Prevalence and antimicrobial resistance of bacterial uropathogens isolated from Iranian kidney transplant recipients: A systematic review and meta-analysis

Background: Urinary tract infection (UTI) is a major complication in patients who receive the kidney transplant. We aimed to evaluate the prevalence and antimicrobial resistance of bacterial uropathogens isolated from Iranian kidney transplant recipients. Methods: We searched according to Prisma protocol for UTI infection, prevalence, occurrence and distribution of bacteria and their pattern of antibiotic resistance among Iranian patients who receive kidney transplant through online electronic databases with MeSh terms and text words in published references in both Persian and English languages during 1990-2017. Data analysis was performed using Comprehensive meta-analysis software (CMA) by Cochrane Q and I2 Random Effects Model. Results: Eleven studies met the eligible inclusion criteria. The prevalence of UTI among kidney transplant patients varied from 11.7 to 67.5. The combined prevalence of UTI was 32.6. Among Gram-negative pathogens causing UTI, E. coli was the most dominant followed by Klebsiella pneumonia with prevalence 41.3 and 11.9, respectively. Also, amongst Gram-positive bacteria, the highest prevalence belonged to Enterococcus spp. (9.8) and coagulase-negative Staphylococci (9.4). Also in Gram-negative pathogens, the most resistance was to ampicillin (91.2), followed by ceftazidime (89.5). The minimum resistance was against imipenem with prevalence 14.3. Conclusion: The combined prevalence of UTI was 32.6. Gram-negative pathogens especially E. coli were the most agents of UTI in Iranian patients who receive kidney transplant. Also, in gram-negative pathogens, the most resistance was to ampicillin that it needs a new strategy for prophylaxis and treatment of UTI after the kidney transplant. © 2019, Iranian Journal of Public Health. All rights reserved

Molecular mechanisms regulating immune responses in thromboangiitis obliterans: a comprehensive review

Thromboangiitis obliterans (TAO) is a thrombotic-occlusive as well as an inflammatory peripheral vascular disease with unknown etiology. Recent evidence has supported the immunopathogenesis of the disease, however, the factors contributing to the altered immune function and vascular tissue inflammation are still unclear. This review was intended to collate the more current knowledge on the regulatory molecules involved in TAO from an immunoreactive perspective. The homeostasis of the immune system as well as a variety of progenitor cell populations appear to be affected during TAO and these alterations are associated with intrinsic signaling defects that are directing to an improved understanding of the crosstalk between angiogenesis and the immune system, as well as the potential of new co-targeting strategies applying both immunotherapy and angiogenic therapy

Anti-inflammatory and immune-modulatory impacts of berberine on activation of autoreactive T cells in autoimmune inflammation

Autoreactive inflammatory CD4+ T cells, such as T helper (Th)1 and Th17 subtypes, have been found to associate with the pathogenesis of autoimmune disorders. On the other hand, CD4+ Foxp3+ T regulatory (Treg) cells are crucial for the immune tolerance and have a critical role in the suppression of the excessive immune and inflammatory response promoted by these Th cells. In contrast, dendritic cells (DCs) and macrophages are immune cells that through their inflammatory functions promote autoreactive T-cell responses in autoimmune conditions. In recent years, there has been increasing attention to exploring effective immunomodulatory or anti-inflammatory agents from the herbal collection of traditional medicine. Berberine, an isoquinoline alkaloid, is one of the main active ingredients extracted from medicinal herbs and has been shown to exert various biological and pharmacological effects that are suggested to be mainly attributed to its anti-inflammatory and immunomodulatory properties. Several lines of experimental study have recently investigated the therapeutic potential of berberine for treating autoimmune conditions in animal models of human autoimmune diseases. Here, we aimed to seek mechanisms underlying immunomodulatory and anti-inflammatory effects of berberine on autoreactive inflammatory responses in autoimmune conditions. Reported data reveal that berberine can directly suppress functions and differentiation of pro-inflammatory Th1 and Th17 cells, and indirectly decrease Th cell-mediated inflammation through modulating or suppressing other cells assisting autoreactive inflammation, such as Tregs, DCs and macrophages. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Lt

