scholarly journals Reacciones adversas a los alimentos: ¿Cuál es el papel de los microorganismos?

2021 ◽  
Vol 51 (3) ◽  
Author(s):  
Alberto Caminero

It is estimated that around 25% of the population worldwide experience adverse reactions to food, which are very diverse based on both etiology and clinical presentation. According to the pathophysiological processes involved, adverse reactions to foods can be broadly classified as sensitivities or intolerances, depending on whether they are immune-mediated, or not. Specifically, food sensitivities have become a growing clinical, economic, and social problem nowadays. Although the reason for the increased prevalence of well-determined food sensitives such as celiac disease and food allergies is not well understood, the role of microbes in both inducing and protecting from these conditions has been proposed. First, several studies suggest that the gut microbiota, the vast number of microbes that live in our digestive tract, influence the appearance of different adverse reactions to food. These studies are based on observational changes in the composition and function of the fecal microbiota of celiac, allergic and food intolerant patients when compared to controls or healthy participants. Second, infectious microbial agents have been related to the loss of oral tolerance towards dietary components and the occurrence of different adverse reactions to foods. However, how could microbes participate in food sensitivities and intolerances from a mechanistic point of view? Preclinical studies with animal models not only support observations in humans, they also show a causal role of microbes in the occurrence and course of these diseases, while informing the specific underlying mechanisms. The aim of this review is to summarize the scientific evidence that supports the role of microbes in the main adverse reactions to food described, with an emphasis on the underlying mechanisms. The discovery of the main molecular pathways involved in pathogenic reactions to diet foods will accelerate the development of new therapeutic approaches with the aim of preventing and treating food sensitivities and intolerances.

2020 ◽  
Author(s):  
Jaap van Krugten ◽  
Noémie Danné ◽  
Erwin J.G. Peterman

AbstractSensing and reacting to the environment is essential for survival and procreation of most organisms. Caenorhabditis elegans senses soluble chemicals with transmembrane proteins (TPs) in the cilia of its chemosensory neurons. Development, maintenance and function of these cilia relies on intraflagellar transport (IFT), in which motor proteins transport cargo, including sensory TPs, back and forth along the ciliary axoneme. Here we use live fluorescence imaging to show that IFT machinery and the sensory TP OCR-2 reversibly redistribute along the cilium after exposure to repellant chemicals. To elucidate the underlying mechanisms, we performed single-molecule tracking experiments and found that OCR-2 distribution depends on an intricate interplay between IFT-driven transport, normal diffusion and subdiffusion that depends on the specific location in the cilium. These insights in the role of IFT on the dynamics of cellular signal transduction contribute to a deeper understanding of the regulation of sensory TPs and chemosensing.


2020 ◽  
Vol 21 (8) ◽  
pp. 2867 ◽  
Author(s):  
Gabsik Yang ◽  
Jin Kyung Seok ◽  
Han Chang Kang ◽  
Yong-Yeon Cho ◽  
Hye Suk Lee ◽  
...  

Atopic dermatitis (AD) is a common and relapsing skin disease that is characterized by skin barrier dysfunction, inflammation, and chronic pruritus. While AD was previously thought to occur primarily in children, increasing evidence suggests that AD is more common in adults than previously assumed. Accumulating evidence from experimental, genetic, and clinical studies indicates that AD expression is a precondition for the later development of other atopic diseases, such as asthma, food allergies, and allergic rhinitis. Although the exact mechanisms of the disease pathogenesis remain unclear, it is evident that both cutaneous barrier dysfunction and immune dysregulation are critical etiologies of AD pathology. This review explores recent findings on AD and the possible underlying mechanisms involved in its pathogenesis, which is characterized by dysregulation of immunological and skin barrier integrity and function, supporting the idea that AD is a systemic disease. These findings provide further insights for therapeutic developments aiming to repair the skin barrier and decrease inflammation.


2021 ◽  
Vol 11 ◽  
Author(s):  
Xiangjun Liu ◽  
Ye Cheng ◽  
Dan Zang ◽  
Min Zhang ◽  
Xiuhua Li ◽  
...  

