1.
Wold, Agnes E, 1955, et al.
(författare)
Breast feeding and the intestinal microflora of the infant--implications for protection against infectious diseases.
2000
Ingår i: Advances in experimental medicine and biology. - Boston : Kluwer Academic Publishers. - 0065-2598. ; 478, s. 77-93
Forskningsöversikt (refereegranskat) abstract
Human breast milk contains an array of factors with anti-infectious potential, such as immunoglobulins (especially secretory IgA), oligosaccharides and glycoproteins with anti-adhesive capacity, and cytokines. Breast-feeding is associated with protection from the following infections or infection-related conditions: gastroenteritis, upper and lower respiratory tract infection, acute otitis media, urinary tract infection, neonatal septicaemia and necrotizing enterocolitis. Some of the protective effects may derive from an altered mucosal colonization pattern in the breast-fed infant. In other instances breast-fed infants develop less symptoms to the same microbe which causes disease in the bottle-fed infant. An example of an altered colonization pattern is that breast-fed infants have less P-fimbriated, but more type 1-fimbriated E. coli. This may protect against urinary tract infection in the breast-fed infant since P. fimbriae are the major virulence factor for urinary tract infection. An example of changed consequences of the same microbial colonization is that secretory IgA in the breast-milk protects very efficiently from translocation of intestinal bacteria across the gut mucosa by coating intestinal bacteria and blocking their interaction with the epithelium. This mechanism may protect the infant from septicaemia of gut origin and, possibly, necrotizing enterocolitis. Breast-milk is also highly anti-inflammatogenic and contains hormone like factors which counteract diarrhea. Thus, breast-fed infants may be colonized by recognized diarrheal pathogens and still remain healthy. Due to a less virulent intestinal microflora and decreased translocation breast-fed infants will obtain less stimuli for the gut immune system, resulting, in e.g., lower salivary IgA antibody titres.
2.
Gorreja, Frida
(författare)
Gene expression changes as predictors of the immune-modulatory effects of probiotics: Towards a better understanding of strain-disease specific interactions
2019
Ingår i: NFS Journal. - : Elsevier BV. - 2352-3646. ; 14-15, s. 1-5
Forskningsöversikt (refereegranskat) abstract
Probiotic bacteria in clinical use grant a health benefit to humans when administered in adequate amount, frequency, and period. The majority of research into probiotics focuses on the usage of probiotics in the prevention and/or treatment of digestive diseases or other diseases related to an aberrant microbiota or inflamed mucosa. Hence, translational research often excludes the underlying multifaceted mechanisms of action of these supplements. This mini-review endeavours to summarize the mechanisms of action related to changes in gene expression, with a focus on studies published from 2015 to 2018. Alteration of gene expression has been described in the justification of the use of probiotics for certain diseases such as irritable bowel disease. The review centers on in vivo studies considering inflammation-related genes and pathways in gastrointestinal tissue and blood, and in vitro studies mainly from human intestinal epithelial cells but also immune cells. Probiotics are prospectively anti-inflammatory therapies in diseases with an impaired gut mucosa. Translational research will aim to target changes in genes expression that are strain- and disease-specific.
3.
4.
von Hertzen, Leena, et al.
(författare)
Helsinki alert of biodiversity and health
2015
Ingår i: Annals of Medicine. - : Informa UK Limited. - 1365-2060 .- 0785-3890. ; 47:3, s. 218-225
Forskningsöversikt (refereegranskat) abstract
Urban living in built environments, combined with the use of processed water and food, may not provide the microbial stimulation necessary for a balanced development of immune function. Many chronic inflammatory disorders, including allergic, autoimmune, metabolic, and even some behavioural disorders, are linked to alteration in the human commensal microbiota. Sedentary lifestyle is associated with reduced exposure to a broad spectrum of environmental micro-organisms and surplus energy balance, both risk factors of chronic inflammatory disorders. According to the Biodiversity Hypothesis, an environment with diverse macrobiota and microbiota modifies and enriches the human microbiota, which in turn is crucial in the development and maintenance of appropriate immune function. These issues were discussed in the symposium 'Chronic Inflammation, Lifestyle and Environment ', held in Helsinki, 20 - 22 August 2014, under the sponsorship of the Yrjo Jahnsson Foundation. This paper briefly outlines the recent findings in the context of the environment, lifestyle, and health; discusses the forces that undermine immune tolerance in urban environments; and highlights the possibilities to restore broken immune tolerance among urban dwellers, summarizing the main messages in four statements and calling for actions to combat major public health threats.
