by which certain patients infected with SARS-CoV-2 develop severity and others did not develop any clinical symptoms.


2018 ◽  
Vol 16 (3) ◽  
pp. 218-223
Author(s):  
Y. Dimcheva ◽  
Kr. Kalinova ◽  
K. Georgiev

The specific purpose of this study was to describe and characterize the systemic inflammatory response to appendicitis in childhood. The clinical symptoms of SIRS are present in a large proportion of patients . A study of high-risk patients showed that over a given period of time, 44-68% of the patients met the criteria for this condition, while at the same time they had proven infection up to 50%.The incidence of SIRS is even higher in the post-operative period and in trauma regardless of the presence or absence of infection. On the other hand, between 10% and 43% of patients with proven sepsis do not meet the SIRS criteria.The inclusion of a number of biological markers (C-reactive protein, procalcitonin, cytokines) aims to help differentiate SIRS with infectious and noninfectious etiology. Sixty six patients were studied, divided into four groups from onset of symptoms to diagnosis. The primary outcome measure was to determine the systemic inflammatory response to appendicitis according to the established groups of time intervals. The secondary outcome measure was the analysis of C-reactive protein for the same purpose. The variables of the systemic inflammatory response, according to diagnostic intervals, showed non-significant differences in white blood cell count. The temperature rose constantly after 48 h, reaching its peak after 72 h (p = 0.001), and the respiratory rate rose after 72 h (p < 0.0001). After 73 h, most patients had three or four systemic inflammatory response criteria (p < 0.0001). C-reactive protein levels rose progressively, showing higher levels after 48 h (p = 0.005). The inflammatory response to appendicitis is progressive, being more marked along the timeline from onset of symptoms to diagnosis. Key words: appendicitis, diagnostic SIRS, children, algoritm.


2018 ◽  
Vol 43 (9) ◽  
pp. 893-901 ◽  
Author(s):  
Jennifer M. Monk ◽  
Wenqing Wu ◽  
Laurel H. McGillis ◽  
Hannah R. Wellings ◽  
Amber L. Hutchinson ◽  
...  

The potential for a chickpea-supplemented diet (rich in fermentable nondigestible carbohydrates and phenolic compounds) to modify the colonic microenvironment and attenuate the severity of acute colonic inflammation was investigated. C57Bl/6 male mice were fed a control basal diet or basal diet supplemented with 20% cooked chickpea flour for 3 weeks prior to acute colitis onset induced by 7-day exposure to dextran sodium sulfate (DSS; 2% w/v in drinking water) and colon and serum levels of inflammatory mediators were assessed. Despite an equal degree of DSS-induced epithelial barrier histological damage and clinical symptoms between dietary groups, biomarkers of the ensuing inflammatory response were attenuated by chickpea pre-feeding, including reduced colon tissue activation of nuclear factor kappa B and inflammatory cytokine production (tumor necrosis factor alpha and interleukin (IL)-18). Additionally, colon protein expression of anti-inflammatory (IL-10) and epithelial repair (IL-22 and IL-27) cytokines were increased by chickpea pre-feeding. Furthermore, during acute colitis, chickpea pre-feeding increased markers of enhanced colonic function, including Relmβ and IgA gene expression. Collectively, chickpea pre-feeding modulated the baseline function of the colonic microenvironment, whereby upon induction of acute colitis, the severity of the inflammatory response was attenuated.


2021 ◽  
pp. 30-38
Author(s):  
V. A. Kubyshkin ◽  
L. M. Samokhodskaya ◽  
Yu. M. Korolev

Despite all the achievements of modern surgery, the number of postoperative infectious complications in the world remains high. Their occurrence leads to a longer period of patients’ hospitalization, requires the use of additional medical and diagnostic measures, which ultimately leads to higher treatment costs and significant financial losses in the health care system. Therefore, it is important to identify postoperative complications at an early stage, even before the development of pronounced clinical symptoms, and to predict their possible development in a certain category of patients. For these purposes, scientists try to use various laboratory markers. In this paper, we analyzed both well-known indicators of the inflammatory response, such as: C-reactive protein, albumin, their ratio, procalcitonin and interleukin-6, and relatively new parameters that research teams are trying to apply for these purposes: neutrophil granularity intensity and neutrophil reactivity intensity, pancreatic stone protein and pancreatitis-associated protein. We tried to collect the most complete information available at the moment, evaluate the opinions of researchers, identify contradictions in their works and try to explain their cause. As a result, it turned out that even the markers of inflammation known for many years are not absolutely specific for postoperative infectious complications. We concluded that most of the laboratory parameters described in this article can be used to some extent in the early diagnosis of postoperative infectious complications, but if we want to obtain more complete information in this area of knowledge, it is necessary to conduct new largescale studies.


