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admin | What Cures Bv | 07.02.2014
A new genomic test developed by researchers at Duke University School of Medicine can accurately sort between viral and bacterial infections, possibly helping to limit the overuse of antibiotics and the emergence of bacterial resistance. A blood test developed by researchers at Duke Medicine showed more than 90-percent accuracy in distinguishing between viral and bacterial infections when tested in people with respiratory illnesses. The test, which detects a specific genetic “signature” that the sick person’s immune system expresses as a response to the virus, demonstrates a potential new method for diagnosing the source of illnesses that have long been tough to pinpoint. When infected by a virus, a person’s immune system responds differently than when fighting a bacterial infection.
In previous work, the Duke team described the development of a blood test, using a special assay, to identify some 30 genes involved in the immune response to viral infection among volunteers who had agreed to be infected with a series of common upper respiratory viruses.
Unlike current tests that rely on evidence of the pathogen in the blood stream – requiring knowledge of that particular bug to detect it – the new approach could be used to detect unknown emerging diseases, including potential bioterrorism threats. The assay provided true positive identifications of viral infection in 89 percent of the cases, and correctly ruled out the negative cases 94 percent of the time.
The researchers said larger studies are planned, and additional work is ongoing to trim the amount of time it takes for the test results to be reported. In addition to Ginsburg, Zaas and Woods, study authors include Thomas Burke, Minhua Chen, Micah McClain, Bradly Nicholson, Timothy Veldman, Ephraim L. The study was supported in part by the Defense Advanced Research Projects Agency, the National Institutes of Allergy and Infectious Diseases (AI066569), and the Department of Veterans Affairs. Ginsburg, Zaas, Woods, Hero, Carin and Lucas have filed for a provisional patent on the respiratory viral signature. Blog about the latest news and commentary pertaining to affordable health insurance and healthcare. It's easy to understand why most people are confused about the difference between a virus and a bacteria infection. The main difference between a virus infection and a bacteria infection is that antibiotics have no affect on viruses.
Although viruses and bacteria are different and not treated the same, they are spread in the same manner. DISCLAIMER: The content or opinions expressed on this web site are not to be interpreted as medical advice. Pharyngitis, a painful inflammation or a viral infection of the throat is the main cause of sore throat.
Viruses that cause viral infections like common cold, coughing, nose blowing, sneezing, swollen glands in the neck (lymph nodes), infection of the tonsils (tonsillitis), and mild fever can be some of the common causes for sore throats virally. Streptococcus and Arcanobacterium  Haemolyticum are the common bacteria that causes sore throat infections.
Gastroesophagea reflux disease (GERD) is caused by the backflow of food and stomach acids into the esophagus, which is a tube that connects the mouth to the stomach.
Indoor and outdoor pollution, complications in postnasal drip, yelling, and low humidity can some of the allergic causes of sore throats. The most common symptom is experiencing pain in the throat and sometimes this pain spreads to the ear.
Lump in the neck, suffering with hoarseness for more than two weeks can be said as the symptoms of sore throat.
Heart burns are the symptoms faced by one if sore throat is caused by Gastroesophageal Reflux.
Initially, instead of seeking a doctor in primary stages it is better if you keep yourself safe at home.
Eating raw garlic can reduce the itchy and the scratchy irritation that caused due to sore throat. Yes, you made find that trying out pepper would be little difficult because of the spiciness of pepper.
As dryness and low humidity is one of the causes for sore throat, using a sore throat at your work place or in your room can reduce the suffering.
Home treatment with antacids and other acid- reducing medicines may decrease the pain caused by mild GERD and sometimes it may even prevent the severe conditions.
As the causes for sore throat may vary from mild to severe it is best if you consult a doctor.
If the sore throat is caused by a bacterial infection it is better suggested if you take antibiotics.
Pain relievers such as ibuprofen, acetaminophen may help you to relieve from the severe pain. All these medicines are taken only under the advice of doctors and you should not exceed recommended dose.
Following these simple measures and carefully taking the medicines would relieve you from the suffering caused by sore throat infections.