5.
Cenci, M. Angela, et al.
(författare)
Animal models of l-dopa-induced dyskinesia in Parkinson's disease
2018
Ingår i: Movement Disorders. - : Wiley. - 0885-3185. ; 33:6, s. 889-899
Forskningsöversikt (refereegranskat) abstract
Understanding the biological mechanisms of l-dopa-induced motor complications is dependent on our ability to investigate these phenomena in animal models of Parkinson's disease. The most common motor complications consist in wearing-off fluctuations and abnormal involuntary movements appearing when plasma levels of l-dopa are high, commonly referred to as peak-dose l-dopa-induced dyskinesia. Parkinsonian models exhibiting these features have been well-characterized in both rodent and nonhuman primate species. The first animal models of peak-dose l-dopa-induced dyskinesia were produced in monkeys lesioned with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and treated chronically with l-dopa to elicit choreic movements and dystonic postures. Seminal studies were performed in these models using both metabolic mapping and electrophysiological techniques, providing fundamental pathophysiological insights that have stood the test of time. A decade later, it was shown possible to reproduce peak-dose l-dopa-induced dyskinesia in rats and mice rendered parkinsonian with nigrostriatal 6-hydroxydopamine lesions. When treated with l-dopa, these animals exhibit abnormal involuntary movements having both hyperkinetic and dystonic components. These models have enabled molecular- and cellular-level investigations into the mechanisms of l-dopa-induced dyskinesia. A flourishing literature using genetically engineered mice is now unraveling the role of specific genes and neural circuits in the development of l-dopa-induced motor complications. Both non-human primate and rodent models of peak-dose l-dopa-induced dyskinesia have excellent construct validity and provide valuable tools for discovering therapeutic targets and evaluating potential treatments.
6.
Erlanson-Albertsson, Charlotte, et al.
(författare)
The importance of food for endotoxemia and an inflammatory response
2021
Ingår i: International Journal of Molecular Sciences. - : MDPI AG. - 1661-6596 .- 1422-0067. ; 22:17
Forskningsöversikt (refereegranskat) abstract
Bacterial endotoxin is a potent inflammatory antigen abundant in the human intestine. Endotoxins circulate in the blood at low concentrations in all healthy individuals. Elevated levels of circulatory endotoxins may cause inflammation with the development of chronic disease, either affecting metabolism, neurological disease, or resistance to viral and bacterial infections. The most important endotoxin is LPS, being a superantigen. In this narrative review, the effect of various food components to postprandially elevate circulating LPS and inflammatory markers is described. There is evidence that the intake of food enriched in fat, in particular saturated fat, may elevate LPS and pro-inflammatory markers. This occurs in both normal-weight and obese subjects. In obese subjects, inflammatory markers are already elevated before meal consumption. The importance of food choice for endotoxemia and inflammatory response is discussed.
7.
8.
Hakansson, A. P., et al.