1999 ◽  
Vol 12 (3) ◽  
pp. 445-453 ◽  
Author(s):  
Laurie R. Hall ◽  
Eric Pearlman

SUMMARY Onchocerciasis is a major cause of blindness. Although the World Health Organization has been successful in reducing onchocerciasis as a public health problem in parts of West Africa, there remain an estimated 17 million people infected with Onchocerca volvulus, the parasite that causes this disease. Ocular pathology can be manifested in any part of the eye, although disease manifestations are frequently characterized as either posterior or anterior eye disease. This review focuses on onchocerca-mediated keratitis that results from an inflammatory response in the anterior portion of the eye and summarizes what is currently known about human disease. This review also describes studies with experimental models that have been established to determine the immunological mechanisms underlying interstitial keratitis. The pathogenesis of keratitis is thought to be due to the host inflammatory response to degenerating parasites in the eye; therefore, the primary clinical symptoms of onchocercal keratitis (corneal opacification and neovascularization) are induced after injection of soluble O. volvulus antigens into the corneal stroma. Experimental approaches have demonstrated an essential role for sensitized T helper cells and shown that cytokines can regulate the severity of keratitis by controlling recruitment of inflammatory cells into the cornea. Chemokines are also important in inflammatory cell recruitment to the cornea, and their role in onchocerciasis is being examined. Further understanding of the molecular basis of the development of onchocercal keratitis may lead to novel approaches to immunologically based intervention.


Neurosurgery ◽  
2019 ◽  
Vol 66 (Supplement_1) ◽  
Author(s):  
Victoria E Sanchez ◽  
John Lynes ◽  
Stuart Walbridge ◽  
Xiang Wang ◽  
Nancy A Edwards ◽  
...  

Abstract INTRODUCTION Preclinical models that accurately recapitulate the immunosuppressive properties of human gliomas are essential to assess immune therapeutics. Glioma-261 (GL261) murine glioma cells are widely used as an in Vivo model of glioma. Our group has previously shown that the red-shifted luciferase-expressing cell line, GL261 Red-FLuc, creates an inflammatory response when implanted intracranially in C57BL/6 mice. However, it remains unclear if this is particular to GL261 Red-Fluc or any GL261 cell line transfected with luciferase-expressing genes. For this reason, we have additionally explored the inflammatory response of stably transfected, monoclonal GL261-luc2 cells. METHODS To evaluate the characteristics of these various cell lines, C57BL/6 mice (n = 10 in each group) underwent stereotaxic, intracranial implantation with GL261, GL261 Red-FLuc, or GL261-Luc2 cells at doses of 5 × 104 cells/5 μL or 3 × 105 cells/5 μL. Immunohistochemistry and flow cytometry of sacrificed mouse brains assess the frequency of immune cell populations. Magnetic resonance imaging (MRI) scans were also performed to monitor relative tumor growth. Finally, in Vitro cytokine profiles were evaluated by proteome microarray. RESULTS Kaplan-Meier survival analysis demonstrated that the median survival for mice implanted with GL261 cells at 5 × 104 cells/5 μL was 21 d. However, even at a higher tumor dose (3 × 105 cells/5 μL), the GL261-Red FLuc implanted mice did not reach median survival. Mice injected with the newly transfected GL261-Luc2 cells at 3 × 105 cells/5 μL reached median survival at 23 d, but median survival was not reached for GL261-Luc2 implanted mice at 5 × 104 cells/5 μL. MRI analysis reveals clear differences in tumor growth that correspond well with the onset of clinical symptoms and median survival. In addition, proteomic analysis reveals significantly elevated inflammatory cytokines such as IFNgamma, IL-7, and TNF-alpha in the supernatant of the GL261 Red-FLuc cells and upregulated IL-1alpha in GL261-Luc2 cells. Further immune characterization is ongoing. CONCLUSION Our data suggest that both GL261 Red-FLuc and GL261-luc2 murine models create an undesirable microenvironment for tumor growth by increasing proinflammatory modulators.


