Differential pattern of cytokine expression by macrophages infected<i>in vitro</i>with different<i>Mycobacterium tuberculosis</i>genotypes

Chacón‐Salinas, Rommel; Serafín‐López, Jeanet; Ramos‐Payán, Rosalío; Méndez-Aragón, Patricia; Hernández-Pando, Rogelio; Soolingen, Dick van; Flores‐Romo, Leopoldo; Estrada‐Parra, Sergio; Estrada-Garcı́a, Iris

doi:10.1111/j.1365-2249.2005.02797.x

Cited by 96 publications

(66 citation statements)

References 23 publications

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“…The elevation in total protein and globulin could be due to good response to treatment. This agrees with the work of Zia et al, in India where he observed increase total protein and globulin in individuals on intensive phase and increased albumin/ globulin ratio in those on continuation phase of treatment [32].…”

Section: Discussionsupporting

confidence: 82%

Serum Albumin/Globulin ratio in Tuberculosis and HIV Patients any Relationship?

Shingdang¹,

Y²

2016

Mycobact Dis

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Background: Tuberculosis (TB) remains an important communicable disease all over the world. The serum protein levels in TB patients may be altered by low immunity, edema and decrease antioxidant activity. This study therefore evaluates the relationship between TB and serum proteins with emphasis on albumin/globulin ratio an important component for treatment and management of TB. The study also aimed at comparing albumin/globulin ratio of tuberculosis patients, HIV patients, those on drugs and naive patients.

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Section: Discussionsupporting

confidence: 82%

Serum Albumin/Globulin ratio in Tuberculosis and HIV Patients any Relationship?

Shingdang¹,

Y²

2016

Mycobact Dis

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“…As the disease severity, drug toxicity, and drug resistance were similar between the two groups (W-Beijing versus others), the authors suggested that these differences may be due to the strains' (W-Beijing) ability to induce a different host response, consistent with the studies described above (51,157,163,165,207). Further studies with human populations are needed.…”

Section: Strain-specific Variations In Immunity and Pathogenesissupporting

confidence: 70%

Molecular Epidemiology of Tuberculosis: Current Insights

et al. 2006

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SUMMARY Molecular epidemiologic studies of tuberculosis (TB) have focused largely on utilizing molecular techniques to address short- and long-term epidemiologic questions, such as in outbreak investigations and in assessing the global dissemination of strains, respectively. This is done primarily by examining the extent of genetic diversity of clinical strains of Mycobacterium tuberculosis. When molecular methods are used in conjunction with classical epidemiology, their utility for TB control has been realized. For instance, molecular epidemiologic studies have added much-needed accuracy and precision in describing transmission dynamics, and they have facilitated investigation of previously unresolved issues, such as estimates of recent-versus-reactive disease and the extent of exogenous reinfection. In addition, there is mounting evidence to suggest that specific strains of M. tuberculosis belonging to discrete phylogenetic clusters (lineages) may differ in virulence, pathogenesis, and epidemiologic characteristics, all of which may significantly impact TB control and vaccine development strategies. Here, we review the current methods, concepts, and applications of molecular approaches used to better understand the epidemiology of TB.

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“…M1 macrophages are generally considered responsible for resistance against intracellular pathogens and characterize infection with Listeria monocytogenes (55), Salmonella typhi, and Salmonella typhimurium (56), as well as the early phases of infection with Mycobacterium tuberculosis (57), Mycobacterium ulcerans, and Mycobacterium avium (58,59). Uncontrolled M1 inflammation associated with acute infections with E. coli or Streptococcus sp.…”

Section: Infectionmentioning

confidence: 99%

Macrophage plasticity and polarization: in vivo veritas

2012

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(Retnla, Fizz1), and chitinase 3-like 3 (Chi3l3, Ym1) (14). IL-10 activates STAT3-mediated expression of genes (Il10, Tgfb1, Mrc1) associated with an M2-like phenotype (4,15,16). STAT-mediated activation of macrophages is regulated by members of the SOCS family. IL-4 and IFN-γ, the latter in concert with TLR stimulation, upregulate SOCS1 and SOCS3, which in turn inhibit the action of STAT1 and STAT3, respectively (17,18).Downstream of, or in parallel with, the IRF/STAT/SOCS pathway, a panel of transcription factors orchestrates polarized macrophage activation. The nuclear receptors PPARγ (19) and PPARδ (20,21) control distinct subsets of genes associated with M2 macrophage activation and oxidative metabolism (Figure 1). Interestingly, STAT6 coordinates and synergizes with both PPARγ (22) and Krüppel-like factor 4 (KLF4), a member of a family of proteins that contribute to macrophage function (23, 24). KLF4 cooperates with Stat6 to induce M2 genes (Arg-1, Mrc1, Fizz1, PPARγ) and inhibit M1 genes (TNFa, Cox-2, CCL5, iNOS) via sequestration of coactivators required for NF-κB activation. KLF2 regulates macrophage activation by inhibiting NF-κB/ HIF-1α activities (25). IL-4 also induces c-Myc activity in human macrophages (26), which controls genes of M2 activation (Scarb1, Alox15, and Mrc1) as well as STAT6 and PPARγ activation (26).TLR engagement leads to NF-κB activation and production of inflammatory mediators (27) associated with M1 macrophages. However, NF-κB activation also activates a genetic program essential for resolution of inflammation (28) and for M2 polarization of tumor-associated macrophages (TAMs) (29). Moreover, induction of p50 NF-κB homodimers is essential for M2 polarization in vitro and in vivo (30). The hypoxia-inducible factors HIF-1α and HIF-2α are expressed differentially in M1- and M2-polarized macrophages (31) and regulate inducible NOS2 (M1) and arginase 1 (M2), respectively. Figure 1Mechanisms of macrophage polarization. The major pathways of macrophage polarization are outlined. The crosstalk between the M1-M2 macrophage-polarizing pathways is also indicated. The balance between activation of STAT1 and STAT3/STAT6 finely regulates macrophage polarization and activity. A predominance of NF-κB and STAT1 activation promotes M1 macrophage polarization, resulting in cytotoxic and inflammatory functions. In contrast, a predominance of STAT3 and STAT6 activation results in M2 macrophage polarization, associated with immune suppression and tumor progression. PPARγ and PPARδ control distinct aspects of M2 macrophage activation and oxidative metabolism. KLF4 and KLF2 participate in the promotion of M2 macrophage functions by cooperating with STAT6 and suppressing the NF-κB/HIF-1α-dependent transcription, respectively. IL-4-induced c-Myc activity controls a subset of M2-associated genes. IL-4 also induces the M2-polarizing Jmjd3-IRF4 axis to inhibit IRF5-mediated M1 polarization. IL-10 promotes M2 polarization through the induction of p50 NF-κB homodimer, c-Maf, and STAT3 activities. Epigenetic ...

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Differential pattern of cytokine expression by macrophages infectedin vitrowith differentMycobacterium tuberculosisgenotypes

Cited by 96 publications

References 23 publications

Serum Albumin/Globulin ratio in Tuberculosis and HIV Patients any Relationship?

Serum Albumin/Globulin ratio in Tuberculosis and HIV Patients any Relationship?

Molecular Epidemiology of Tuberculosis: Current Insights

Macrophage plasticity and polarization: in vivo veritas

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