Impact of Dietary Cholesterol on the Pathophysiology of Infectious and Autoimmune Disease.

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Term Occurence Count Dictionary
trachoma 1 infectiousdiseases
tuberculosis 15 infectiousdiseases
AIDS 3 infectiousdiseases
dexamethasone 1 infectiousdiseasesdrugs
hepatitis C 3 infectiousdiseases
infectious disease 14 infectiousdiseases
pneumonia 12 infectiousdiseases
pulmonary tuberculosis 2 infectiousdiseases

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dexamethasone 14568 ovalalbumin-sensitized BALB/c mouse models of asthma, whereas cholesterol content is normalized by dexamethasone treatment [[89]]. Pulmonary cholesterol levels were negatively correlated with numbers of macrophages,
Select Disease Character Offset Disease Term Instance
AIDS 39237 energy) diet on simian immunodeficiency virus (SIV) progression to acquired immunodeficiency syndrome ( AIDS ) in infected macaques primates. Interestingly, animals fed the high cholesterol/high fat diet exhibited
AIDS 54519 expression of LXRα, LXRβ, SREBP-1c, ABCA1 ↓ % Th17 cells, serum IL-17, IL-22, TGFβ, HA[[26]]HIV/ AIDS SIV-infected macaque primatesHigh-fat (40% of energy)/high-cholesterol (1%) diet↑ peak viral loads,
AIDS 54879 no change or difference between groups. Abbreviations: ABCA1: ATP-binding cassette transporter A 1; AIDS : acquired immunodeficiency syndrome; apoE: apolipoprotein E; HA: hyaluronic acid; HCV: hepatitis C virus;
hepatitis C 11695 and its associated efflux transporters have been implicated in human immunodeficiency virus (HIV) and hepatitis C virus (HCV) infection [[69],[70]]. HIV infection has been shown to suppress ABCA1-mediated efflux via
hepatitis C 51652 cassette transporter A 1; ABCG1: ATP-binding cassette transporter G 1; apoA1: apolipoprotein A 1; HCV: hepatitis C virus; HIV: human immunodeficiency virus; LDLR: low-density lipoprotein receptor; LPS: lipopolysaccharide;
hepatitis C 54971 transporter A 1; AIDS: acquired immunodeficiency syndrome; apoE: apolipoprotein E; HA: hyaluronic acid; HCV: hepatitis C virus; HIV: human immunodeficiency virus; IL-17: interleukin 17; IL-18: interleukin 18; IL-22: interleukin
infectious disease 2060 controversial studies on the role of dietary cholesterol and lipid metabolism in the pathophysiology of infectious disease and autoimmune disorders, highlighting the need for further investigation in this developing area of
infectious disease 4859 important regulator of immune cell activity and inflammation, with implications for risk and treatment of infectious disease and chronic autoimmune disorders [[24],[25],[26],[27],[28]]. Understanding the relationship between
infectious disease 12860 very high (>100 mg/dL) HDL-cholesterol levels were shown to be associated with an increased risk of infectious disease [[77]]. Low HDL-cholesterol appeared to have a greater impact on infectious disease risk, with a 75%
infectious disease 12944 increased risk of infectious disease [[77]]. Low HDL-cholesterol appeared to have a greater impact on infectious disease risk, with a 75% increased risk of disease, vs. a 43% increased risk in individuals with very high HDL-cholesterol
infectious disease 13469 [[38],[70],[78],[79]].2.2. Role of Cholesterol in the Pathophysiology of Autoimmune DiseaseIn addition to infectious disease pathways, cholesterol metabolism appears to play an important role in autoimmune disease. In patients
infectious disease 15475 asthma, or whether lipoprotein metabolism contributes to disease progression.Similar to observations in infectious disease , altered lipoprotein patterns and dysfunctional HDL have been identified in patients with SLE, RA, asthma,
infectious disease 16174 research shows that lipid rafts and lipoprotein interactions are not only essential in the pathogenesis of infectious disease , but also in the compensatory immune response to ameliorate infection (Figure 1). Dysregulation of lipid
infectious disease 16845 elucidate the impact of lipid- and immune-modulating dietary components on risk and treatment of specific infectious disease s and autoimmune disorders.3. Effects of Dietary Cholesterol and Egg Intake on Lipoprotein Metabolism