2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Tangyou Mao ◽  
Junxiang Li ◽  
Lijuan Liu ◽  
Weihan Zhao ◽  
Yuyue Liu ◽  
...  

Ulcerative colitis (UC) is a chronic, nonspecific, inflammatory disease for which an effective treatment is lacking. Our previous study found that Qingchang Wenzhong Decoction (QCWZD) can significantly improve the clinical symptoms of UC and ameliorate dextran sulphate sodium- (DSS-) induced ulcerative colitis in rats by downregulating the IP10/CXCR3 axis–mediated inflammatory response. The purpose of the present study was to further explore the mechanism of QCWZD for UC in rats models, which were established by 7-day administration of 4.5% dextran sulphate sodium solution. QCWZD was administered daily for 7 days; then we determined the serum macrophage-stimulating protein concentration (MSP) and recepteur d’origine nantais (RON) expression and its downstream proteins (protein kinase B [Akt], phosphorylated [p] Akt, occludin, zona occluden- [ZO-] 1, and claudin-2) in colon tissue using Western blotting and quantitative polymerase chain reaction. In DSS-induced UC, QCWZD significantly alleviated colitis-associated inflammation, upregulated serum MSP expression and RON expression in the colon, reduced the pAkt levels, promoted colonic occluding and ZO-1 expression, and depressed claudin-2 expression. In conclusion, the MSP/RON signalling pathway plays an important role in the pathogenesis of UC by involving the inflammatory response and improving intestinal barrier function. QCWZD appears to attenuate DSS-induced UC in rats by upregulating the MSP/RON signalling pathway.


2021 ◽  
Vol 11 ◽  
Author(s):  
Junyu Ren ◽  
Bei Yue ◽  
Hao Wang ◽  
Beibei Zhang ◽  
Xiaoping Luo ◽  
...  

Acacetin, a natural dietary flavonoid abundantly found in acacia honey and citrus fruits, reportedly exerts several biological effects, such as anti-tumor, anti-inflammatory, and anti-oxidative effects. However, the effects of acacetin on intestinal inflammation remain unclear. We sought to investigate whether acacetin ameliorates inflammatory bowel disease (IBD) in mice with dextran sulfate sodium (DSS)-induced ulcerative colitis (UC). Our results suggest that acacetin alleviates the clinical symptoms of DSS-induced colitis, as determined by body weight loss, diarrhea, colon shortening, inflammatory infiltration, and histological injury. Further studies showed that acacetin remarkably inhibited both the macrophage inflammatory response in vitro and levels of inflammatory mediators in mice with colitis. In addition, some features of the gut microbiota were disordered in mice with DSS-induced colitis, as evidenced by a significant reduction in microbiota diversity and a marked shift in bacterial profiles. However, acacetin treatment improved this imbalance and restored gut microbiota to levels that were similar to those in normal mice. In conclusion, our work presents evidence that acacetin attenuates DSS-induced colitis in mice, at least in part, by inhibiting inflammation and regulating the intestinal microbiota.


Neurosurgery ◽  
1991 ◽  
Vol 28 (1) ◽  
pp. 130-135 ◽  
Author(s):  
Mark S. Dias ◽  
Dachling Pang

Abstract Juvenile intervertebral disc calcification is an uncommon disorder of childhood, characterized by calcification of the nucleus pulposus of one or more intervertebral discs. Calcification may remain dormant or subsequently become symptomatic. The symptoms include fever, malaise, and neck pain and are associated with an elevated erythrocyte sedimentation rate and, occasionally, leukocytosis. Although disc protrusion occurs in 38% of patients, neurological signs are distinctly uncommon. We report the case of a patient with a herniated T2-T3 calcified intervertebral disc and compressive myelopathy. Juvenile intervertebral disc calcification is generally a self-limiting disease that seldom requires an operation. The symptoms are transient, and resorption of the disc calcification is the rule once symptoms occur. Neither the cause of the disc calcification nor the trigger for the onset of symptoms is known. An inflammatory response within the disc appears to give rise to clinical symptoms and is associated with eventual resorption of the disc calcification.


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