Effects of antibiotics on expression and function of Toll-like receptors 2 and 4 on mononuclear cells in patients with advanced cirrhosis

Testro, Adam; Gow, Paul J; Angus, Peter W; Wongseelashote, Sarah; Skinner, Narelle; Markovska, V.; Visvanathan, Kumar

doi:10.1016/j.jhep.2009.11.006

Cited by 23 publications

(30 citation statements)

References 47 publications

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“…Both of these TLRs activate nuclear factor kappa β (NFKβ) in liver cells 40. Studies have shown decreased TLR2 function in early cirrhosis41,42 but decreased TLR4 function in advanced cirrhosis only 41,43–46. A study performed by Nischelke et al 47.…”

Section: Immunological Dysfunction In Cirrhosismentioning

confidence: 99%

Immune Dysfunction in Cirrhosis

Noor¹,

Manoria²

2017

Journal of Clinical and Translational Hepatology

118

105

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Cirrhosis due to any etiology disrupts the homeostatic role of liver in the body. Cirrhosis-associated immune dysfunction leads to alterations in both innate and acquired immunity, due to defects in the local immunity of liver as well as in systemic immunity. Cirrhosis-associated immune dysfunction is a dynamic phenomenon, comprised of both increased systemic inflammation and immunodeficiency, and is responsible for 30% mortality. It also plays an important role in acute as well as chronic decompensation. Immune paralysis can accompany it, which is characterized by increase in antiinflammatory cytokines and suppression of proinflammatory cytokines. There is also presence of increased gut permeability, reduced gut motility and altered gut flora, all of which leads to increased bacterial translocation. This increased bacterial translocation and consequent endotoxemia leads to increased blood stream bacterial infections that cause systemic inflammatory response syndrome, sepsis, multiorgan failure and death. The gut microbiota of cirrhotic patients has more pathogenic microbes than that of noncirrhotic individuals, and this disturbs the homeostasis and favors gut translocation. Prompt diagnosis and treatment of such infections are necessary for better survival. We have reviewed the various mechanisms of immune dysfunction and its consequences in cirrhosis. Recognizing the exact pathophysiology of immune dysfunction will help treating clinicians in avoiding its complications in their patients and can lead to newer therapeutic interventions and reducing the morbidity and mortality rates. Citation of this article: Noor MT, Manoria P. Immune dysfunction in cirrhosis.

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Section: Immunological Dysfunction In Cirrhosismentioning

confidence: 99%

Immune Dysfunction in Cirrhosis

Noor¹,

Manoria²

2017

Journal of Clinical and Translational Hepatology

118

105

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“…Other authors also found a decrease TLR2-and TLR4-response in immune cells, particularly in advanced stages of disease, that was associated with decreased, normal or increased levels of TLRs, depending on the study (Riordan et al, 2003;Stadlbauer et al, 2008;Stadlbauer et al, 2009;Tazi et al, 2006;Testro et al, 2009;Wasmuth et al, 2005). The data of these studies are compared in table 1.…”

Section: Role Of Innate Immunity Impairment In Ald Infection Riskmentioning

confidence: 95%

“…Hence, we believe that the frequent episodes of bacteraemia that occur in cirrhosis, by changing TLR expression on immune cells, can help explain these discrepancies concerning TLR expression. This also might be the reason why Stadlbauer et al (Stadlbauer et al, 2008), using probiotics, promoted the decrease, and Testro et al (Testro et al, 2009), using antibiotics, the increase in TLR4 levels, both trending towards normal levels of expression. Possibly, these two different therapeutic agents decrease episodes of bacteraemia, consequently with less fluctuation of TLR levels.…”

Section: Role Of Innate Immunity Impairment In Ald Infection Riskmentioning

confidence: 98%

“…Fourthly, taking together the discrepancies in the expression levels of TLRs, it appears that other factors, probably intracellular, are fundamental to this immunodeficiency. Finally, this process may be reversible with antibiotics and/or probiotics (Stadlbauer et al, 2008;Testro et al, 2009). However, further studies are needed before generalization since Riordan et al (Riordan et al, 2003) showed that the use of a symbiotic (mixture of probiotic and probiotic) further compromised TLR2 function, in contrast to the positive immunological effects obtained by Stadlbauer et al (Stadlbauer et al, 2008) and Testro et al (Testro et al, 2009 Table 1.…”

Section: Role Of Innate Immunity Impairment In Ald Infection Riskmentioning

confidence: 99%

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Innate Immunity in Alcohol Liver Disease

Soares¹,

Pimentel‐Nunes²

2012

Trends in Alcoholic Liver Disease Research - Clinical and Scientific Aspects

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“…Loss-of function TLR4 variants are associated with reduced risk for liver fibrosis progression in chronic hepatitis-virus-C infection (Huang et al, 2007) and increased TLR2 and TLR4 liver expression were associated with cirrhosis (Manigold et al, 2003;Tazi et al, 2006;Testro et al, 2010). Similarly TLR2 deficient mice display diminished inflammatory and fibrotic responses via reduced TLR4 signaling (Hartmann et al, 2012).…”

Section: Liver Fibrosismentioning

confidence: 99%