infectious disease 27327 metabolic status. These findings have important implications for the pathophysiology and management of infectious disease and autoimmune disorders, suggesting that immunomodulatory lipid pathways may serve as a therapeutic
infectious disease 28626 findings from research studies evaluating the effects of dietary cholesterol on the pathogenesis of infectious disease s. 4.1. TuberculosisTuberculosis is one of the leading causes of death from infectious disease worldwide
infectious disease 28720 pathogenesis of infectious diseases. 4.1. TuberculosisTuberculosis is one of the leading causes of death from infectious disease worldwide [[139]]. Tuberculosis can further lead to, and be complicated by, malnutrition and nutrient
infectious disease 34421 consumption in humans may lead to clinical benefits overall (Table 1).4.3. Hepatitis C VirusIn addition to infectious disease s affecting pulmonary tissues, dietary cholesterol may further impact mechanisms of viral infection by
infectious disease 40194 infection and treatment in humans. 5. Dietary Cholesterol Effects in Autoimmune DiseaseIn addition to infectious disease s, dietary cholesterol has the potential to impact risk, severity, and treatment of chronic autoimmune
infectious disease 50364 cholesterol-rich dietary patterns differentially impact pathophysiology and clinical outcomes of distinct infectious disease s by various bacterial and viral pathogens, and that dietary cholesterol may either exasperate or mitigate
pneumonia 8416 infection by multiple Chlamydia species associated with urogenital tract infections and respiratory pneumonia (C. trachomatis and C. pneumonia)[[45],[46]], tick-borne pathogens Anaplasma phagocytophilium and Ehrlichia
pneumonia 8449 species associated with urogenital tract infections and respiratory pneumonia (C. trachomatis and C. pneumonia )[[45],[46]], tick-borne pathogens Anaplasma phagocytophilium and Ehrlichia chaffeensis [[47]], as MβCD-mediated
pneumonia 9922 also important to note that bacterial infections disrupt cellular and systemic lipid metabolism. C. pneumonia infection has been shown to increase LDL uptake, suppress expression of ABCA1 and ABCG1, and reduce
pneumonia 31224 dietary cholesterol appears to impact the pathogenesis of other types of pulmonary infections, including pneumonia . Klebsiella pneumoniae—a pneumonia-causing Gram-negative pathogen—additionally utilizes host lipid
pneumonia 31246 to impact the pathogenesis of other types of pulmonary infections, including pneumonia. Klebsiella pneumonia e—a pneumonia-causing Gram-negative pathogen—additionally utilizes host lipid rafts for infection,
pneumonia 31261 pathogenesis of other types of pulmonary infections, including pneumonia. Klebsiella pneumoniae—a pneumonia -causing Gram-negative pathogen—additionally utilizes host lipid rafts for infection, whereas depletion
pneumonia 31440 rafts for infection, whereas depletion of host cell cholesterol by MβCD and LXR activation impairs K. pneumonia internalization and subsequent host defenses [[144],[145]]. These findings suggest that cholesterol
pneumonia 31576 subsequent host defenses [[144],[145]]. These findings suggest that cholesterol enrichment may promote K. pneumonia clearance.Animal studies have demonstrated that high cholesterol feeding modifies the lipid composition
pneumonia 33098 [[134]]. Together, these findings suggest that cholesterol dose-dependently modulates pathways of K. pneumonia in a tissue-specific manner, which may ultimately impact disease outcomes.The effects of dietary cholesterol
pneumonia 33241 which may ultimately impact disease outcomes.The effects of dietary cholesterol on clinical outcomes of pneumonia have additionally been investigated in humans. In a study by Wang and Hong [[135]], pneumonia patients
pneumonia 33335 outcomes of pneumonia have additionally been investigated in humans. In a study by Wang and Hong [[135]], pneumonia patients were supplemented with an additional 600 mg of cholesterol from egg yolks per day for 10 days.