(författare)
Bacterial-host interactions : Physiology and pathophysiology of respiratory infection
2018
Ingår i: Physiological Reviews. - : American Physiological Society. - 0031-9333 .- 1522-1210. ; 98:2, s. 781-811
Forskningsöversikt (refereegranskat) abstract
It has long been thought that respiratory infections are the direct result of acquisition of pathogenic viruses or bacteria, followed by their overgrowth, dissemination, and in some instances tissue invasion. In the last decades, it has become apparent that in contrast to this classical view, the majority of microorganisms associated with respiratory infections and inflammation are actually common members of the respiratory ecosystem and only in rare circumstances do they cause disease. This suggests that a complex interplay between host, environment, and properties of colonizing microorganisms together determines disease development and its severity. To understand the pathophysiological processes that underlie respiratory infectious diseases, it is therefore necessary to understand the host-bacterial interactions occurring at mucosal surfaces, along with the microbes inhabiting them, during symbiosis. Current knowledge regarding host-bacterial interactions during asymptomatic colonization will be discussed, including a plausible role for the human microbiome in maintaining a healthy state. With this as a starting point, we will discuss possible disruptive factors contributing to dysbiosis, which is likely to be a key trigger for pathobionts in the development and pathophysiology of respiratory diseases. Finally, from this renewed perspective, we will reflect on current and potential new approaches for treatment in the future.
9.
Kakooza-Mwesige, Angelina, et al.
(författare)
Emerging Viral Infections in Sub-Saharan Africa and the Developing Nervous System : A Mini Review
2018
Ingår i: Frontiers in Neurology. - : Frontiers Media S.A.. - 1664-2295. ; 9
Forskningsöversikt (refereegranskat) abstract
The global public health concern is heightened over the increasing number of emerging viruses, i.e., newly discovered or previously known that have expanded into new geographical zones. These viruses challenge the health-care systems in sub-Saharan Africa (SSA) countries from which several of them have originated and been transmitted by insects worldwide. Some of these viruses are neuroinvasive, but have been relatively neglected by neuroscientists. They may provide experiments by nature to give a time window for exposure to a new virus within sizeable, previously non-infected human populations, which, for instance, enables studies on potential long-term or late-onset effects on the developing nervous system. Here, we briefly summarize studies on the developing brain by West Nile, Zika, and Chikungunya viruses, which are mosquito-borne and have spread worldwide out of SSA. They can all be neuroinvasive, but their effects vary from malformations caused by prenatal infections to cognitive disturbances following perinatal or later infections. We also highlight Ebola virus, which can leave surviving children with psychiatric disturbances and cause persistent infections in the non-human primate brain. Greater awareness within the neuroscience community is needed to emphasize the menace evoked by these emerging viruses to the developing brain. In particular, frontline neuroscience research should include neuropediatric follow-up studies in the field on long-term or late-onset cognitive and behavior disturbances or neuropsychiatric disorders. Studies on pathogenetic mechanisms for viral-induced perturbations of brain maturation should be extended to the vulnerable periods when neurocircuit formations are at peaks during infancy and early childhood.
10.
Rostedt Punga, Anna, et al.
(författare)
Circulating microRNAs as potential biomarkers in myasthenia gravis patients.
2018
Ingår i: Annals of the New York Academy of Sciences. - : Wiley. - 0077-8923 .- 1749-6632. ; 1412:1, s. 33-40
Forskningsöversikt (refereegranskat) abstract
MicroRNAs (miRNAs) are small noncoding RNA molecules that bind to specific mRNA targets and regulate a wide range of important biological processes within cells. Circulating miRNAs are released into the extracellular space and can be measured in most biofluids, including blood serum and plasma. Recently, circulating miRNAs have emerged as easily accessible markers in various body fluids with different profiles and quantities specific for different human disorders, including autoimmune diseases. In myasthenia gravis (MG), diagnostic tests such as titers of serum autoantibodies specific for either the acetylcholine receptor (AChR+) or muscle‐specific tyrosine kinase (MuSK+) do not necessarily reflect disease progression, and there is a great need for reliable objective biomarkers to monitor the disease course and therapeutic response. Recent studies in AChR+ MG revealed elevated levels of the immuno‐miRNAs miR‐150‐5p and miR‐21‐5p. Of particular importance, levels of miR‐150‐5p were lower in immunosuppressed patients and in patients with clinical improvement following thymectomy. In MuSK+ MG, another profile of circulating miRNAs was found, including upregulation of the let‐7 family of miRNAs. Here, we summarize the potential role of circulating miRNAs as biomarkers in general and in MG, and highlight important considerations for the analysis of circulating miRNA.
