Pub Date : 2018-06-07DOI: 10.15406/MOJI.2018.06.00200
O. Anatskaya, J. Erenpreisa, K. Salmina, A. VazquezMartin, A. Huna, N. Nikolsky, A. Vinogradov
Polyploid cells contain several copies of diploid genomes. These cells were found in all mammalian tissues where they were searched. In physiological conditions, genome accumulation is a part of development and differentiation programs. Polyploid cells present in heart, skin epithelium, placenta, liver, brain, and blood.1 In stressful condition polyploidy accompanies and stimulates pathological processes. Thus, the increase of polyploidy was documented in hypertensive heart, atherosclerotic vessels, cirrhotic liver and cancer.2 Despite ubiquitous distribution, the effect of polyploidy on gene expression remains not completely understood. Increasing evidence suggests that cell polyploidy may epigenetically alter gene expression and miRNA gene transcription in plants as well as in animals.3,4 miRNA which are short (20-22 nucleotide long) noncoding RNA reported to play various roles in human, plant and in some viruses.5,6 The impact of polyploidy on the transcriptome was investigated in hepatocytes, megakaryocytes, vascular epithelial cells, and placenta. Investigation of the differences in expression using the conservative double threshold led investigators to the conclusion that among several thousand genes not a single one is affected by polyploidy (as in the case of hepatocytes) or only several dozen genes are reactive.7 Moreover, for each cell type, this small set of genes turned out to be different. For instance, in the cells of vascular epithelium, several genes associated with the immune system were suppressed;8 in megakaryocytes, activation of tissue specific genes was registered; and, in decidual cells, activation of nuclear genes encoding mitochondrial proteins was detected.9 These differences suggest that the full effect of somatic polyploidy (if it exists) has not been identified yet. The absence of consensus is not surprising because mmaintaining gene dosage balance, polyploidy has little impact on separate gene activity. The weakness of ploidy associated effects make it difficult to identify common gene expression signature. At the same time, modifying activity of thousands of genes at a time, polyploidy participates in coordination of postnatal development, developmental programming, differentiation and pathogenesis of many diseases, including cardiovascular diseases and cancer.2,7,10–12
{"title":"Polyploidy activates biological pathways related to morphogenesis in mammalian tissues","authors":"O. Anatskaya, J. Erenpreisa, K. Salmina, A. VazquezMartin, A. Huna, N. Nikolsky, A. Vinogradov","doi":"10.15406/MOJI.2018.06.00200","DOIUrl":"https://doi.org/10.15406/MOJI.2018.06.00200","url":null,"abstract":"Polyploid cells contain several copies of diploid genomes. These cells were found in all mammalian tissues where they were searched. In physiological conditions, genome accumulation is a part of development and differentiation programs. Polyploid cells present in heart, skin epithelium, placenta, liver, brain, and blood.1 In stressful condition polyploidy accompanies and stimulates pathological processes. Thus, the increase of polyploidy was documented in hypertensive heart, atherosclerotic vessels, cirrhotic liver and cancer.2 Despite ubiquitous distribution, the effect of polyploidy on gene expression remains not completely understood. Increasing evidence suggests that cell polyploidy may epigenetically alter gene expression and miRNA gene transcription in plants as well as in animals.3,4 miRNA which are short (20-22 nucleotide long) noncoding RNA reported to play various roles in human, plant and in some viruses.5,6 The impact of polyploidy on the transcriptome was investigated in hepatocytes, megakaryocytes, vascular epithelial cells, and placenta. Investigation of the differences in expression using the conservative double threshold led investigators to the conclusion that among several thousand genes not a single one is affected by polyploidy (as in the case of hepatocytes) or only several dozen genes are reactive.7 Moreover, for each cell type, this small set of genes turned out to be different. For instance, in the cells of vascular epithelium, several genes associated with the immune system were suppressed;8 in megakaryocytes, activation of tissue specific genes was registered; and, in decidual cells, activation of nuclear genes encoding mitochondrial proteins was detected.9 These differences suggest that the full effect of somatic polyploidy (if it