An eye infection or an eye ailment refers to a bacterial or viral infection of the eye or the immediate tissue adjacent to the eye, such as conjunctivitis (or pink eye) that affects the membrane lining the internal side of the eyelids and covering the whites of the eyes, and blepharitis that affects the margin of the eyelids.
London, June 30 : The speed and accuracy with which certain tests can tell the difference between bacterial and viral infections, is extremely vital for the patient's recovery.
Since current diagnostic methods are both time-consuming and not very accurate, researchers have developed a new test to help doctors rapidly pinpoint the condition - whether it is a bacterial infection or a viral infection. Robert Marks, professor in biotechnology engineering, and Daria Prilutsky, doctoral student in virology at the Negev Ben-Gurion University, developed a test based on those differences.
Marks and Prilutsky found that the immune systems of patients with bacterial infections behaved differently than the immune systems of patients with viral infections, reports the journal, Analytical Chemistry. If left untreated until results of a throat culture are received, bacterial infections can get worse.
But needlessly giving antibiotics to patients with a viral infection could contribute to the growing problem of antibiotic-resistant bacteriam, according to a Ben-Gurion statement. We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you.
Initially, indoleamine-2,3-dioxygenase (IDO) has been introduced as a bactericidal effector mechanism and has been linked to T-cell immunosuppression and tolerance.
Indoleamine-2,3-dioxygenase (IDO) is an intracellular, non-secreted enzyme, which catabolizes the production of kynurenine (Kyn) derivates from tryptophan (Trp). Exogenous inflammatory stimuli induce the expression of IDO in antigen-presenting cells (APCs), such as dendritic cells (DC) (7), macrophages (4), and B-cells. Apparently, pathogens are able to highjack the immunosuppressive effects of IDO and make use of them to facilitate their own life cycle.
Infection with HIV causes a severe impairment of T-cell responses by loss of proliferative capacity of T-cells accompanied by a depletion of functionally competent CD4+ T helper cells and by induction of regulatory T-cells (Treg) during the chronic phase of HIV infection (Figure 1). In simian immunodeficiency virus (SIV)-infected macaques, treatment with a combination of antiretroviral therapy (ART) and 1-MT successfully diminished viral loads in plasma and lymph nodes and restored Trp levels but did not reduce Kyn (34). Another mechanism of IDO expression in APCs is mediated by regulatory T-cells (Treg) (39, 40). The influence of IDO expression on viral loads in mice infected with the retroviral leukemia virus LP-BM5 is controversially discussed. An interesting link between chronic inflammatory diseases and neurological disorders has been recently made with IDO being involved.
Indoleamine-2,3-dioxygenase has also been linked to chronic infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) (57).
Yet another mechanism for induction of IDO expression was demonstrated in a murine hepatitis model. Additional evidence for an important role for IDO in viral infection was provided in studies of human papilloma viruses (HPV). Overall, IDO seems to play an important role in chronic viral infections mainly by contributing to the establishment of an immunotolerogenic microenvironment.
Further controversy about the role of IDO in Tb comes from a recent report demonstrating no essential role for IDO in a murine model of Tb (81). There have been numerous studies during the last 20 years demonstrating a correlation between Tb and depressive disorders in patients (Figure 2) (83–86), but many of the underlying molecular mechanisms remain unclear. Indoleamine-2,3-dioxygenase was also shown to be important in the defense against the ubiquitous intracellular bacterium Chlamydia pneumoniae (C. An interesting link between IDO and iron metabolism has been suggested by Krausse-Opatz and colleagues (91). 18, 2013, issue of the journal Science Translational Medicine, the finding moves the technology closer to clinical use, where it could help patients get quicker diagnoses and treatments, while curbing the unnecessary use of antibiotics that don’t work on viral infections. These differences are evident at the genetic level, where certain genes are switched on during a viral attack, creating a fingerprint that broadly identifies the culpable pathogen. Among 102 people arriving at a hospital’s emergency department with fever, 28 had a viral infection, 39 had a bacterial infection and 35 were healthy controls.
