Biochemical Mediators Of Inflammation Research Articles

Correlation Relationship of Interferons, Cytokines with Biochemical Mediators of Inflammation in The Blood in The Association of Covid-19 and Type 2 Diabetes

The study included 103 patients hospitalized for SARS-CoV-2 pneumonia at the Bukhara Regional Infectious Diseases Hospital, which was reorganized into the Covid Center. Immunological studies of the blood of sick children were carried out in the laboratory of immunomorphology of the Institute of Human Immunology and Genomics of the Academy of Sciences of the Republic of Uzbekistan. The indicators of interferon (INF-a, IFN-γ), cytokines (IL4, IL18) and biochemical tests in the blood were studied. In patients with SARS-CoV-2 pneumonia and type 2 diabetes, total bilirubin has a high relationship with the diabetogenic cytokine IL-18 - r = 0.42, against the background of a noticeable negative relationship with IL-4 (r = -0.30) and INF γ -r=-0.34. At the same time, the free fraction of bilirubin, like total bilirubin, has noticeable negative connections with IL-4 (r = -0.22) and IFN-γ r = -0.34, and has a significant positive connection with IL-18 - r = 0.34

Correlation Relationship of Interferons, Cytokines with Biochemical Mediators of Inflammation in The Blood in The Association of Covid-19 and Type 2 Diabetes

The study included 103 patients hospitalized for SARS-CoV-2 pneumonia at the Bukhara Regional Infectious Diseases Hospital, which was reorganized into the Covid Center. Immunological studies of the blood of sick children were carried out in the laboratory of immunomorphology of the Institute of Human Immunology and Genomics of the Academy of Sciences of the Republic of Uzbekistan. The indicators of interferon (INF-a, IFN-γ), cytokines (IL4, IL18) and biochemical tests in the blood were studied.

Biochemical mediators of inflammation and basic principles of wound healing in the skin

Biochemical mediators released during inflammation intensify and propagate the inflammatory response. These mediators are soluble, diffusible molecules that can act locally and systemically. Mediators derived from plasma include complement and complement-derived peptides and kinins. Released via the classic or alternative pathways of the complement cascade, complement-derived peptides (C3a, C3b, and C5a) increase vascular permeability, cause smooth muscle contraction, activate leukocytes, and induce mast-cell degranulation. C5a is a potent chemotactic factor for neutrophils and mononuclear phagocytes. The kinins are also important inflammatory mediators. The most important kinin is bradykinin, which increases vascular permeability and vasodilation and, importantly, activates phospholipase A2 (PLA2) to liberate arachidonic acid (AA). Here, we review mediators of inflammation and process of wound healing.

In vitro and In vivo Models for Anti-inflammation: An Evaluative Review

Anti-inflammatory activity study involves developing a model that mimics, or provokes the production or release of, the biochemical mediators of inflammation, and monitoring the response of these biochemicals to the test drugs. This report constitutes an updated review of the in vitro and in vivo study models for assessing anti-inflammatory activity in plant extracts and synthetic drugs. The materials, instrumentation, and methods involved, as well as the mechanism of anti-inflammatory activity tested in each model, are extensively described. The merits and limitations of each method have also been discussed. A comparative assessment of the in vivo animal models vis-à-vis, the in vitro enzyme models have been made to assist scientists and researchers in the choice of assay method in terms of sensitivity, reliability, duration of test, ethical, and cost considerations.

Peri-implant and Paracrestal Inflammatory Biomarkers at Failing Versus Surviving Implant Sites in a Beagle Dog Study.