exists) has not been identified yet. The absence of consensus is not surprising because mmaintaining gene dosage balance, polyploidy has little impact on separate gene activity. The weakness of ploidy associated effects make it difficult to identify common gene expression signature. At the same time, modifying activity of thousands of genes at a time, polyploidy participates in coordination of postnatal development, developmental programming, differentiation and pathogenesis of many diseases, including cardiovascular diseases and cancer.2,7,10–12","PeriodicalId":90928,"journal":{"name":"MOJ immunology","volume":"6 1","pages":"90-93"},"PeriodicalIF":0.0,"publicationDate":"2018-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43746079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-06-06DOI: 10.15406/MOJI.2018.06.00219
P. Lissoni, G. Messina, Vezika Cenaj, F. Rovelli, G. Porro, A. Lissoni, T. Aymerich, G. Fede
Several experimental and clinical investigations have shown that stress may predispose to the most severe systemic illnesses, including cancer and autoimmune diseases.1 According to the recent discoveries of the Psycho-neuroendocrino-immunology (PNEI),2 cancer-and autoimmunity-related immune alterations may depend at least at the beginning of disease on an altered psychoneuroendocrine regulation of the immune responses. From an immune point of view, despite the great complexity of immune interactions involved in the onset of human systemic diseases, cancer and autoimmunity may be considered as the result of two opposite manners of immune reaction, consisting of a deficiency in the immune response in cancer and an exaggerated reaction in the autoimmunity, which allows a consequent reaction also against self-antigens. More in detail, the differences in the immune behavior occurring in cancer and in autoimmune diseases would synthetically depend on the different interactions among the three main subsets of CD4+T lymphocytes, consisting of T helper (TH) (CD4+CD25-CD17-), regulatory T lymphocytes (T reg) (CD4+CD25+) and TH-17 lymphocytes (CD4+CD17+).3–5 In particular, T reg cell number and function have been shown to be abnormally high in cancer and abnormally low in the autoimmunity.3–6
{"title":"The role of IL-17 secretion in mediating the influence of stress on cancer and other human systemic diseases","authors":"P. Lissoni, G. Messina, Vezika Cenaj, F. Rovelli, G. Porro, A. Lissoni, T. Aymerich, G. Fede","doi":"10.15406/MOJI.2018.06.00219","DOIUrl":"https://doi.org/10.15406/MOJI.2018.06.00219","url":null,"abstract":"Several experimental and clinical investigations have shown that stress may predispose to the most severe systemic illnesses, including cancer and autoimmune diseases.1 According to the recent discoveries of the Psycho-neuroendocrino-immunology (PNEI),2 cancer-and autoimmunity-related immune alterations may depend at least at the beginning of disease on an altered psychoneuroendocrine regulation of the immune responses. From an immune point of view, despite the great complexity of immune interactions involved in the onset of human systemic diseases, cancer and autoimmunity may be considered as the result of two opposite manners of immune reaction, consisting of a deficiency in the immune response in cancer and an exaggerated reaction in the autoimmunity, which allows a consequent reaction also against self-antigens. More in detail, the differences in the immune behavior occurring in cancer and in autoimmune diseases would synthetically depend on the different interactions among the three main subsets of CD4+T lymphocytes, consisting of T helper (TH) (CD4+CD25-CD17-), regulatory T lymphocytes (T reg) (CD4+CD25+) and TH-17 lymphocytes (CD4+CD17+).3–5 In particular, T reg cell number and function have been shown to be abnormally high in cancer and abnormally low in the autoimmunity.3–6","PeriodicalId":90928,"journal":{"name":"MOJ immunology","volume":"2 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2018-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48144445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-05-24DOI: 10.15406/MOJI.2018.06.00218
D. Liberati
{"title":"Could systemic capillary leakage syndrome post-episodic recovery light-up our knowledge about less evident and less known key properties of the lymphatic system?","authors":"D. Liberati","doi":"10.15406/MOJI.2018.06.00218","DOIUrl":"https://doi.org/10.15406/MOJI.2018.06.00218","url":null,"abstract":"","PeriodicalId":90928,"journal":{"name":"MOJ immunology","volume":"2 1","pages":"1-1"},"PeriodicalIF":0.0,"publicationDate":"2018-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48703233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-05-22DOI: 10.15406/moji.2018.06.00197