But until viral infection is conclusively decided it is usual to take anti-biotics so that worst will not happen to the patient, knowing pretty well that antibiotics will cut no ice on the disease until the patient develops resistance himself. When you are sick, these two terms are often used interchangeably to describe what type of infection you have. A virus usually has more widespread symptoms where a bacteria infection tends to stay within one area, such as the throat. Please consult with your doctor or medical practictioner before utilizing any suggestions on this web site.
Sore throat, a distressing infection is commonly seen in all age groups from infants to aged persons. Mononucleosis, a virus, effluent in causing flu, breathing difficulties is responsible for sore throat infection in extremes.  Other viral infections such as mumps, laryngitis (infection of voice box), and measles can also lead to sore throat infections. This may usually occur when your immune system gets heated up due to some changes in climatic conditions. You may experience pain radiating to your ear and other symptoms include sudden weight loss, blood in saliva and phlegm that leads to sore throat infection caused by tumors. This in overtime, leads to inflammation, sores and narrowing of the esophagus which is the cause of sore throats. Chewing tobacco, drinking alcohol, and intake of any spicy foods irritate the throat and make you feel scratchy and itchy. As the suffering may occur in any form you cannot easily find out whether it causes sore throat or other common flues.
You need to let the garlic juices coat through your complete throat and mouth but not just by biting the garlic cloves.


Generally, the causes for sore throat are tested in lab by taking the samples of your saliva.
Increase the intake of citrus fruits in your diet and liquids in order to prevent sore throats and other mouth infections. Though the infections of the cornea are not very common, they can have a serious effect on the vision. Those common afflictions often have similar symptoms but vastly different treatments - antibiotics work for bacterial infections but not for viruses. This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button.
This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. In recent years, evidence has been accumulated that IDO also plays an important role during viral infections including HIV, influenza, and hepatitis B and C. Anti-proliferative features of IDO on bacteria, protozoa, and tumor cells have been first described in 1984 by Pfefferkorn (1) as well as Taylor and Feng (2).
For instance, uropathogenic Escherichia coli (UPEC) induce IDO in epithelial cells of the urinary tract and in polymorphonuclear leukocytes (21). The exact T-cell impairing mechanism is still not completely understood, but inhibitory molecules on T-cell function have been investigated intensely [reviewed elsewhere (26)].
Schematic summary of immunosuppressive functions of indoleamine-2,3-dioxygenase (IDO) during HIV infection. It is worth to mention that 1-MT alone was not able to restrain viremia in this animal model. In HIV patients, an elevated enzymatic activity of IDO in APCs was associated with a reduced anti-viral T-cell response [reviewed elsewhere (41)], while depletion of Treg cells reconstituted anti-HIV immune responses (42).
In an earlier study, higher numbers of pDC in IDO KO mice correlated with increased levels of type I IFN and reduced viral load (46). Patients suffering from chronic inflammatory diseases show often signs of depressive mood behavior (Figure 2).
Infection with murine influenza virus PR8 has been shown to induce IDO expression in mouse lung tissue (53, 54) and lung-associated lymph nodes (54).
Despite an appropriate T-cell response during the acute phase of HCV infection and subsequent viral clearance, T-cell responses in the chronic phase are weak [summarized by Hiroishi et al.
New strategies to target IDO itself or upstream mechanisms inducing IDO might help in the development of therapeutic drugs for patients with chronic viral infections.
Wild-type as well as IDO KO mice showed comparable bacterial burden, T-cell responses, and survival rates, leading to the conclusion that IDO activity is not required for the control of M. Using the test, the Duke researchers were able to accurately classify more than 90 percent of the patients as having viral infection or not. Thus this test if accurately decides viral infection indiscriminate use of drugs and follow up of bacterial resistance to the drugs can be avoided. Strep throat, tuberculosis, and urinary tract infections are examples of infections caused by bacteria. They also have similar symptoms, such as coughing and sneezing, fever, inflammation, vomiting, diarrhea, fatigue, and cramping. The irritation caused by sore throat may be mild enough and it may leave you without any medication. Streptococcus is the bacterium that causes strep throat infection in both adults and children. Also smoking or breathing through mouth may lead to excessive nose and throat dryness which is one of the causes for throat infections.
