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Eosinophil–Epithelial Interactions and Transepithelial Migration
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
Mary K. Schroth, James M. Stark, Julie B. Sedgwick, William W. Busse
Eotaxin is a relatively new C-C chemokine identified in guinea pig lungs following an aerosol allergen challenge (62,63). When injected into the lungs or skin, eotaxin induces the selective recruitment of eosinophils (62,63). High levels of constitutive eotaxin mRNA have been identified in guinea pig lungs and these are increased in response to allergen during the late-phase response (5). Human eotaxin has been identified and cloned; it has the same receptor as RANTES and macrophage chemotactic protein-3 (61). Finally, human eotaxin has recently been identified as an early response gene in cytokine-stimulated epithelial and endothelial cells (158). Stimulation of the epithelial cell line, BEAS-2B, with IL-1β or TNF-α yields a marked increase in eotaxin mRNA.
Analyzing Complex Polygenic Traits
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Bernard R. Lauwerys, Edward K. Wakeland
In another group of modified animals, disruption of pathways that regulate apoptosis in the immune system results in the accumulation of autoreactive T and B lymphocytes and the production of antinuclear antibodies. This phenomenon has been extensively studied in Fas and Fas-Ligand MRL deficient mice that are classical models of SLE. Similarly, bcl-2 transgenic mice produce high levels of anti-dsDNA autoantibodies due to an increased lifespan of autoantibody producing B cells.83 IEX-1 (Immediate Early Response gene X1) transgenic mice display reduced apoptosis rates of activated T cells, resulting in accumulation of effector/memory T cells, splenomegaly, lymphadenopathy, production of IgG2a anti-dsDNA antibodies and proteinuria.84
Photobiomodulation Therapy in Orthopedics
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
Zhang et al. [125] showed that secondary brain injury occurred to a worse degree in mice that had been genetically engineered to lack “Immediate Early Response” gene X-1 (IEX-1) when exposed to a gentle head impact (this injury is thought to closely resemble mild TBI in humans). Exposing IEX-1 knockout mice to PBM 4 hours post injury, suppressed proinflammatory cytokine expression of interleukin (IL)-Iβ and IL-6, but upregulated TNF-α. The lack of IEX-1 decreased ATP production, but exposing the injured brain to PBM elevated ATP production back to near normal levels.
Multiple brain regions are involved in reaction to acute restraint stress in CYLD-knockout mice
Published in Stress, 2023
Yuan-Yuan Han, Jian-Wen Zhou, Zhi-Wei Guo, Zhuo-Qing Wu, Zai-Yong Zhang, De-xiang Liu, Cheng Long
In this study, we explored the impact of environmental challenges on Cyld−/− mice by evaluating whether and how CYLD-knockout mice respond to the acute challenge posed by a single episode of ARS. The elevated plus maze (EPM) test was employed to assess anxious behavior in CYLD-knockout mice following ARS. We also used c-Fos immunochemical staining to characterize activated brain areas in CYLD-knockout mice after ARS. It is upregulated soon after a stimulus is delivered, so c-Fos is known as an early response gene and shows activity-dependent expression; consequently, it has been widely used to identify stimulation-induced neuronal activation (Bullitt, 1990). Our data highlight several new brain regions for studying the role of CYLD in the central nervous system.
Experimental in vivo model to evaluate the impact of Cernitin™ on pain response on induced chronic bladder inflammation
Published in Scandinavian Journal of Urology, 2022
Céline Augé, Nishtman Dizeyi, Lena Ramnemark, Philippe Lluel, Magnus Grabe
Cyclophosphamide-induced BPS in rodents is a well-characterized model [11–13]. Systemic CYP is metabolized in the liver but eliminated primarily through the kidneys. CYP’s major uro-toxic metabolite is acrolein, which causes mucosal inflammation as indicated by microscopic changes in the bladder and the presence of inflammatory cell infiltrations as well as visceral pain [2,14]. This experimental model makes CYP-induced BPS the optimal choice to elucidate mechanisms, identify specific biomarkers related to this chronic condition and subsequently finding effective therapeutic options. A chronic condition, inducing inflammation and tissue damage, can change the properties of sensory pathways leading to a reduction in pain threshold (allodynia) and an amplification of painful sensations (hyperalgesia) [2]. Furthermore, chronic CYP-induced BPS may involve alterations in neurotrophic factors, chemokines [12,15] and cytokines [16]. The presence of pro-inflammatory cytokines can induce cyclooxygenase-2 (COX-2) enzyme, an inflammatory early response gene [17] and generate prostaglandins, a substance that plays a role in the inflammation process. In this study, we hypothesize that CYP-induced BPS upregulates COX-2 [18] and prostanoids [19] in the urinary bladder, which contributes to altered urodynamic function. Cyclooxygenase-2 has also been reported to have a nociceptive (analgesic) effect in both the central and peripheral nervous systems. They show the improvement in bladder function with administration of a specific COX-2 inhibitor [20] suggesting the pivotal role of COX-2 and prostanoids in BPS.
Low-dose ionizing radiation attenuates mast cell migration through suppression of monocyte chemoattractant protein-1 (MCP-1) expression by Nr4a2
Published in International Journal of Radiation Biology, 2019
Chin-Hee Song, Hae Mi Joo, So Hyun Han, Jeong-In Kim, Seon Young Nam, Ji Young Kim
Nr4a2 (Nurr1) is a member of the Nr4A subfamily that includes three nuclear orphan receptors. It is an immediate- or early-response gene that is activated in a ligand-independent manner, and is involved in the regulation of proliferation, apoptosis, and inflammation (Zhao and Bruemmer 2010). It was recently reported that Nr4a2 expression is up-regulated in activated mast cells (Wang et al. 2014). Nr4a2-mediated cell migration has been described in several cell types, including synoviocytes, mesenchymal stromal cells, and colorectal carcinoma cells (Han and Cao 2012; Maijenburg et al. 2012; Mix et al. 2012). We confirmed that Nr4a2 expression was increased in activated mast cells and was inhibited by irradiation (Figure 2(A)). To assess the direct involvement of Nr4a2 on mast cell migration, we performed mast cell migration assays following Nr4a2 knockdown. As shown in Figure 2(B), migration of RBL-2H3 cells was induced following mast cell activation and suppressed following Nr4a2 knockdown. Furthermore, the phosphorylation of both PI3K and Btk was diminished in cells pretreated with Nr4a2 siRNA (Figure 2(C)). These findings indicate that migration-associated signaling pathways are modulated by Nr4a2.