R. Ghaderi, Maryam Rashavi
Inhalation allergens in allergic diseases (atopy) are very important. These types of allergens are classified indoors and out door allergen. The indoor allergens include mites, Cockroach, pets, mold, and andfungus. Of course, other factors such as tobacco smoke, color smell and detergents are also important as immune system stimulants. Outdoor allergens include pollen from trees, grasses, grasses, weeds, dust, molds and fungi. Environmental pollutants should also be considered as stimuli.2,3
{"title":"Prevalence of common allergens among patients with atopic dermatitis in Eastern Iran","authors":"R. Ghaderi, Maryam Rashavi","doi":"10.15406/moji.2018.06.00197","DOIUrl":"https://doi.org/10.15406/moji.2018.06.00197","url":null,"abstract":"Inhalation allergens in allergic diseases (atopy) are very important. These types of allergens are classified indoors and out door allergen. The indoor allergens include mites, Cockroach, pets, mold, and andfungus. Of course, other factors such as tobacco smoke, color smell and detergents are also important as immune system stimulants. Outdoor allergens include pollen from trees, grasses, grasses, weeds, dust, molds and fungi. Environmental pollutants should also be considered as stimuli.2,3","PeriodicalId":90928,"journal":{"name":"MOJ immunology","volume":"6 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2018-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45271823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-05-21DOI: 10.15406/MOJI.2018.06.00196
A. Tabbabi
anesthesia and prevent the blood from clotting in the trunk. Most of these salivary compound have been identified by studies to develop the transcriptome and proteome of salivary glands from several adult female mosquito species. It has thus been possible to identifie new transcrits associated with mosquito nutrition and new salivary protein and peptide séquences.2 Disposition of databases containing such sequences is a prerequisite for establishing salivary protein profiles of mosquitoes, studying their characteristics and properties, checking their roles and developing strategies to block them.
{"title":"Salivary biomarkers in the control of mosquito-borne diseases","authors":"A. Tabbabi","doi":"10.15406/MOJI.2018.06.00196","DOIUrl":"https://doi.org/10.15406/MOJI.2018.06.00196","url":null,"abstract":"anesthesia and prevent the blood from clotting in the trunk. Most of these salivary compound have been identified by studies to develop the transcriptome and proteome of salivary glands from several adult female mosquito species. It has thus been possible to identifie new transcrits associated with mosquito nutrition and new salivary protein and peptide séquences.2 Disposition of databases containing such sequences is a prerequisite for establishing salivary protein profiles of mosquitoes, studying their characteristics and properties, checking their roles and developing strategies to block them.","PeriodicalId":90928,"journal":{"name":"MOJ immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41913945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-05-08DOI: 10.15406/moji.2018.06.00195
Kunjan Khanna, K. Mishra, L. Ganju, B. Kumar, S. Singh
An altitude above 8000 feet is considered as high altitude which includes oxygen-compromised environment. Such environment results in a condition called hypobaric hypoxia (HH) which may induce diseases/problems in different organ systems. Diseases like Acute Mountain Sickness (AMS), High Altitude Pulmonary Edema (HAPE), and High Altitude Cerebral Edema (HACE) occur commonly in natives, mountaineers and soldiers recruited at high altitude. While much work has been done on the effects of high altitude but its impact on immune system is less studied so far. Immune system is a network of different cells, tissues and organs which help in defending the body from foreign substances and other harmful stressors. It gets affected by extreme environments, invading harmful micro-organisms and disease conditions. It is now established that stressful conditions do affect the immune system. In some reports, high altitude environment has shown to affect different immune cells like T-cells, B-cells, NK cells and macrophages.1,2 Studies on harsh environment of Antarctica also suggested that stressful conditions of Antarctica lead to increased serum IgA levels.3 One of the important branches of immune system is