Also straining your throat muscles by speaking loudly in a noisy environment stresses your throat membranes that lead to irritation. However there are certain symptoms and you can avoid by taking necessary preventive measures.
Repeat this gargling at least 3 to 4 times a day and this helps in rehydrating the dry tissues in the throat.
All you need to do is add 4 to 5 shakes of cayenne pepper to a glass of warm water and add 2 to 3 drops of lime juice to it. If the sore throat persists for more than a week it is better if you visit your nearby doctor.
Taking antibiotics unnecessarily may not solve the problem as some bacteria may become resistant to the antibiotics. Aspirin is taken generally to get rid of the mild fever in adults but not in children and teens as it leads to serious illness called Reye syndrome. Further, use of contact lenses for prolonged period can also lead to eye infections, and also if not cleaned properly.
Moreover, novel aspects about the role of IDO in bacterial infections and sepsis have been revealed. Induction of IDO in cells of the immune system by IFNγ was introduced for the first time in the late 1980s (3, 4). As mode of action for IDO, O2▪-radical scavenging (2, 10) and later suppression of T-cell responses (11, 12) were discussed.
The dampened immune response upon IDO induction enables a successful colonization of urinary epithelium by UPEC.
Elevated serum levels of IFNγ (27, 28) and Kyn (29) in HIV patients pointed toward a participation of IDO in suppression of T-cell function, yet molecular mechanisms were unknown. Direct induction of IDO in antigen-presenting cells (APC) by viral Tat protein is established via an intracellular signaling cascade including kinases (JakI, PI3K) or CTLA-4-B7 interaction on regulatory T (Treg)-cells with B7 co-receptor on the APC, which leads in consequence to a breakdown of tryptophan (Trp) into kynurenine (Kyn).
Probably, IDO was only partially inhibited since reconstituted Trp levels were accompanied with elevated Kyn levels in sera of treated animals.
Similarly, in SIV-infected macaques, the expression of the Treg markers CTLA-4 and FoxP3 was increased in T-cells of mesenteric lymph nodes, spleen, and colon, organs with high viral load (43).
However, in a more recent study using the same model, IDO had no impact on disease progression (47). In patients with chronic HIV infection, the elevated Trp catabolism maintained by IDO expression is associated with reduced levels of free serum Trp (48, 49). Underlying mechanisms of the connection between chronic infection with viruses or bacteria and the onset of mental disorders in men are unknown. IDO activity increased during influenza infection and peak expression correlated with increased lymphocyte numbers in the respiratory tract, albeit the study did not discriminate between T-cell and B-cell subpopulations (53).
It was speculated that IDO suppresses an overactive immune response triggered by TNFα-producing NK cells and macrophages infiltrating the liver. This might be important since NK cells have been suggested to control the proliferation of EBV-infected B-cells in the acute phase. Immunotherapy against the tumor is often inefficient because of the existence of a local immunosuppressive tumor milieu with impaired tumor cell antigen presentation and resistance of tumor cells against effector mechanisms of T-cells.
In Tb patients elevated levels of anti-inflammatory molecules in the sputum, amongst them IDO have been detected (70). Activation of IDO activity in bacteria-infected cells induces a potent bactericidal growth restrain to fight against spreading of the infection.
In general, the life cycle of Chlamydia species can be divided into two phases: (1) a stage of infectious but metabolically inactive form directly after uptake of the bacteria into the host cell, and (2) a stage of differentiation and multiplication enabled by an active metabolism. If you compare a virus to a bacteria it is like comparing a mouse to an elephant in corresponding proportionate sizes and anything to attack an elephant cannot destroy a mouse and vice versa.Thank you. A virus may produce phlegm that is clear or cloudy, but a bacterial infection may produce phlegm that is green, yellow, bloody or brown. Sometimes the pain persists for several days that it becomes difficult to chew and swallow your own food, sometimes you even might go speechless because of the severe pain. Inflammation of epiglottis is one of the serious causes affecting sore throat because it becomes difficult for you to swallow food which is usually the function of epiglottis. If you have any further queries and doubts that hover your mind after reading this article feel free to comment via the comments section.
