Treating Depression with Exercise
Henning Budde, Mirko Wegner in The Exercise Effect on Mental Health, 2018
Exercise-induced cellular neuroimmune factors also include increased CD11b and CD66b enhanced gene expression from peripheral blood mononuclear cells (i.e. IL-5, IL-8, IL-2), increased regulatory T cells (Tregs) and increased CD14+, CD16+ monocytes (Timmerman, Flynn, Coen, Markofski, & Pence 2008; Coen, Flynn, Markofski, Pence, & Hannemann 2010; Wang et al. 2012; Stewart et al. 2005). Exercise has also shown to increase, in parallel to IL-10, the levels of chemokine (C-X-C motif) ligand 1 (CXCL1), CXCL12, and systemic macrophage-released MAPK phosphatise-1 (MKP-1) in rodent brain tissues (Parachikova et al. 2008). CXCL1 is considered to be a neuroprotective biomolecule, and the up-regulation of CXCL12 is known to exert several enhancing effects on: (1) glutamate release from astrocytes, hence regulating neuronal excitability, (2) signal propagation within glial networks, and (3) synaptic transmission; while MKP-1 negatively regulates pro-inflammatory macrophages activation. Finally, exercise also increases hippocampal T cells population due to C-C chemokine receptor type 2 (CCR2), a microglial chemoattractant factor (Parachikova et al. 2008). T cells are responsible for neuroregeneration and modulation of microglia. These effects are associated with other benefits such as a decrease in pro-inflammatory visceral white fat mass (Esposito et al. 2003; Petersen et al. 2005; Donges et al. 2010). Thus, it could be concluded that the better mental well-being experienced by individuals who regularly exercise might be partly explained by IL-6-induced anti-inflammatory mechanisms.
The S100A7/8/9 Proteins: Novel Biomarker and Therapeutic Targets for Solid Tumor Stroma
Surinder K. Batra, Moorthy P. Ponnusamy in Gene Regulation and Therapeutics for Cancer, 2021
The overexpression of S100A8/A9 has also been appreciated in lung cancer. Recently, higher expression of S100A8 and S100A9 was reported in 71.2% and 76.9% non-small cell lung cancer patient samples, respectively, in comparison to adjacent normal [98]. The higher expression of S100A8/A9 was also associated with degree of tumor differentiation [98]. S100A8/A9 plays a crucial role in the formation of pre-metastatic niche. Tumor secreted factors (TSFs) such as VEGF-A, TGF-β and TNF-α may induce expression of S100A8/A9 in pre-metastatic endothelial cells and macrophages [65]. S100A8/A9 secreted by lung stromal cells promotes recruitment of CD11b+ myeloid cells to establish a pre-metastatic niche in the lungs, to which tumor cells migrate [65]. Subsequently, it was shown that S100A8 induces the expression of serum amyloid A 3 (SAA3) in pre-metastatic lungs, followed by activation of NF-κβ signaling, resulting in accumulation of CD11b+ myeloid cells [99]. In addition, S100A8/A9 can also induce the expression of CXCL1 in pre-metastatic lungs, which has been shown to attract tumor cells [68]. The role of S100A8/A9 in pre-metastatic niche formation has been summarized in Fig. 2.
Immunology
M. Alan Menter, Caitriona Ryan in Psoriasis, 2017
As a first line of defense against an immune attack, neutrophils have many intracellular antimicrobial peptides. In psoriatic skin, the presence of neutrophils in the epidermis and the formation of Munro,s microabscesses are histological hallmarks of psoriasis. There is also an abundant expression of neutrophil chemokines, such as CXCL1, CXCL2, and CXCL8/IL-8, in psoriatic skin. However, neutrophils are inconsistently found in chronic psoriatic lesions and are absent from some mouse models of psoriasis.2 Neutrophils have been also suggested as a source of IL-17, potentially having another role in psoriasis pathophysiology.34 It has been suggested that a neutrophil–keratinocyte cross talk is an early target of IL-17 inhibitory treatment for psoriasis.35 However, it is unclear whether cutaneous neutrophils in psoriatic skin synthesize new IL-17 or if neutrophils containing preformed IL-17 are entering the skin.
