Effect of morphine on Mycobacterium smegmatis infection in mice and macrophages

Singh, Raman P.; Jhamb, Sarbjit Singh; Singh, Prati Pal

doi:10.1007/s12088-009-0045-6

Cited by 4 publications

(2 citation statements)

References 23 publications

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“…A possible explanation is that opioids affect the immune response directly; in vitro and animal studies have found deleterious effects of opioids in infections [ 20 ]. In relation to mycobacteria specifically, studies show mixed results; some finding advantageous effects of opioids [ 32 ], others showing deleterious effects [ 33 , 34 ]. In addition, we have previously shown biological effects of heroin use on the expression of chemokines and chemokine receptors among HIV-infected individuals [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Active and latent tuberculosis among HIV‐positive injecting drug users in Indonesia

Meijerink

Wisaksana

Lestari

et al. 2015

Journal of the International AIDS Society

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IntroductionInjecting drug use (IDU) is associated with tuberculosis but few data are available from low-income settings. We examined IDU in relation to active and latent tuberculosis (LTBI) among HIV-positive individuals in Indonesia, which has a high burden of tuberculosis and a rapidly growing HIV epidemic strongly driven by IDU.MethodsActive tuberculosis was measured prospectively among 1900 consecutive antiretroviral treatment (ART)-naïve adult patients entering care in a clinic in West Java. Prevalence of LTBI was determined cross-sectionally in a subset of 518 ART-experienced patients using an interferon-gamma release assay.ResultsPatients with a history of IDU (53.1%) more often reported a history of tuberculosis treatment (34.8% vs. 21.9%, p<0.001), more often received tuberculosis treatment during follow-up (adjusted HR=1.71; 95% CI: 1.25–2.35) and more often had bacteriologically confirmed tuberculosis (OR=1.67; 95% CI: 0.94–2.96). LTBI was equally prevalent among people with and without a history of IDU (29.1 vs. 30.4%, NS). The risk estimates did not change after adjustment for CD4 cell count or ART.ConclusionsHIV-positive individuals with a history of IDU in Indonesia have more active tuberculosis, with similar rates of LTBI. Within the HIV clinic, LTBI screening and isoniazid preventive therapy may be prioritized to patients with a history of IDU.

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Section: Discussionmentioning

confidence: 99%

Active and latent tuberculosis among HIV‐positive injecting drug users in Indonesia

Meijerink

Wisaksana

Lestari

et al. 2015

Journal of the International AIDS Society

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“…Cells were lysed for bacterial counts in PBS containing 0.05% Tween 80 (59). The number of cfu per 1 ϫ 10 6 cells was determined by plating 10-fold serial dilutions of cell lysates on Middlebrook 7H10 plates complemented with 0.5% glycerol and 10% oleic albumin dextrose complex enrichment (59,60). For selective medium, 40 g/ml kanamycin was added.…”

Section: Assessment Of Intracellular Bacterial Cfumentioning

confidence: 99%

The R753Q polymorphism in Toll-like receptor 2 (TLR2) attenuates innate immune responses to mycobacteria and impairs MyD88 adapter recruitment to TLR2

Pattabiraman

Panchal

Medvedev

2017

Journal of Biological Chemistry

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Toll-like receptor 2 (TLR2) plays a critical role in host defenses against mycobacterial infections. The R753Q TLR2 polymorphism has been associated with increased incidence of tuberculosis and infections with non-tuberculous mycobacteria in human populations, but the mechanisms by which this polymorphism affects TLR2 signaling are unclear. In this study, we determined the impact of the R753Q TLR2 polymorphism on macrophage sensing of Upon infection with, macrophages from knock-in mice harboring R753Q TLR2 expressed lower levels of TNF-α, IL-1β, IL-6, and IL-10 compared with cells from WT mice, but both R753Q TLR2- and WT-derived macrophages exhibited comparable bacterial burdens. The decreased cytokine responses in R753Q TLR2-expressing macrophages were accompanied by impaired phosphorylation of IL-1R-associated kinase 1 (IRAK-1), p38, ERK1/2 MAPKs, and p65 NF-κB, suggesting that the R753Q TLR2 polymorphism alters the functions of the myeloid differentiation primary response protein 88 (MyD88)-IRAK-dependent signaling axis. Supporting this notion, HEK293 cells stably transfected with YFP-tagged R753Q TLR2 displayed reduced recruitment of MyD88 to TLR2, decreased NF-κB activation, and impaired IL-8 expression upon exposure to Collectively, our results indicate that the R753Q polymorphism alters TLR2 signaling competence, leading to impaired MyD88-TLR2 assembly, reduced phosphorylation of IRAK-1, diminished activation of MAPKs and NF-κB, and deficient induction of cytokines in macrophages infected with.

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