Here, we review these recent findings highlighting the central role of IDO and tryptophan metabolism in many major human infections. Since many microbial organisms rely on the essential amino acid Trp, its degradation by IDO-expressing cells of the innate immune system was favored as the major IDO-mediated mechanism against infections (13). In addition, viruses like human immunodeficiency virus 1 (HIV) use the immunosuppressive activity of IDO to drive HIV infection into the chronic phase (25). Further support came from increased IDO mRNA levels measured in peripheral blood mononuclear cells (PBMCs) of HIV-infected patients (30). Further, a compensatory counterregulatory mechanism for 1-MT was suggested due to increased IDO and TGFβ production in lymph nodes of treated animals. Simultaneously, IDO expression in spleen and gut-associated lymphoid tissues was suggested to support immunological suppression in favor of viral replication. Viral loads of IDO KO mice were comparable to those of wild-type B6 mice and both IDO KO and WT mice showed decreased responsiveness to B-cell and T-cell mitogens. This correlates with a reduction of serotonin (5-HT) and serotonin transporter (5-HTT) expression, as well as an accumulation of neurotoxic Trp metabolites (50). Insufficient levels of serotonin in chronically infected and depressive patients are thought to be the consequence of constitutively elevated levels of IDO. A massive amount of HCV-specific CD8 T-cells are recruited to the liver; however, recognition of viral epitopes is barely present. In the same report, it was shown that IL18 suppressed the effect of Kyn on NKG2D expression. The immunosuppressive milieu might be created during the stage of cervical intraepithelial neoplasia (CIN), since numbers of IDO, IFNγ, IL10, and FoxP3 expressing cells are elevated in CIN compared to normal cervical tissue (66). Besides the induction of reactive oxygen species (ROS) and nitric oxide radicals, activity of IDO aids in Trp degradation to starve Trp auxotroph bacteria.
The authors present no evidence IDO is indeed expressed in the myeloid cell compartment, like in human disease, indicating that this mouse model might not reflect the human situation.
It can be assumed that immune responses of host cells might differ according to the life cycle of Chlamydia.
Similarly, the human monocytic cell line THP-1 has been shown to be sensitive to low iron concentrations, which showed an inhibitory effect on IFNγ signaling resulting in decreased Trp metabolism (92).
A sore throat usually mentioned as a throat infection or pharyngitis, causes pain in the back part of the throat.


Inflammation of uvulitis and is responsible for the food to enter into the digestive system. Within two days of experiencing these symptoms, a physician should be contacted for immediate treatment. Moreover, we also shed light on issues concerning human-specific and mouse-specific host–pathogen interactions that need to be considered when studying the biology of IDO in the context of infections. It participates in a broad spectrum of immune responses during chronic infections, immune-escape of cancer cells, tissue inflammation, transplantation, and maternal tolerance toward the fetus and autoimmunity (6).
In infectious disease states, IDO has been shown to exert pleiotropic effects, even with opposing outcomes.
In the following chapters, we will focus on new insights into the role of IDO and Kyn derivates in major viral and bacterial infections in mice and men.
Decreased numbers of CD4+ T-cells during the course of HIV infection are accompanied by a loss of type I IFN producing cells, like pDC (35, 36).
Therefore, therapeutic targeting of Treg in HIV patients thereby reducing IDO expression in APCs and subsequently immunosuppression seemed promising. One might postulate that an important denominator of efficacy targeting IDO might simply be the time when IDO is induced during the course of the infection. Especially, Kyn and quinolinic acid (QA) can be detected in cerebrospinal fluids of HIV patients and are linked to the development of neuropsychiatric disorders, as part of the Neuro-AIDS complex of symptoms (50). Murine models of chronic infections are established to decipher the involvement of IDO in the development of depressive-like behavior. Similarly, in chronic HBV infection, cytotoxic T lymphocytes (CTLs) show only a weak response against the HBV surface antigen (HBsAg).
Upon immunization, expression of the cytokines IL-2 and IL-12b were only increased in IDO KO mice leading to the induction of HBsAg-specific CTLs.
