Biologics in Microangiopathic Wounds

2018 ◽  
Vol 17 (4) ◽  
pp. 205-213
Author(s):  
Massimo Papi ◽  
Claudia Papi

In the last decades the possibility to diagnose a skin ulcer has greatly improved. We learnt that a consistent percentage of nonhealing ulcers may be caused by a microangiopathic disorder that has not been properly investigated and cured. Pathogenetically, we can distinguish 2 main groups: (1) ulcers due to inflammatory microangiopathy, mainly including cutaneous small and medium vessel vasculitis, pyoderma gangrenosum, and connective tissue diseases, and (2) ulcers due to occlusive microangiopathy. The group of microangiopathic occlusive ulcers is more heterogeneous and includes different disorders ranging from livedo vasculopathy to calciphylaxis, hydroxyurea-induced ulcers, antiphospholipid antibodies ulcers, and various other types. These conditions can induce thromboses or anatomo-functional occlusion of cutaneous microvessels. Despite different physiopathologic mechanisms, the ulcer resulting from a primitive microangiopathy may receive basic treatments that are in the complex similar to other pathogenetically different wounds, including MOIST-based local therapy and elastic compression when it is not contraindicated. Persistent inflammatory processes are increasingly demonstrated as responsible for the chronicity of many skin ulcers. New data concerning the biological phases of wound healing and the molecules that play crucial roles in this process suggested the use of new specific therapies. Some of them such as growth factors and platelet-rich plasma are prevalently used as topical biologic agents with variable benefits. In recent years, a new class of systemic anti-inflammatory molecules, better known as biologic drugs, have been introduced in the cure of chronic inflammatory diseases that can induce microangiopathic injuries and ulcerative complication. They enlarged the therapeutic options in case of nonresponder microangiopathic ulcers and could represent a future model of “pathogenetically based” therapy of skin ulcers.

2019 ◽  
pp. 78-86 ◽  
Author(s):  
G. V. Poryadin ◽  
J. M. Salmasi ◽  
A. N. Kazimirsky

Local inflammatory diseases caused by various infections are one of the most common pathologies in medical practice. For example, tonsillopharyngitis. This disease is extremely frequent for a physician’s practice. There is a fair amount of drugs, which supposed to be helpful against tonsillopharyngitis, but different drugs are also not the same in their pharmacological effects. In gynecological practice, frequent diseases are specific and non-specific vulvovaginitis, which have inflammatory and infectious components. For administrating local pharmacotherapy in gynecology against inflammation, a large number of drugs with different mechanisms of action are proposed. In this study, we focused on key pathological mechanisms associated with acute and chronic inflammation, for which these drugs should be exposed by their pharmacokinetic and pharmacodynamic properties. The best combination of these properties is available for benzydamine hydrochloride. Benzydamine hydrochloride has a wide antimicrobic activity against bacteria and Candida spices both albicans and non-albicans strains and allows to influence on etiologic cause of the disease. Also benzydamine hydrochloride associated with «cytokine» mechanism of anti-inflammatory action, which means that he does not affect COX enzymes and it allows to avoid gastrotoxic adverse events. Also, in this work showed and discussed aspects of the interaction of benzydamine with local immune system and justification of useful usage the benzydamine for local therapy of acute and chronic inflammatory processes caused by various infections.


2009 ◽  
Vol 7 (2) ◽  
pp. 63-69 ◽  
Author(s):  
M.L. Castellani ◽  
P. Felaco ◽  
F. Pandolfp ◽  
V. Salini ◽  
D. De Amicis ◽  
...  

Inflammatory diseases represent one of the major causes of morbidity and mortality throughout the world and they affect the functions of several tissues. The pathophysiology of these diseases involves release of many pro-inflammatory mediators such as cytokines/chemokines, histamine, C3a, C5a (complement components), bradykinin, leukotrienes (LTC4, LTD4, LTE4), PAF, and substance P, in addition to anti-inflammatory molecules. Recently, it has been demonstrated that neuroimmune interactions are important in the initiation and progress of inflammatory processes. Substance P is an 11-amino acid neuropeptide that is released from nerve endings in many tissues. It acts via membrane-bound NK1 receptors (NK1R). Inflammatory and neuropeptides such as substance P stimulate the release of chemokines, in particular IL-8, a potent neutrophil chemoattractant. Expression of IL-8 is regulated mainly by the transcription factors NF-kappaB, activating protein-1. Substance P plays an important role in immunological and inflammatory states, and it is a mediator of tissue injury, asthma, arthritis, allergy and autoimmune diseases. In this article, our studies revisited the interrelationship between these two powerful inflammatory compounds: substance P and cytokines. These observations suggest that these inflammatory molecules may represent a potential therapeutic target to treat several inflammatory states.


