scholarly journals Binding of CXCL8/IL-8 toMycobacterium tuberculosisModulates the Innate Immune Response

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Agnieszka Krupa ◽  
Marek Fol ◽  
Bozena R. Dziadek ◽  
Ewa Kepka ◽  
Dominika Wojciechowska ◽  
...  
Keyword(s):  
Immune Response ◽  
Mycobacterium Tuberculosis ◽  
Innate Immune Response ◽  
Respiratory Diseases ◽  
Underlying Mechanism ◽  
Innate Immune ◽  
Major Goal ◽  
Adequate Response ◽  
Inflammatory Processes ◽  
First Time

Interleukin-8 (IL-8) has been implicated in the pathogenesis of several human respiratory diseases, including tuberculosis (TB). Importantly and in direct relevance to the objectives of this report quite a few findings suggest that the presence of IL-8 may be beneficial for the host. IL-8 may aid with mounting an adequate response during infection withMycobacterium tuberculosis (M. tb); however, the underlying mechanism remains largely unknown. The major goal of our study was to investigate the contribution of IL-8 to the inflammatory processes that are typically elicited in patients with TB. We have shown for the first time that IL-8 can directly bind to tubercle bacilli. We have also demonstrated that association of IL-8 withM. tbmolecules leads to the augmentation of the ability of leukocytes (neutrophils and macrophages) to phagocyte and kill these bacilli. In addition, we have shown that significant amount of IL-8 present in the blood of TB patients associates with erythrocytes. Finally, we have noted that IL-8 is the major chemokine responsible for recruiting T lymphocytes (CD3+, CD4+, and CD8+T cells). In summary, our data suggest that the association of IL-8 withM. tbmolecules may modify and possibly enhance the innate immune response in patients with TB.

scholarly journals Innate Immune Response to Mycobacterium tuberculosis Beijing and Other Genotypes

PLoS ONE ◽  
2010 ◽  
Vol 5 (10) ◽  
pp. e13594 ◽  
Author(s):  
Chongzhen Wang ◽  
Pascale Peyron ◽  
Olga Mestre ◽  
Gilla Kaplan ◽  
Dick van Soolingen ◽  
...  
Keyword(s):  
Immune Response ◽  
Mycobacterium Tuberculosis ◽  
Innate Immune Response ◽  
Innate Immune

scholarly journals Mycobacterium tuberculosis Lineage Influences Innate Immune Response and Virulence and Is Associated with Distinct Cell Envelope Lipid Profiles

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e23870 ◽  
Author(s):  
Nitya Krishnan ◽  
Wladimir Malaga ◽  
Patricia Constant ◽  
Maxine Caws ◽  
Tran Thi Hoang Chau ◽  
...  
Keyword(s):  
Immune Response ◽  
Mycobacterium Tuberculosis ◽  
Innate Immune Response ◽  
Cell Envelope ◽  
Lipid Profiles ◽  
Innate Immune ◽  
Distinct Cell

scholarly journals 1-Trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo) Induces the Apoptosis of Dopaminergic Neurons via Oxidative Stress and Neuroinflammation

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Yihang Yang ◽  
Bo Pang ◽  
Zihao Liu ◽  
Jie Li ◽  
Zhen Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Innate Immune Response ◽  
Diffusion Tensor ◽  
Underlying Mechanism ◽  
Innate Immune ◽  
Motor Dysfunction ◽  
Mass Spectrometry Analysis ◽  
Nigrostriatal System

Several in vitro studies have revealed the neurotoxicity of 1-trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo). However, the underlying mechanism has not been completely elucidated, particularly in vivo. This study was designed to study the neurotoxicity of TaClo in vivo by stereotactically injecting TaClo into the striatum of Wistar rats. After the TaClo injections, rats were subjected to an open field test, and their distance travelled and tracks showed decreasing trends over time. The results of liquid chromatography-mass spectrometry analysis showed that the motor dysfunction of the TaClo-treated rats was accompanied by reduced dopamine levels in the striatum. Based on the diffusion tensor imaging data, the apparent diffusion coefficient of the nigrostriatal pathway was significantly increased, and subsequent histological staining revealed the demyelination of nigrostriatal fibres after the TaClo treatment. TaClo induced a loss of tyrosine hydroxylase-positive cells in the substantia nigra compacta. Regarding the underlying mechanism, TaClo caused oxidative stress in the nigrostriatal system by increasing the production of reactive oxygen species and reducing the mitochondria membrane potential. Meanwhile, the elevated expression of Iba-1, TNF-α, IL-6, Cox-2, and iNOS indicated microglial activation and a strong innate immune response in the nigrostriatal system. In addition, activated caspase-3 levels were increased. Thus, both mitochondrial impairments and the innate immune response are involved in TaClo-induced neurotoxicity.

scholarly journals Mycobacterium tuberculosis Strains Lacking Surface Lipid Phthiocerol Dimycocerosate Are Susceptible to Killing by an Early Innate Host Response

2014 ◽  
Vol 82 (12) ◽  
pp. 5214-5222 ◽  
Author(s):  
Tracey A. Day ◽  
John E. Mittler ◽  
Molly R. Nixon ◽  
Cullen Thompson ◽  
Maurine D. Miner ◽  
...  
Keyword(s):  
Immune Response ◽  
Mycobacterium Tuberculosis ◽  
Innate Immune Response ◽  
Host Response ◽  
Innate Immune ◽  
Dependent Manner ◽  
Surface Lipid ◽  
Content Type ◽  
Ifn Γ ◽  
Phthiocerol Dimycocerosate

ABSTRACTThe innate immune response plays an important but unknown role in host defense againstMycobacterium tuberculosis. To define the function of innate immunity during tuberculosis, we evaluatedM. tuberculosisreplication dynamics during murine infection. Our data show that the early pulmonary innate immune response limitsM. tuberculosisreplication in a MyD88-dependent manner. Strikingly, we found that littleM. tuberculosiscell death occurs during the first 2 weeks of infection. In contrast,M. tuberculosiscells deficient in the surface lipid phthiocerol dimycocerosate (PDIM) exhibited significant death rates, and consequently, total bacterial numbers were reduced. Host restriction of PDIM-deficientM. tuberculosiswas not alleviated by the absence of interferon gamma (IFN-γ), inducible nitric oxide synthase (iNOS), or the phagocyte oxidase subunit p47. Taken together, these data indicate that PDIM protectsM. tuberculosisfrom an early innate host response that is independent of IFN-γ, reactive nitrogen intermediates, and reactive oxygen species. By employing a pathogen replication tracking tool to evaluateM. tuberculosisreplication and death during infection, we identify both host and pathogen factors affecting the outcome of infection.

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