It might be speculated that the suppression of NK cell activation by IDO-expressing EBV-infected B-cells serves as an escape strategy of the virus. When HPV16 E7, an envelope- and oncoprotein of HPV was expressed under the keratin-14 promoter (K14E7) in a skin grafting model, graft rejection was prevented suggesting that HPV16E7 induced an immunotolerogenic environment (67). It was assumed that all these inhibitory molecules dampen Th1 responses in the lung thereby contributing to immune-escape of the bacteria. A further species-specific bactericidal effect of increased IDO activation is the production of toxic Kyn metabolites.
In contrast, another report demonstrates a direct connection between IFNγ and IDO expression in non-hematopoietic cells, during the chronic phase of murine M.
This observation led to the hypothesis that immune cells retain iron during inflammatory diseases to enable efficient IFNγ driven immune responses. Interestingly, accumulating evidence also connects enhanced Trp metabolism to mental disorders based on serotonin starvation. One reason for the low pDC numbers might be their redistribution to peripheral lymph nodes, as observed in the acute phase of SIV-infected macaques (36).
However, when blocking CTLA-4 signaling in SIV-infected macaques, an unexpected increase in IDO expression and Kyn levels was observed (44). Clearly, more work is necessary to determine the role of IDO in murine retroviral infections. HIV-1 associated dementia (HAD) is correlated to IDO and Kyn induced by Tat of HIV-1 clade B in human primary astrocytes (51) while Tat of HIV-1 clade C does not induce IDO activity in human primary astrocytes and is not associated with HAD. While the molecular mechanisms of the tolerogenic state in chronic HBV and HCV infection are not completely understood, an increased IDO expression in the liver of patients with chronic HBV or HCV infection has been observed (57).
Recently, it was shown that in vitro generated macrophages expressed IDO after infection with EBV and displayed T-cell suppressive activities (64). Recruitment of Treg cells and increasing levels of free ions might help as negative feedback loop to terminate inflammatory responses.
On the other hand, reduction of iron levels by deferoxamine did not reconstitute IDO activity, but still suppressed bacterial growth (90, 91). Besides Trp depletion, production of Trp metabolites with bactericidal activity, like Kyn, were identified in human macrophages upon infection with diverse bacteria species as another defense mechanism mediated by IDO (23). Also, numbers of myeloid DC (mDC) are diminished in blood of HIV patients during primary infection (37).
Moreover, even under conditions of increased T-cell activation due to loss of the regulatory CTLA-4 signaling, viral replication was still promoted. Further evidence for the role of Tat for IDO expression in the brain came from experiments injecting Tat protein intracerebroventricularly into different mice strains. These results indicate that inhibition of IDO might improve flu vaccine activity, might aid in heterosubtypic immunity and support a faster recovery. In fact, IDO seems to have a pivotal role in K14E7 graft tolerance, since IDO inhibition by 1-MT leads to rejection of K14E7 skin grafts (67). In this model, IDO was expressed in endothelial and epithelial cells, and IFN receptor deficiency reduced the levels of expression of IDO in these cells thereby leading to an impaired long-term control of M. IFNγ induced Trp degradation leading to anti-toxoplasmosis activity in infected human fibroblasts was first described by Pfefferkorn in 1984 (1). Further, when injecting Tat, induction of IDO and several other pro-inflammatory cytokines in the brain was associated with reduced mobility and depressive-like behavior (52), demonstrating the important role of IDO in the pathophysiology of HIV infection. This view is also supported by data reporting reduced morbidity rates in IDO KO mice when challenged with RP8 or X31 influenza viruses (54).
In a recent study including 176 patients suffering from chronic HCV infection and 37 healthy controls, it could be shown that Kyn levels correlated with advanced liver inflammation and fibrosis (59).
Only a few years later, several studies linked this effect to enhanced IDO activity against pathogens like Toxoplasma gondii, certain Chlamydia psittaci strains and Leishmania donovani (14–16).
In monocyte-derived DC (moDC), the N-terminal domain of HIV-1 transactivator regulatory protein (Tat) induced IFNγ and IDO expression and therefore further led to a suppression of T-cell proliferation. To investigate, if HIV alters the function of infected mDC, PBMC-derived DC were transfected with a HIV containing vector construct as a model system (38).