Roles of GM-CSF in the Pathogenesis of Autoimmune Diseases: An Update.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) was first described as a growth factor that induces the differentiation and proliferation of myeloid progenitors in the bone marrow. GM-CSF also has an important cytokine effect in chronic inflammatory diseases by stimulating the activation and migration of myeloid cells to inflammation sites, promoting survival of target cells and stimulating the renewal of effector granulocytes and macrophages. Because of these pro-cellular effects, an imbalance in GM-CSF production/signaling may lead to harmful inflammatory conditions. In this context, GM-CSF has a pathogenic role in autoimmune diseases that are dependent on cellular immune responses such as multiple sclerosis (MS) and rheumatoid arthritis (RA). Conversely, a protective role has also been described in other autoimmune diseases where humoral responses are detrimental such as myasthenia gravis (MG), Hashimoto\u27s thyroiditis (HT), inflammatory bowel disease (IBD), and systemic lupus erythematosus (SLE). In this review, we aimed for a comprehensive analysis of literature data on the multiple roles of GM-CSF in autoimmue diseases and possible therapeutic strategies that target GM-CSF production

How the redox state regulates immunity

Oxidative stress is defined as an imbalance beween the levels of reactive oxygen species (ROS) and antioxidant defences. The view of oxidative stress as a cause of cell damage has evolved over the past few decades to a much more nuanced view of the role of oxidative changes in cell physiology. This is no more evident than in the field of immunity, where oxidative changes are now known to regulate many aspects of the immune response, and inflammatory pathways in particular. Our understanding of redox regulation of immunity now encompasses not only increases in reactive oxygen and nitrogen species, but also changes in the activities of oxidoreductase enzymes. These enzymes are important regulators of immune pathways both via changes in their redox activity, but also via other more recently identified cytokine-like functions. The emerging picture of redox regulation of immune pathways is one of increasing complexity and while therapeutic targeting of the redox environment to treat inflammatory disease is a possibility, any such strategy is likely to be more nuanced than simply inhibiting ROS production

The ERK and JNK pathways in the regulation of metabolic reprogramming.

Most tumor cells reprogram their glucose metabolism as a result of mutations in oncogenes and tumor suppressors, leading to the constitutive activation of signaling pathways involved in cell growth. This metabolic reprogramming, known as aerobic glycolysis or the Warburg effect, allows tumor cells to sustain their fast proliferation and evade apoptosis. Interfering with oncogenic signaling pathways that regulate the Warburg effect in cancer cells has therefore become an attractive anticancer strategy. However, evidence for the occurrence of the Warburg effect in physiological processes has also been documented. As such, close consideration of which signaling pathways are beneficial targets and the effect of their inhibition on physiological processes are essential. The MAPK/ERK and MAPK/JNK pathways, crucial for normal cellular responses to extracellular stimuli, have recently emerged as key regulators of the Warburg effect during tumorigenesis and normal cellular functions. In this review, we summarize our current understanding of the roles of the ERK and JNK pathways in controlling the Warburg effect in cancer and discuss their implication in controlling this metabolic reprogramming in physiological processes and opportunities for targeting their downstream effectors for therapeutic purposes.Brunel Research Initiative & Enterprise Fund, Brunel University of London (to CB), Kay Kendall Leukemia Fund (KKL443) (to CB), 250 Great Minds Fellowship, University of Leeds (to SP), AMMF Cholangiocarcinoma Charity (to SP and PMC), and Bloodwise (17014) (to SP and CB)

The Effect of Massage with Medium-Chain Triglyceride Oil on Weight Gain in Premature Neonates

Prematurity and poor weight gaining are important causes for neonatal hospitalization. The present study aimed to investigate the role of medium-chain triglyceride (MCT) oil via massage therapy as a supplementary nutritional method on the weight gain of Neonatal Intensive Care Units (NICU)-hospitalized neonates. This randomized clinical trial performed among 121 stable premature neonates hospitalized in the NICU of Qaem Educational Hospital, Mashhad, Iran. They were randomly divided into three groups: oil-massage, massage alone and control groups. These groups were compared on the basis of weight gain during a one-week interval. The three groups were matched for sex, mean gestational age, birth weight, head circumference, delivery, and feeding type (P>0.05). The mean weight gain on the 7th day in the oil massage group was 105±1.3gr and 52±0.1gr in the massage group; whereas 54±1.3gr weight loss was observed in the control group. Significant differences were observed between the oil-massage group and the other two groups, respectively (P=0.002 and P=0.000). The findings of this study suggest that transcutaneous feeding with MCT oil massage therapy in premature neonates can result in accelerated weight gain in this age group with no risk of NEC