pneumonia 34243 [[24],[101],[102]]. Thus, while excess dietary cholesterol may exasperate pulmonary dysfunction during K. pneumonia infection in animal models [[134]], systemic effects and egg consumption in humans may lead to clinical
pulmonary tuberculosis 29277 levels are reduced and negatively associated with clinical radiological and smear positivity measures on pulmonary tuberculosis patients [[142],[143]]. Thus, cellular cholesterol enrichment may promote M. tuberculosis infection,
pulmonary tuberculosis 30628 patients who consumed a cholesterol-rich diet (800 mg/day) while undergoing inpatient treatment for active pulmonary tuberculosis had faster reductions in positive sputum cultures and sputum production, as compared to patients receiving
trachoma 8430 multiple Chlamydia species associated with urogenital tract infections and respiratory pneumonia (C. trachoma tis and C. pneumonia)[[45],[46]], tick-borne pathogens Anaplasma phagocytophilium and Ehrlichia chaffeensis
tuberculosis 28899 complicated by, malnutrition and nutrient deficiencies [[140]]. Research on nutritional support for tuberculosis has been inconsistent, leading to a lack of nutritional guidelines and recommendations for tuberculosis
tuberculosis 29003 tuberculosis has been inconsistent, leading to a lack of nutritional guidelines and recommendations for tuberculosis treatment [[140]]. Lipid raft formation is essential for Mycobacterium tuberculosis internalization
tuberculosis 29087 recommendations for tuberculosis treatment [[140]]. Lipid raft formation is essential for Mycobacterium tuberculosis internalization and survival in host cells [[141]], whereas serum lipid levels are reduced and negatively
tuberculosis 29287 reduced and negatively associated with clinical radiological and smear positivity measures on pulmonary tuberculosis patients [[142],[143]]. Thus, cellular cholesterol enrichment may promote M. tuberculosis infection,
tuberculosis 29377 pulmonary tuberculosis patients [[142],[143]]. Thus, cellular cholesterol enrichment may promote M. tuberculosis infection, whereas systemic cholesterol depletion may contribute to disease progression.Accordingly,
tuberculosis 29537 depletion may contribute to disease progression.Accordingly, conflicting effects of dietary cholesterol on tuberculosis pathology have been reported (Table 1). In apolipopotein E (apoE)-deficient mice, high cholesterol feeding
tuberculosis 29672 reported (Table 1). In apolipopotein E (apoE)-deficient mice, high cholesterol feeding exasperated M. tuberculosis infection, as evidenced by reduced T helper 1 (Th1)-mediated immune responses, increased bacterial burden
tuberculosis 29993 found that high cholesterol (1.25% cholesterol) feeding resulted in a greater bacterial burden of M. tuberculosis H37Rv in both wild type and SB-BI knockout mice, as compared to mice consuming a low cholesterol (0.15%)
tuberculosis 30385 Chinese Health Study, dietary cholesterol intake was dose-dependently associated with risk of active tuberculosis , where individuals consuming the greatest amount of cholesterol had the greatest risk of tuberculosis
tuberculosis 30487 tuberculosis, where individuals consuming the greatest amount of cholesterol had the greatest risk of tuberculosis [[132]]. Conversely, patients who consumed a cholesterol-rich diet (800 mg/day) while undergoing inpatient
tuberculosis 30638 consumed a cholesterol-rich diet (800 mg/day) while undergoing inpatient treatment for active pulmonary tuberculosis had faster reductions in positive sputum cultures and sputum production, as compared to patients receiving
tuberculosis 30959 Together, these findings suggest that habitually high intakes of dietary cholesterol may promote M. tuberculosis infection, whereas supplementation during active infection may promote pathogen clearance and recovery.
tuberculosis 31105 supplementation during active infection may promote pathogen clearance and recovery. 4.2. PneumoniaIn addition to tuberculosis , dietary cholesterol appears to impact the pathogenesis of other types of pulmonary infections, including
tuberculosis 53626 Physiology Score II; SGA: Subjective Global Assessment; SR-BI: scavenger receptor class B type I; TB: tuberculosis ; Th1: T helper 1 lymphocytes; TNFα: tumor necrosis factor α.nutrients-10-00764-t002_Table 2Table 2Effects
tuberculosis 55280 mononuclear cell; SIV: simian immunodeficiency virus; SREBP-1c: sterol regulatory binding protein 1 c; TB: tuberculosis ; TGFβ: transforming growth factor β; Th17: T helper 17 lymphocytes; TNFα: tumor necrosis factor α;

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