Age-associated Ligand-receptor Interactions Imputed from Nasopharyngeal Transcriptomes of COVID-19 Patients
Published in Immunological Investigations, 2022
A recent study of immune cell composition in bronchoalveolar lavage fluid has shown increased expression of pro-inflammatory immune cells expressing more CCR1 and CXCR2 receptors in severe COVID-19 cases (Liao et al. 2020). Indeed, the present study has also shown increased interactions with these receptors in older patients between the NP-M interactions (Figure 1A). Interactions with these receptors were also increased within the microenvironment (M-M) in older patients (Figure 2A). CXCR2 signaling is also a chemokine axis that regulates neutrophil release form the bone marrow (Eash et al. 2010). This is further supported by the increased relative proportions of neutrophils in older patients suggested from computational gene expression deconvolution (Figure 3). Furthermore, CXCL1 and CXCL6 ligands were also shown to be involved in these interactions. CXCL1 secretion has been associated with pro-inflammatory immune cell infiltration (Susek et al. 2018). Formyl peptide receptor 2 (FPR2) interaction with amyloid precursor protein (APP) was also higher in older patients and is implicated in regulating the activation of inflammatory cells (Park et al. 2019). Some notable M-M interactions included SELL receptor interactions with complement factor H (CFH), PODXL2, and CD34, which were decreased relative to the younger patient cohort (Figure 2A). CFH participates in regulation of complement activation (Rodríguez de Córdoba et al. 2004).
The temporal pattern of immune and inflammatory proteins prior to a recurrent coronary event in post-acute coronary syndrome patients
Published in Biomarkers, 2019
Maxime M. Vroegindewey, Rohit M. Oemrawsingh, Isabella Kardys, Folkert W. Asselbergs, Pim van der Harst, Anton J. Oude Ophuis, G. Etienne Cramer, Arthur Maas, S. Hong Kie The, Alexander J. Wardeh, Henk Mouthaan, Eric Boersma, K. Martijn Akkerhuis
CXCL1 is a cytokine that attracts neutrophils by chemotaxis and stimulates monocyte arrest (Dusi et al.2016). Oxidized LDL and wall shear stress on endothelial cells have been shown to induce the expression of CXCL1 (Hagiwara et al.1998, Zhou et al.2011). Subsequently, CXCL1 stimulates monocyte adhesion to the endothelial wall (Breland et al.2008, Papadopoulou et al.2008). These monocytes migrate into the endothelial wall and stimulate the accumulation of macrophages. Eventually, this process promotes atherosclerotic plaque formation and instability and is therefore a key process in pathological atherosclerosis. Since we found higher serum levels of CXCL1 in early cases, a possible mechanism may be that CXCL1 is upregulated due to the index ACS, but subsequently also promotes early recurrent events by inducing atherosclerotic plaque instability.
Lactobacillus fermentum species ameliorate dextran sulfate sodium-induced colitis by regulating the immune response and altering gut microbiota
Published in Gut Microbes, 2019
You Jin Jang, Woon-Ki Kim, Dae Hee Han, Kiuk Lee, Gwangpyo Ko
Furthermore, the L. fermentum KBL374 and KBL375 treatments reduced the innate immune response, which agrees with a previous study.43 Changes in MPO levels reflect the degree of neutrophil infiltration and tissue damage in the colon. TNF and CCL2, which are a key pro-inflammatory cytokine and chemokine, respectively, are primarily produced by monocytes and macrophages. Moreover, TNF-ɑ is an activator of nuclear factor-κB, which further promotes the secretion of TNF and upregulates other pro-inflammatory cytokines, such as IL-1β and IL-6.44–47 CXCL1 is a chemokine with dual roles in recruiting and activating neutrophils.48 Overall, the colons of the L. fermentum KBL374- and KBL375-treated DSS mice contained reduced levels of these inflammatory markers (Figure 3).
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