This study sought to quantify three biochemical mediators of inflammation (tumor necrosis factor alpha [TNF-α], superoxide anion [SOA], and myeloperoxidase [MPO]) by analyzing crestal (peri-implants) and paracrestal gingival biopsy samples obtained from an experimental study on beagle dogs treated with implants inserted immediately into fresh sockets with circumferential defects. In 10 beagle dogs, 4 roughened titanium implants (3.8 mm wide × 8 mm high) were placed in the distal sockets of the third and fourth premolars, where a circumferential defect (5 mm wide and 5 mm deep) had been previously created by trephination. After varying follow-up periods, ranging from 80 to 190 days, the dogs were explored clinically to assess implant survival, peri-implant pocket depth, and implant stability. The levels of three biochemical mediators of inflammation (MPO, TNF-α, and SOA) were investigated using the crestal and paracrestal gingival biopsy samples with ELISA tests. It was found that 37.5% of the implants were either absent or mobile. Higher levels of the inflammatory mediators were found in the crestal samples than in the paracrestal samples. The final implant stability values were significantly correlated with the final probing depth (r = -0.83, P < .01), but neither of the clinical measures were significantly correlated with any biochemical marker. The risk of implant failure was significantly proportional to the level of MPO (odds ratio: 1.1) and TNF-α (odds ratio: 1.1) in both the crestal and paracrestal regions. All the inflammatory mediators studied were higher in the crestal areas than in the paracrestal regions, but only the values of MPO and TNF-α were significant predictors of implant failure.

Suppression of ongoing experimental arthritis by a chinese herbal formula (huo-luo-xiao-ling dan) involves changes in antigen-induced immunological and biochemical mediators of inflammation.

Rheumatoid arthritis (RA) is one of the major autoimmune diseases of global prevalence. The use of the anti-inflammatory drugs for the treatment of RA is associated with severe adverse reactions and toxicity. This limitation has necessitated the search for novel therapeutic products. We report here a traditional Chinese medicine-based herbal formula, Huo luo xiao ling dan (HLXL), which has potent antiarthritic activity as validated in the rat adjuvant-induced arthritis (AA) model. HLXL (2.3 g/Kg) was fed to Lewis (RT.11) rats daily by gavage beginning at the onset of arthritis and then continued through the observation period. HLXL inhibited the severity of ongoing AA. This suppression of arthritis was associated with significant alterations in the T cell proliferative and cytokine responses as well as the antibody response against the disease-related antigen, mycobacterial heat-shock protein 65 (Bhsp65). There was a reduction in the level of the proinflammatory cytokines IL-17 and IL-1β but enhancement of the anti-inflammatory cytokine IL-10 level. In addition, there was inhibition of both the anti-Bhsp65 antibody response and the serum level of nitric oxide. Thus, HLXL is a promising CAM modality for further testing in RA patients.

The role of mast cells in disc herniation inflammation.

A study of herniated lumbar disc tissue samples and control disc material to determine the presence of mast cells in disc herniations. To analyze whether mast cells have any involvement in disc herniation pathophysiology and lumbar pain, because mast cells may have an important role in acute and chronic inflammatory responses. Studies of inflammatory cells, biochemical mediators of inflammation, and tissue degrading enzymes have suggested that these factors may be involved--and perhaps play an important role--in the pathophysiology of lumbar pain and radiculopathy. Mast cells are known to play an important role in acute and chronic inflammatory responses. It was therefore of interest to clarify their possible role in intervertebral disc herniation inflammation. Fifty herniated lumbar discs from 50 patients who had undergone disc surgery and three normal control discs were obtained. Sections from every disc then were examined histologically and immunocytochemically for mast cells by using monoclonal antibodies to either of two types of specific proteases of mast cells, tryptase and chymase. By none of the methods could any mast cells be observed in any of the control disc samples. With toluidine blue staining, mast cells were observed in 9 of 50 (18%) of discs. Mast cells immunoreactive to either tryptase or chymase were observed in 10 of 50 disc samples (20%) and immunoreactive for tryptase and chymase simultaneously in 4 of 50 disc samples (8%). However, the majority of the samples studied (80%) demonstrated immunoreactivity to neither tryptase nor chymase. Among the samples studied were five disc protrusions that totally lacked mast cells. A minority of disc herniations exhibited mast cells, as verified by toluidine blue staining and immunocytochemistry. The results may suggest a role of mast cells in intervertebral disc herniation inflammation, but only in a subset of these cases. Massive infiltration by mast cells never was observed.