2019 ◽  
Vol 20 (3) ◽  
pp. 459 ◽  
Author(s):  
Leila Kheirandish-Gozal ◽  
David Gozal

Obstructive sleep apnea syndrome (OSAS) is a markedly prevalent condition across the lifespan, particularly in overweight and obese individuals, which has been associated with an independent risk for neurocognitive, behavioral, and mood problems as well as cardiovascular and metabolic morbidities, ultimately fostering increases in overall mortality rates. In adult patients, excessive daytime sleepiness (EDS) is the most frequent symptom leading to clinical referral for evaluation and treatment, but classic EDS features are less likely to be reported in children, particularly among those with normal body-mass index. The cumulative evidence collected over the last two decades supports a conceptual framework, whereby sleep-disordered breathing in general and more particularly OSAS should be viewed as low-grade chronic inflammatory diseases. Accordingly, it is assumed that a proportion of the morbid phenotypic signature in OSAS is causally explained by underlying inflammatory processes inducing end-organ dysfunction. Here, the published links between OSAS and systemic inflammation will be critically reviewed, with special focus on the pro-inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), since these constitute classical prototypes of the large spectrum of inflammatory molecules that have been explored in OSAS patients.


2021 ◽  
Vol 13 ◽  
pp. 1759720X2110026
Author(s):  
Chinar R. Parikh ◽  
Jaya K. Ponnampalam ◽  
George Seligmann ◽  
Leda Coelewij ◽  
Ines Pineda-Torra ◽  
...  

The treatment of inflammatory arthritis has been revolutionised by the introduction of biologic treatments. Many biologic agents are currently licensed for use in both paediatric and adult patients with inflammatory arthritis and contribute to improved disease outcomes compared with the pre-biologic era. However, immunogenicity to biologic agents, characterised by an immune reaction leading to the production of anti-drug antibodies (ADAs), can negatively impact the therapeutic efficacy of biologic drugs and induce side effects to treatment. This review explores for the first time the impact of immunogenicity against all licensed biologic treatments currently used in inflammatory arthritis across age, and will examine any significant differences between ADA prevalence, titres and timing of development, as well as ADA impact on therapeutic drug levels, clinical efficacy and side effects between paediatric and adult patients. In addition, we will investigate factors associated with differences in immunogenicity across biologic agents used in inflammatory arthritis, and their potential therapeutic implications.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wen-Teng Chang ◽  
Ming-Yuan Hong ◽  
Chien-Liang Chen ◽  
Chi-Yuan Hwang ◽  
Cheng-Chieh Tsai ◽  
...  

Abstract Background Glucocorticoids (GCs) have been extensively used as essential modulators in clinical infectious and inflammatory diseases. The GC receptor (GR) is a transcription factor belonging to the nuclear receptor family that regulates anti-inflammatory processes and releases pro-inflammatory cytokines, such as interleukin (IL)-6. Results Five putative GR binding sites and other transcriptional factor binding sites were identified on theIL-6 promoter, and dexamethasone (DEX) was noted to reduce the lipopolysaccharide (LPS)-induced IL-6 production. Among mutant transcriptional factor binding sites, nuclear factor-kappa B (NF-κB), activator protein (AP)-1, and specificity protein (Sp)1–2 sites reduced basal and LPS-induced IL-6 promoter activities through various responses. The second GR binding site (GR2) was noted to play a crucial role in both basal and inducible promoter activities in LPS-induced inflammation. Conclusions We concluded that selective GR2 modulator might exert agonistic and antagonistic effects and could activate crucial signaling pathways during the LPS-stimulated inflammatory process.


1995 ◽  
Vol 4 (1) ◽  
pp. 5-15 ◽  
Author(s):  
C. Haanen ◽  
I. Vermes

During the last few decades it has been recognized that cell death is not the consequence of accidental injury, but is the expression of a cell suicide programme. Kerr et al. (1972) introduced the term apoptosis. This form of cell death is under the influence of hormones, growth factors and cytokines, which depending upon the receptors present on the target cells, may activate a genetically controlled cell elimination process. During apoptosis the cell membrane remains intact and the cell breaks into apoptotic bodies, which are phagocytosed. Apoptosis, in contrast to necrosis, is not harmful to the host and does not induce any inflammatory reaction. The principal event that leads to inflammatory disease is cell damage, induced by chemical/physical injury, anoxia or starvation. Cell damage means leakage of cell contents into the adjacent tissues, resulting in the capillary transmigration of granulocytes to the injured tissue. The accumulation of neutrophils and release of enzymes and oxygen radicals enhances the inflammatory reaction. Until now there has been little research into the factors controlling the accumulation and the tissue load of granulocytes and their histotoxic products in inflammatory processes. Neutrophil apoptosis may represent an important event in the control of intlamtnation. It has been assumed that granulocytes disintegrate to apoptotic bodies before their fragments are removed by local macrophages. Removal of neutrophils from the inflammatory site without release of granule contents is of paramount importance for cessation of inflammation. In conclusion, apoptotic cell death plays an important role in inflammatory processes and in the resolution of inflammatory reactions. The facts known at present should stimulate further research into the role of neutrophil, eosinophil and macrophage apoptosis in inflammatory diseases.