the Complement system which helps the immune cells to get activated against the invading micro-organisms and different inflammatory molecules, thus provides a bridge between innate and adaptive immune response.4 Complement system is activated via three pathways namely classical, alternate and lectin.5 In many studies, Complement system has also been shown to get activated by different stressful environments. In a study, performed on human subjects who went to Antarctica, it has been shown that stressful conditions led to the activation of complement cascade. Factors like C3, C4, C3a, C4a, C5a and Complement Factor B were modulated in the summer as well as winter over expedition members.6 A Study on rats sensitive to hypoxia revealed activation of complement system components with different degrees of hypoxia exposure for maximum of 3 days.7 Also, levels of complement protein like C4 has been seen to alter on acute HH exposure8 HH is a stressful condition; human go to pilgrimages, mountains or works at such high altitude which results in immune compromisation. IgA has been seen to play a major role in defending to infections on mucous membranes. It has been seen that there is a higher incidence of infections in people going to high altitudes, therefore the study was done in an attempt to understand immunity of people at high altitude, changes in IgA levels and complement factors were studied. As in rats, pathological changes are majorly seen at an altitude of 25,000 ft,9 the rats were exposed to simulated hypobaric hypoxic conditions in specially designed decompression chamber. Our study revealed that HH significantly modulated the levels of IgA and complement factors in rats. The results can be applied to unfold mechanism of immune system activation in human
{"title":"Alterations in IgA and complement system of rats exposed to intense hypobaric hypoxia (7620m) at different time duration","authors":"Kunjan Khanna, K. Mishra, L. Ganju, B. Kumar, S. Singh","doi":"10.15406/moji.2018.06.00195","DOIUrl":"https://doi.org/10.15406/moji.2018.06.00195","url":null,"abstract":"An altitude above 8000 feet is considered as high altitude which includes oxygen-compromised environment. Such environment results in a condition called hypobaric hypoxia (HH) which may induce diseases/problems in different organ systems. Diseases like Acute Mountain Sickness (AMS), High Altitude Pulmonary Edema (HAPE), and High Altitude Cerebral Edema (HACE) occur commonly in natives, mountaineers and soldiers recruited at high altitude. While much work has been done on the effects of high altitude but its impact on immune system is less studied so far. Immune system is a network of different cells, tissues and organs which help in defending the body from foreign substances and other harmful stressors. It gets affected by extreme environments, invading harmful micro-organisms and disease conditions. It is now established that stressful conditions do affect the immune system. In some reports, high altitude environment has shown to affect different immune cells like T-cells, B-cells, NK cells and macrophages.1,2 Studies on harsh environment of Antarctica also suggested that stressful conditions of Antarctica lead to increased serum IgA levels.3 One of the important branches of immune system is the Complement system which helps the immune cells to get activated against the invading micro-organisms and different inflammatory molecules, thus provides a bridge between innate and adaptive immune response.4 Complement system is activated via three pathways namely classical, alternate and lectin.5 In many studies, Complement system has also been shown to get activated by different stressful environments. In a study, performed on human subjects who went to Antarctica, it has been shown that stressful conditions led to the activation of complement cascade. Factors like C3, C4, C3a, C4a, C5a and Complement Factor B were modulated in the summer as well as winter over expedition members.6 A Study on rats sensitive to hypoxia revealed activation of complement system components with different degrees of hypoxia exposure for maximum of 3 days.7 Also, levels of complement protein like C4 has been seen to alter on acute HH exposure8 HH is a stressful condition; human go to pilgrimages, mountains or works at such high altitude which results in immune compromisation. IgA has been seen to play a major role in defending to infections on mucous membranes. It has been seen that there is a higher incidence of infections in people going to high altitudes, therefore the study was done