The influence of microbiota on host health and disease has attracted adequate attention, and gut microbiota components and microbiota-derived metabolites affect host immune homeostasis locally and systematically. Some studies have found that gut dysbiosis, disturbance of the structure and function of the gut microbiome, disrupts pulmonary immune homeostasis, thus leading to increased disease susceptibility; the gut-lung axis is the primary cross-talk for this communication. Gut dysbiosis is involved in carcinogenesis and the progression of lung cancer through genotoxicity, systemic inflammation, and defective immunosurveillance. In addition, the gut microbiome harbors the potential to be a novel biomarker for predicting sensitivity and adverse reactions to immunotherapy in patients with lung cancer. Probiotics and fecal microbiota transplantation (FMT) can enhance the efficacy and depress the toxicity of immune checkpoint inhibitors by regulating the gut microbiota. Although current studies have found that gut microbiota closely participates in the development and immunotherapy of lung cancer, the mechanisms require further investigation. Therefore, this review aims to discuss the underlying mechanisms of gut microbiota influencing carcinogenesis and immunotherapy in lung cancer and to provide new strategies for governing gut microbiota to enhance the prevention and treatment of lung cancer.


PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7224 ◽  
Author(s):  
Héla Mkaouar ◽  
Nizar Akermi ◽  
Aicha Kriaa ◽  
Anne-Laure Abraham ◽  
Amin Jablaoui ◽  
...  

Serine Protease Inhibitors (Serpins) control tightly regulated physiological processes and their dysfunction is associated to various diseases. Thus, increasing interest is given to these proteins as new therapeutic targets. Several studies provided functional and structural data about human serpins. By comparison, only little knowledge regarding bacterial serpins exists. Through the emergence of metagenomic studies, many bacterial serpins were identified from numerous ecological niches including the human gut microbiota. The origin, distribution and function of these proteins remain to be established. In this report, we shed light on the key role of human and bacterial serpins in health and disease. Moreover, we analyze their function, phylogeny and ecological distribution. This review highlights the potential use of bacterial serpins to set out new therapeutic approaches.


2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Yuqin Ye ◽  
Hongyu Xu ◽  
Xinhong Su ◽  
Xiaosheng He

Although synaptic plasticity in neural circuits is orchestrated by an ocean of genes, molecules, and proteins, the underlying mechanisms remain poorly understood. Recently, it is well acknowledged that miRNA exerts widespread regulation over the translation and degradation of target gene in nervous system. Increasing evidence suggests that quite a few specific miRNAs play important roles in various respects of synaptic plasticity including synaptogenesis, synaptic morphology alteration, and synaptic function modification. More importantly, the miRNA-mediated regulation of synaptic plasticity is not only responsible for synapse development and function but also involved in the pathophysiology of plasticity-related diseases. A review is made here on the function of miRNAs in governing synaptic plasticity, emphasizing the emerging regulatory role of individual miRNAs in synaptic morphological and functional plasticity, as well as their implications in neurological disorders. Understanding of the way in which miRNAs contribute to synaptic plasticity provides rational clues in establishing the novel therapeutic strategy for plasticity-related diseases.


Bone Research ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Lijun Wang ◽  
Huiliang Yang ◽  
Jiahui Huang ◽  
Shaopeng Pei ◽  
Liyun Wang ◽  
...  

AbstractThe maturation and function of osteoblasts (OBs) rely heavily on the reversible phosphorylation of signaling proteins. To date, most of the work in OBs has focused on phosphorylation by tyrosyl kinases, but little has been revealed about dephosphorylation by protein tyrosine phosphatases (PTPases). SHP2 (encoded by PTPN11) is a ubiquitously expressed PTPase. PTPN11 mutations are associated with both bone and cartilage manifestations in patients with Noonan syndrome (NS) and metachondromatosis (MC), although the underlying mechanisms remain elusive. Here, we report that SHP2 deletion in bone gamma-carboxyglutamate protein-expressing (Bglap+) bone cells leads to massive osteopenia in both trabecular and cortical bones due to the failure of bone cell maturation and enhanced osteoclast activity, and its deletion in Bglap+ chondrocytes results in the onset of enchondroma and osteochondroma in aged mice with increased tubular bone length. Mechanistically, SHP2 was found to be required for osteoblastic differentiation by promoting RUNX2/OSTERIX signaling and for the suppression of osteoclastogenesis by inhibiting STAT3-mediated RANKL production by osteoblasts and osteocytes. These findings are likely to explain the compromised skeletal system in NS and MC patients and to inform the development of novel therapeutics to combat skeletal disorders.