In another attempt to refine ART by combining CTLA-4-blockade and 1-MT treatment, severe side effects causing acute pancreatitis with massive lymphocyte infiltration into the pancreas and loss of Langerhans islets were induced (45).
Blockade of IDO or upstream events of IDO induction in chronic infection might be a novel approach to treat chronic HIV infections. Especially, IDO deficiency led to enhanced development of memory T-cells, which protected mice from lethal virus infection.
From in vitro studies, there is evidence that TNFα might play a role during the acute and chronic phase of Tb (9, 76).
Downstream of IDO, BCG also increased the expression of 3-hydroxyanthranilic acid oxygenase (3-HAO), which participates in the generation of the neurotoxic Kyn metabolite QA (88). This resulted in the induction of IDO in immature and matured DC, accompanied by increased levels of Kyn. Moreover, all tested animals developed diabetes and hyperglycemic coma while SIV-specific responses were not observed. Further, it was demonstrated that non-hematopoietic cells from lung-draining lymph nodes were major IDO producing cells in response to X31-induced IFNγ secretion. Along these lines, in vitro stimulation of the HCV-infected hepatocellular carcinoma cell line Huh7 with IFNγ led to an induction of IDO, yet HCV replication was not altered by IDO activity (57). Clearly, this murine model strongly suggests an important participation of IDO in HPV evasion from host immunity. Moreover, treatment of patients with anti-TNFα antibodies can lead to exacerbation of Tb and the induction of Tb sepsis (78).
Application of 1-MT also prevented the development of depressive-like behavior after BCG inoculation in mice, suggesting that elevated IDO, like TNFα, contributes to the onset of depressive disorders during chronic inflammation caused by mycobacteria. IDO expression was initially induced by Tat and followed by the induction of IFNγ leading to a feed forward loop.
These results clearly illustrate that the reversal of immunosuppression by targeting CTLA-4 in chronic viral infection is not a promising approach. As a feed forward loop, IFN type I and II induced subsequently IDO activity in hematopoietic cells. IDO was considered as the major mediator of the IFNγ-induced anti-viral response, since it mediated Trp depletion followed by suppression of HBV replication. This virostatic effect could be reverted by addition of exogenous Trp indicating an involvement of IDO (17, 19, 20). Interestingly, IFNγ signaling pathways leading to IDO expression could be blocked by JAKs and PI3K inhibitors but Tat-induced IDO expression could not be inhibited, suggesting a novel so far not characterized mechanism of IDO induction by Tat proteins in HIV infection (33).
Further, HIV-transduced mature DC induced only modest T-cell proliferation in mixed-lymphocyte reactions, which might be due to IDO activity depleting Trp, a necessary molecule for T-cell function.
Interestingly, the activity of inducible nitric oxide synthetase (iNOS) was suggested to be able to substitute for the IDO-mediated anti-viral mechanism (18, 24). The addition of 1-MT restored the immunostimulatory capacity of these DC, suggesting a central role of IDO in the suppression induced by HIV-infected DC. Since then, it was demonstrated that other viruses, such as herpes simplex virus type 2 (HSV-2) (17), measles virus (19), and vaccinia virus (20), are sensible to IDO-induced Trp depletion. The induction of a tolerogenic milieu including the recruitment of FoxP3+ regulatory T-cells by IDO-expressing cells together with depletion of Trp most likely aids in the restriction of bacterial spread. However, IDO activation in combination with increased Trp degradation as well as IFNγ treatment had no effect on numbers or growth of C. However, there is still controversy about this, since a recent report demonstrated expression of IDO in macrophages of leprotic skin lesions (80).
An interesting aspect of this study was the comparison of chlamydia infection in THP-1 cells and human endothelial cells.
The authors also argued that the differences between the two cell types might also reflect different stages of the C. The bacteria might use immune competent monocytes as transportation vessels for systemic dissemination, while endothelial cells might serve as habitats for differentiation and proliferation, especially under iron rich conditions.



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