IFNγ primes macrophages for inflammatory activation by high molecular weight hyaluronan

Wallet, Mark A.; Wallet, Shannon M.; Guiulfo, Giorgio; Sleasman, John W.; Goodenow, Maureen M.

doi:10.1016/j.cellimm.2010.02.013

Cited by 19 publications

(21 citation statements)

References 19 publications

(34 reference statements)

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“…Upon analysis of specific macrophage subset marker expression under in vitro M1 (IFN-␥, LPS) and M2 (IL-4) conditions, we noticed some variations. 5 Fig. 4C and D).…”

Section: M1(f4/80mentioning

confidence: 88%

“…Stimulation of undifferentiated macrophages with lipopolysaccharide (LPS) and gamma interferon (IFN-␥), or tumor necrosis factor alpha (TNF-␣), induces polarization to the M1 phenotype (4,5). They can be recognized both in vitro and in vivo by the production of nitric oxide species (NOS), as well as other proinflammatory molecules, including TNF-␣, interleukin 1 (IL-1), IL-6, and CCL2 (6).…”

mentioning

confidence: 99%

“…Asterisks indicate data that are significantly different from control data at a P value of Ͻ0.05 as determined by ANOVA followed by Dunnett's test. 5-LOX products are also important for the transcellular biosynthesis of the proresolution lipoxins, which are important mediators of the resolution of inflammation (49). In vitro stimulation of BMDM from 5-LOX Ϫ/Ϫ mice resulted in shift toward the M1 subtype and slightly away from the M2 or rM phenotypes.…”

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confidence: 99%

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Macrophage Polarization during Murine Lyme Borreliosis

2015

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Infection of C3H mice with Borrelia burgdorferi, the causative agent of Lyme disease, reliably produces an infectious arthritis and carditis that peak around 3 weeks postinfection and then spontaneously resolve. Macrophage polarization has been suggested to drive inflammation, the clearance of bacteria, and tissue repair and resolution in a variety of infectious disease models. During Lyme disease it is clear that macrophages are capable of clearing Borrelia spirochetes and exhausted neutrophils; however, the role of macrophage phenotype in disease development or resolution has not been studied. Using classical (NOS2) and alternative (CD206) macrophage subset-specific markers, we determined the phenotype of F4/80 ؉ macrophages within the joints and heart throughout the infection time course. Within the joint, CD206؉ macrophages dominated throughout the course of infection, and NOS2؉ macrophage numbers became elevated only during the peak of inflammation. We also found dual NOS2 ؉ CD206 ؉ macrophages which increased during resolution. In contrast to findings for the ankle joints, numbers of NOS2 ؉ and CD206؉ macrophages in the heart were similar at the peak of inflammation. 5-Lipoxygenase-deficient (5-LOX ؊/؊ ) mice, which display a failure of Lyme arthritis resolution, recruited fewer F4/80 ؉ cells to the infected joints and heart, but macrophage subset populations were unchanged. These results highlight differences in the inflammatory infiltrates during Lyme arthritis and carditis and demonstrate the coexistence of multiple macrophage subsets within a single inflammatory site. Macrophages play a dynamic role in the immune system as both inflammatory and anti-inflammatory mediators. Their phenotype is highly flexible and dependent upon the cytokine stimulus of the microenvironment they infiltrate (1). They are routinely classified as proinflammatory and immunomodulatory (M1) or anti-inflammatory and remodeling (M2) macrophages, but their phenotype actually lies within a spectrum of inflammatory to anti-inflammatory polarization (2). The language within the field is currently being modified to ensure that the macrophages being studied have a clear phenotypic description, and we use the nomenclature recently suggested (3). Within the last 15 years, much work has been done to phenotypically characterize macrophage subsets. Identifying unique surface and intracellular markers, as well as understanding transcriptional regulation, has allowed the importance of specific macrophage phenotypes in infectious and autoimmune models to be uncovered.Classically activated M1 macrophages are proinflammatory cells capable of destroying pathogens, tumor cells, and various foreign compounds. Stimulation of undifferentiated macrophages with lipopolysaccharide (LPS) and gamma interferon (IFN-␥), or tumor necrosis factor alpha (TNF-␣), induces polarization to the M1 phenotype (4, 5). They can be recognized both in vitro and in vivo by the production of nitric oxide species (NOS), as well as other proinflammatory molecules, including ...

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“…Upon analysis of specific macrophage subset marker expression under in vitro M1 (IFN-␥, LPS) and M2 (IL-4) conditions, we noticed some variations. 5 Fig. 4C and D).…”

Section: M1(f4/80mentioning

confidence: 88%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Macrophage Polarization during Murine Lyme Borreliosis

2015

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“…Moreover, resident tissue macrophages are long-lived and may naturally produce low levels of virus. HIV ϩ perivascular macrophages and macrophage-like microglia (39,40) in the brain have been associated with the emergence of antiretroviral drug resistance (41,42) and HIV-associated neurocognitive disorders (HAND) (43,44). HIV ϩ patients may also harbor viral populations in cerebrospinal fluid (CSF) that are genetically distinct from virus in the blood (45)(46)(47)(48)(49)(50) and that exhibit characteristics of macrophage/microglia tropism (51).…”

mentioning

confidence: 99%

HIV DNA Is Frequently Present within Pathologic Tissues Evaluated at Autopsy from Combined Antiretroviral Therapy-Treated Patients with Undetectable Viral Loads