2020 ◽  
Vol 18 ◽  
Author(s):  
Qianyu Shi ◽  
Quancheng Cheng ◽  
Chunhua Chen

: Autophagy is a strictly regulated process which degrades and recycles long-lived or misfolded proteins and damaged organelles for the maintenance of energy and function homeostasis of cells. Insufficient oxygen and glucose supply caused by cerebral ischemia leads to higher ratio of AMP/ATP, which will activate AMPK pathway to initiate the process of autophagy. Accumulating evidence shows that autophagy participates in the pathogenesis of ischemic stroke as a doubleedge sword. However, the exact role of autophagy in the pathogenesis of ischemic stroke is controversial and yet to be elucidated. In this review, we expounded the autophagy pathway both in physiological condition and in ischemic stroke. We also focused on discussing the double-edge sword effect of autophagy in brain ischemia and its underlying mechanisms. In addition, we reviewed potential therapeutic strategies for ischemic stroke targeting autophagy pathway.


2021 ◽  
Vol 11 ◽  
Author(s):  
Ana Ghenciulescu ◽  
Rebecca J. Park ◽  
Philip W. J. Burnet

The human gut microbiome is emerging as a key modulator of homeostasis, with far-reaching implications for various multifactorial diseases, including anorexia nervosa (AN). Despite significant morbidity and mortality, the underlying mechanisms of this eating disorder are poorly understood, but the classical view defining AN as a purely psychiatric condition is increasingly being challenged. Accumulating evidence from comparative studies of AN and healthy fecal microbial composition reveals considerable low divergence and altered taxonomic abundance of the AN gut microbiome. When integrated with preclinical data, these findings point to a significant role of the gut microbiome in AN pathophysiology, via effects on host energy metabolism, intestinal permeability, immune function, appetite, and behavior. While complex causal relationships between genetic risk factors, dietary patterns and microbiome, and their relevance for AN onset and perpetuation have not been fully elucidated, preliminary clinical studies support the use of microbiome-based interventions such as fecal microbiota transplants and probiotics as adjuvants to standard AN therapies. Future research should aim to move from observational to mechanistic, as dissecting how specific microbial taxa interact with the host to impact the development of AN could help design novel therapeutic approaches that more effectively address the severe comorbidities and high relapse rate of this serious disorder.


2017 ◽  
Vol 131 (15) ◽  
pp. 1923-1940 ◽  
Author(s):  
Steven Horsburgh ◽  
Nicola Fullard ◽  
Mathilde Roger ◽  
Abbie Degnan ◽  
Stephen Todryk ◽  
...  

The skin is the largest organ of the integumentary system and possesses a vast number of functions. Due to the distinct layers of the skin and the variety of cells which populate each, a tightly regulated network of molecular signals control development and regeneration, whether due to programmed cell termination or injury. MicroRNAs (miRs) are a relatively recent discovery; they are a class of small non-coding RNAs which possess a multitude of biological functions due to their ability to regulate gene expression via post-transcriptional gene silencing. Of interest, is that a plethora of data demonstrates that a number of miRs are highly expressed within the skin, and are evidently key regulators of numerous vital processes to maintain non-aberrant functioning. Recently, miRs have been targeted as therapeutic interventions due to the ability of synthetic ‘antagomiRs’ to down-regulate abnormal miR expression, thereby potentiating wound healing and attenuating fibrotic processes which can contribute to disease such as systemic sclerosis (SSc). This review will provide an introduction to the structure and function of the skin and miR biogenesis, before summarizing the literature pertaining to the role of miRs. Finally, miR therapies will also be discussed, highlighting important future areas of research.


2020 ◽  
Vol 21 (9) ◽  
pp. 3070 ◽  
Author(s):  
Manuela Labbozzetta ◽  
Monica Notarbartolo ◽  
Paola Poma

Multidrug resistance (MDR), of the innate and acquired types, is one of major problems in treating tumor diseases with a good chance of success. In this review, we examine the key role of nuclear factor-kappa B (NF-κB) to induce MDR in three tumor models characterized precisely by innate or acquired MDR, in particular triple negative breast cancer (TNBC), hepatocellular carcinoma (HCC), and acute myeloid leukemia (AML). We also present different pharmacological approaches that our group have employed to reduce the expression/activation of this transcriptional factor and thus to restore chemo-sensitivity. Finally, we examine the latest scientific evidence found by other groups, the most significant clinical trials regarding NF-κB, and new perspectives on the possibility to consider this transcriptional factor a valid drug target in neoplastic diseases.


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