in an attempt to understand immunity of people at high altitude, changes in IgA levels and complement factors were studied. As in rats, pathological changes are majorly seen at an altitude of 25,000 ft,9 the rats were exposed to simulated hypobaric hypoxic conditions in specially designed decompression chamber. Our study revealed that HH significantly modulated the levels of IgA and complement factors in rats. The results can be applied to unfold mechanism of immune system activation in human","PeriodicalId":90928,"journal":{"name":"MOJ immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45682305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-05-01DOI: 10.15406/MOJI.2018.06.00193
R. Villa, K. Moreno, Manuela Giraldo
The presence of bronchial asthma, chronic rhinosinusitis (CRS) with nasal polyps, and a hypersensitivity reaction of the airway to aspirin (acetylsalicylic acid–ASA), as well as other non-selective inhibitors of the cyclooxygenase enzyme (COX),1‒3 commonly characterizes the Aspirin-exacerbated respiratory disease (AERD). It is within the broad spectrum of hypersensitivity reactions induced by non-steroidal anti-inflammatory drugs (NSAIDs), in minutes after administration. The prevalence of AERD is unknown, although, it is estimated that it can affect between 5.5% and 12.4% of the general population.4 The exact prevalence of nasal polyps is not known. However, it is estimated that it can be around 100%.5,6 For the diagnosis, the clinical history of hypersensitivity reaction, exacerbation type of asthma or secondary rhinitis to the consumption of NSAIDs is highly suggestive of AERD, especially if there is the presence of anosmia and nasal polyps. Provocation with inhibitors of COX,7‒9 makes the confirmation. This challenging test is mainly performed with aspirin, although protocols with other NSAIDs such as ketorolac also exist.5 The administration route can be oral, nasal, bronchial and intravenous inhalation.10,11
{"title":"Desensitization with asa a successful treatment for a patient with aspirin exacerbated respiratory disease","authors":"R. Villa, K. Moreno, Manuela Giraldo","doi":"10.15406/MOJI.2018.06.00193","DOIUrl":"https://doi.org/10.15406/MOJI.2018.06.00193","url":null,"abstract":"The presence of bronchial asthma, chronic rhinosinusitis (CRS) with nasal polyps, and a hypersensitivity reaction of the airway to aspirin (acetylsalicylic acid–ASA), as well as other non-selective inhibitors of the cyclooxygenase enzyme (COX),1‒3 commonly characterizes the Aspirin-exacerbated respiratory disease (AERD). It is within the broad spectrum of hypersensitivity reactions induced by non-steroidal anti-inflammatory drugs (NSAIDs), in minutes after administration. The prevalence of AERD is unknown, although, it is estimated that it can affect between 5.5% and 12.4% of the general population.4 The exact prevalence of nasal polyps is not known. However, it is estimated that it can be around 100%.5,6 For the diagnosis, the clinical history of hypersensitivity reaction, exacerbation type of asthma or secondary rhinitis to the consumption of NSAIDs is highly suggestive of AERD, especially if there is the presence of anosmia and nasal polyps. Provocation with inhibitors of COX,7‒9 makes the confirmation. This challenging test is mainly performed with aspirin, although protocols with other NSAIDs such as ketorolac also exist.5 The administration route can be oral, nasal, bronchial and intravenous inhalation.10,11","PeriodicalId":90928,"journal":{"name":"MOJ immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43821843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-04-19DOI: 10.15406/MOJI.2018.06.00192
Joseph F. Murphy
The past few years has witnessed a blossoming of research revolving around the human microbiome. Increased knowledge about this field has led to realizing its crucial role in modulating human health. The microbiome genome, compromised of bacteria, fungi, viruses, and protozoa is referred to as our second genome. It is estimated that there are 100 trillion microbes, comprised of over 1,000 species. The composition varies from person to person based on several factors, such as diet, health history, geographic location, and ancestry. They are intertwined with our immune system, interacting directly with our body’s natural killer T-cells. Moreover, this complex ecosystem must be properly balanced and nurtured to remain healthy. Imbalances within our microbiome can lead to illness. Our microbiome also helps control gene expression, which ultimately affects several facets of our physiology.