ChemInform ◽  
2009 ◽  
Vol 40 (20) ◽  
Author(s):  
Y. S. Sadanandam ◽  
Meera M. Shetty ◽  
A. Bhaskar Rao ◽  
Y. Rambabu

1938 ◽  
Vol 34 (1) ◽  
pp. 108-108
Author(s):  
B. Ivanov

Antivirus is used in surgery, firstly, to treat infected wounds and inflammatory processes of the skin and mucous membranes, and, secondly, to prevent and treat inflammatory diseases of the peritoneum and abdominal cavity.


2017 ◽  
Vol 23 (2) ◽  
Author(s):  
Natalya Drohomyretska

Hemomicrocirculatory system – is a complex structure that reacts in every pathological process even before the clinical period and takes the first blow. The study of microhemocirculation will provide an opportunity to solve the important for practical medicine questions of pathogenesis of many diseases, as for the prevention and treatment of regional disorders of blood circulation.The objective of the research is to study the state of the hemomicrocirculatory bed (HMCB) of adventitia of varicose veins of the small pelvis (VVSP) in women with chronic inflammatory processes of the organs of the small pelvis (CIPOSP).Materials and methods of research. To evaluate the restructuring of the HMCB of adventitia of VVSP, the operating material of 12 women of reproductive age was used. Mainly, there were pieces of the ovarian vein. The study of the HMCB in the vein wall was performed by the non-injecting method of silver impregnation according to V.V. Kupriyanov. To standardize the results, the condition of the HMCB of adventitia of the venous wall in norm was studied in 5 women of reproductive age, who died as a result of various traumas.Results of the research. After the performed studies, the structural-morphological changes of the HMCB of the adventitia of the small pelvis veins were revealed. The dilation of capillaries, postcapillaries, postcapillary venules was observed. The diameter of the vessels of the HMCB of the ovarian vein adventitia was: venule – 94.21 ± 1.38 μM in comparison with the norm – 48.78 ± 1.60 μM (p<0.001); post-capillary venules – 46.76 ± 1.04 μM in comparison with the norm – 28.29 ± 1.1.01 μM (p<0.001); the capillaries were 11.22 ± 0.14 μM in comparison with the norm – 8.24 ± 0.16 μM (p<0.05), arterioles – 29.02 ± 0.76 μM in comparison with the norm – 25.19 ± 1.15 μM (p<0.01). The architectonics of the arterioles is almost unchanged. Lumen of venules is filled with formed elements. The structure of capillaries is polymorphic. The capillary net was localized and concentrated or was formed as a thick planar net, the capillaries were expanded. There were arterio-venulous anastomoses. Endothelial nuclei are shortened. In some preparations, the diameter of the arterioles corresponded to the diameter of the collection venules.  Conclusions:1. The first discovered by us changes in HMCB of adventitia of varicose veins of the small pelvis in women with CIPOSP can be one of the pathogenetic links of the development and progression of the varicose vein itself, which in turn aggravates the course of chronic inflammation.      2. The timely appointment of drugs that improve microcirculation will enable to prevent the development of dystrophic changes in the vein wall, improve the course of chronic inflammatory processes and reduce or completely eliminate the syndrome of “chronic pelvic pain”.


Pharmaceutics ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 1802
Author(s):  
Elena Munoz-Perez ◽  
Ainhoa Gonzalez-Pujana ◽  
Manoli Igartua ◽  
Edorta Santos-Vizcaino ◽  
Rosa Maria Hernandez

Considering the high prevalence and the complex pharmacological management of immune-mediated inflammatory diseases (IMIDs), the search for new therapeutic approaches for their treatment is vital. Although the immunomodulatory and anti-inflammatory effects of mesenchymal stromal cells (MSCs) have been extensively studied as a potential therapy in this field, direct MSC implantation presents some limitations that could slow down the clinical translation. Since the beneficial effects of MSCs have been mainly attributed to their ability to secrete a plethora of bioactive factors, their secretome has been proposed as a new and promising pathway for the treatment of IMIDs. Formed from soluble factors and extracellular vesicles (EVs), the MSC-derived secretome has been proven to elicit immunomodulatory effects that control the inflammatory processes that occur in IMIDs. This article aims to review the available knowledge on the MSC secretome, evaluating the advances in this field in terms of its composition, production and application, as well as analyzing the pending challenges in the field. Moreover, the latest research involving secretome administration in IMIDs is discussed to provide an updated state-of-the-art for this field. Finally, novel secretome delivery alternatives are reviewed, paying special attention to hydrogel encapsulation as one of the most convenient and promising strategies.


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