Lamers¹,

Rose²,

Maidji

et al. 2016

J Virol

135

125

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HIV infection treatment strategies have historically defined effectiveness through measuring patient plasma HIV RNA. While combined antiretroviral therapy (cART) can reduce plasma viral load (pVL) to undetectable levels, the degree that HIV is eliminated from other anatomical sites remains unclear. We investigated the HIV DNA levels in 229 varied autopsy tissues from 20 HIV-positive (HIV ؉ ) cART-treated study participants with low or undetectable plasma VL and cerebrospinal fluid (CSF) VL prior to death who were enrolled in the National Neurological AIDS Bank (NNAB) longitudinal study and autopsy cohort. Extensive medical histories were obtained for each participant. Autopsy specimens, including at least six brain and nonbrain tissues per participant, were reviewed by study pathologists. HIV DNA, measured in tissues by quantitative and droplet digital PCR, was identified in 48/87 brain tissues and 82/142 nonbrain tissues at levels >200 HIV copies/million cell equivalents. No participant was found to be completely free of tissue HIV. Parallel sequencing studies from some tissues recovered intact HIV DNA and RNA. Abnormal histological findings were identified in all participants, especially in brain, spleen, lung, lymph node, liver, aorta, and kidney. All brain tissues demonstrated some degree of pathology. Ninety-five percent of participants had some degree of atherosclerosis, and 75% of participants died with cancer. This study assists in characterizing the anatomical locations of HIV, in particular, macrophage-rich tissues, such as the central nervous system (CNS) and testis. Additional studies are needed to determine if the HIV recovered from tissues promotes the pathogenesis of inflammatory diseases, such as HIV-associated neurocognitive disorders, cancer, and atherosclerosis. IMPORTANCEIt is well-known that combined antiretroviral therapy (cART) can reduce plasma HIV to undetectable levels; however, cART cannot completely clear HIV infection. An ongoing question is, "Where is HIV hiding?" A well-studied HIV reservoir is "resting" T cells, which can be isolated from blood products and succumb to cART once activated. Less-studied reservoirs are anatomical tissue samples, which have unknown cART penetration, contain a comparably diverse spectrum of potentially HIV-infected immune cells, and are important since <2% of body lymphocytes actually reside in blood. We examined 229 varied autopsy specimens from 20 HIV ؉ participants who died while on cART and identified that >50% of tissues were HIV infected. Additionally, we identified considerable pathology in participants' tissues, especially in brain, spleen, lung, lymph node, liver, aorta, and kidney. This study substantiates that tissueassociated HIV is present despite cART and can inform future studies into HIV persistence.

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“…HMW HA can reduce bleomycin-induced apoptosis in alveolar epithelial cells from wild type mice and the protective effect was not seen in TLR4 −/− mice (Jiang et al, 2005). Using TLR4-specific small interfering RNA (siRNA), the expressions of matrix metalloprotease 2 (MMP2) and IL-8 induced by HA were blocked (Wallet et al, 2010). Taylor et al (2007) also found that recognition of hyaluronan released in sterile injury involves a unique receptor complex dependent on TLR4, CD44, and MD-2.…”

Section: Discussionmentioning

confidence: 99%

Hyaluronic acid as a rescue therapy for trinitrobenzene sulfonic acid-induced colitis through Cox-2 and PGE2 in a Toll-like receptor 4-dependent way

Chen

Mahaseth

Zhang

2011

J. Zhejiang Univ. Sci. B

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Abstract:We hypothesized whether systemic administration of high-molecular-weight hyaluronic acid (HMW HA) could rescue trinitrobenzene sulfonic acid (TNBS)-induced colitis through Toll-like receptor 4 (TLR4) signal. C3H/HeN mice and C3H/HeJ mice were used. Mice were divided into four groups: control, 50% ethanol treatment group, TNBS treatment group, and TNBS plus HA treatment group. The weight changes, clinical scores, macroscopic scores, and histological scores were recorded. Cyclooxygenase 2 (Cox-2) and prostaglandin E 2 (PGE 2 ) expressions were measured both in colons and peritoneal macrophages from these mice. HA was a rescue therapy for the colitis induced by TNBS only in C3H/HeN mice. The clinical score, macroscopic score, and histological score were much lower in C3H/HeN mice receiving TNBS plus HA treatment. Cox-2 and PGE 2 expressions only increased in C3H/HeN mice. These Cox-2 expressing cells were macrophages. HA can also promote the production of Cox-2 and PGE 2 in peritoneal macrophages from C3H/HeN mice. Our data demonstrated that HMW HA can rescue TNBS-induced colitis through inducing Cox-2 and PGE 2 expressions in a TLR4-dependent way. Macrophages may be the effector cells of HMW HA.

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IFNγ primes macrophages for inflammatory activation by high molecular weight hyaluronan

Cited by 19 publications

References 19 publications

Macrophage Polarization during Murine Lyme Borreliosis

Macrophage Polarization during Murine Lyme Borreliosis

HIV DNA Is Frequently Present within Pathologic Tissues Evaluated at Autopsy from Combined Antiretroviral Therapy-Treated Patients with Undetectable Viral Loads

Hyaluronic acid as a rescue therapy for trinitrobenzene sulfonic acid-induced colitis through Cox-2 and PGE2 in a Toll-like receptor 4-dependent way

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