{"title":"The human microbiome: an emerging paradigm for better health","authors":"Joseph F. Murphy","doi":"10.15406/MOJI.2018.06.00192","DOIUrl":"https://doi.org/10.15406/MOJI.2018.06.00192","url":null,"abstract":"The past few years has witnessed a blossoming of research revolving around the human microbiome. Increased knowledge about this field has led to realizing its crucial role in modulating human health. The microbiome genome, compromised of bacteria, fungi, viruses, and protozoa is referred to as our second genome. It is estimated that there are 100 trillion microbes, comprised of over 1,000 species. The composition varies from person to person based on several factors, such as diet, health history, geographic location, and ancestry. They are intertwined with our immune system, interacting directly with our body’s natural killer T-cells. Moreover, this complex ecosystem must be properly balanced and nurtured to remain healthy. Imbalances within our microbiome can lead to illness. Our microbiome also helps control gene expression, which ultimately affects several facets of our physiology.","PeriodicalId":90928,"journal":{"name":"MOJ immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46086158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-04-11DOI: 10.15406/MOJI.2018.06.00191
N. Deebii, H. Kagbo, B. Aleme
The kidneys can be susceptible to antiretroviral drug toxicity because of their layout and function. A growing number of cross sectional reports and longitudinal studies have described an association between treatment with antiretroviral therapy and proximal tubular dysfunction or impaired glomerular filtration rate (GFR) in patients with human immunodeficiency virus (HIV) infection.1, 2 Alterations on tenofovir secretion by proximal renal tubule may lead directly to a greater drug accumulation in the renal tubular cells and, consequently lead to proximal tubular damage and renal toxicity.3,4 Several studies have found that CKD is associated with increased mortality among HIV-infected individuals.5 Studies of TDF toxicity suggested that mitochondria were unlikely to be the targets.6 Studies by Hall et al.7 have consistently observed marked ultrastructural abnormalities in mitochondria in the proximal tubule in cases of TDF-induced Fanconi syndrome. Further evidence in support of the fact that mitochondria are the major targets of TDF toxicity in the kidney has been provided by 2 recent rodent studies.8−10 However, the animals were exposed to about twice the normal dose in humans when adjusted for body weight.9 Interactions with other nephrotoxic agents and/or underlying genetic polymorphisms in transporters might help explain why TDF accumulates in proximal tubule cells in some patients, but do not shed further light on the exact intracellular targets of toxicity.11 Finally, there is evidence that TDF is specifically toxic to mitochondria in the proximal tubule, and the exact mechanisms of this damage remain unknown till date.
{"title":"Improved immunological profile of HIV infected patients with renal abnormalities on antiretroviral therapy","authors":"N. Deebii, H. Kagbo, B. Aleme","doi":"10.15406/MOJI.2018.06.00191","DOIUrl":"https://doi.org/10.15406/MOJI.2018.06.00191","url":null,"abstract":"The kidneys can be susceptible to antiretroviral drug toxicity because of their layout and function. A growing number of cross sectional reports and longitudinal studies have described an association between treatment with antiretroviral therapy and proximal tubular dysfunction or impaired glomerular filtration rate (GFR) in patients with human immunodeficiency virus (HIV) infection.1, 2 Alterations on tenofovir secretion by proximal renal tubule may lead directly to a greater drug accumulation in the renal tubular cells and, consequently lead to proximal tubular damage and renal toxicity.3,4 Several studies have found that CKD is associated with increased mortality among HIV-infected individuals.5 Studies of TDF toxicity suggested that mitochondria were unlikely to be the targets.6 Studies by Hall et al.7 have consistently observed marked ultrastructural abnormalities in mitochondria in the proximal tubule in cases of TDF-induced Fanconi syndrome. Further evidence in support of the fact that mitochondria are the major targets of TDF toxicity in the kidney has been provided by 2 recent rodent studies.8−10 However, the animals were exposed to about twice the normal dose in humans when adjusted for body weight.9 Interactions with other nephrotoxic agents and/or underlying genetic polymorphisms in transporters might help explain why TDF accumulates in proximal tubule cells in some patients, but do not shed further light on the exact intracellular targets of toxicity.11 Finally, there is evidence that TDF is specifically toxic to mitochondria in the proximal tubule, and the exact mechanisms of this damage remain unknown till date.","PeriodicalId":90928,"journal":{"name":"MOJ immunology","volume":" ","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2018-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48873271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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