The pain of rheumatoid arthritis

R heumatoid arthritis, the most common chronic polyartitular inflammatory disease, is estimated to occur in 1 to 3 percent of the population. The inflammatory process primarily involves synovial membranes, producing synovitis of both small and large joints with potential involvement of virtually any joint in the body, the periarticular bursae, tendon sheaths, and contiguous supporting structures. The systemic nature of the disease is often made apparent by a spectrum of extra-articular symptoms. These include weakness, fatigue, malaise, and weight loss, accompanied by varying degrees of anorexia, fever, and anemia. The clinical onset of rheumatoid arthritis is highly variable: it may range from an acute, almost explosive, generalized joint and extra-articular disease with prominent incapacitating constitutional symptoms, to a creeping, insidious, low-grade condition apparently confined to a few joints, and evolving slowly over several months or years. In either case, the underlying histopathology undergoes an orderly evolution from an acute to a chronic selfsustaining inflammation with characteristic synovial infiltration by lymphocytes, macrophages, and plasma ceils. Pain was recognized by Hippocrates as one of the cardinal manifestations of inflammation, along with redness, warmth, and swelling. Modern research has done much to elucidate the biochemical and cellular mechanisms of inflammation, but their relationship to pain is less well understood. Many biochemical mediators of inflammation are also thought to participate in the development of pain, such as superoxide radicals from leukocytes and macrophages, as well as cycle-oxygenase and lipoxygenase, which mediate tissue damage. As important as these individual factors may be to the inflammatory process at the cellular level, the clinical variability of pain associated with inflammation is not yet explainable. The intensity of pain varies immensely from individual to individual, and often does not correlate well with other clinical and laboratory parameters of inflammation. It is pain that motivates patients to seek medical attention for rheumatoid arthritis, and it is the relief of pain, more than any other manifestation of the disease, upon which the success or failure of treatment is judged by these patients. The treatment of rheumatoid arthritis is, therefore, directed toward suppression of pain and underlying inflammation. In the past two decades, aspirin, with its biphasic analgesic and anti-inflammatory effects, has been used as the standard against which all of the newer nonsteroidal antiinflammatory drugs are compared for efficacy and safety. Over the years, however, it has become increasingly clear that relatively few patients with rheumatoid arthritis are able to tolerate the prolonged high doses of aspirin needed to control inflammation. Recent studies suggest that traditional anti-inflammatory therapy with aspirin should be reassessed. A previously unpublished, large-scale study by Dr. Lomen and his colleagues follows. In the more than 800 patients with classic or definite rheumatoid arthritis who were evaluated, flurbiprofen was equivalent in analgesic and antiinflammatory efficacy to aspirin, and superior in tolerability.

Endothelial changes and microvascular leakage due to hyperthermia in chick embryos.

The effects of hyperthermia on the developing 2- and 3-day chick embryo were studied by vital microscopy, in vivo microangiography and electron microscopy of post-capillary venules of the pellucid area of the yolk sac. Hyperthermia of 3 degrees C and 4 degrees C produced significant microvascular changes and perivascular oedema. The microvascular defects were characterized by interruption of the endothelial lining and the presence of blood cells breaking through the vessel walls. In addition, there were numerous inter-endothelial gaps with wide subendothelial spaces. Microangiography showed leakage from the vessel walls. It is concluded that hyperthermia produces vessel wall injury and induces the formation of gaps between endothelial cells resulting in extravasation of plasma and blood cells. These gaps are similar to those produced by biochemical mediators of inflammation. It is suggested that these microvascular changes with pathological leakage may play important roles in abnormal vascular and embryonic development.