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The immune response to fungal challenge
Published in Mahmoud A. Ghannoum, John R. Perfect, Antifungal Therapy, 2019
Jeffery Hu, Jeffery J. Auletta
Like cytokines, chemokines have critical roles in immune cell activation and recruitment in the context of fungal infection [118] and inflammation [119]. For example, macrophage inflammatory protein-1 alpha (MIP-1α)/CCL3 and monocyte chemoattractant protein-1 (MCP-1)/CCL2 mediate phagocyte recruitment to sites of infection [120]. Likewise, chemokines such as Epstein-Barr I1 ligand chemokine (ELC)/CCL19 and secondary lymphoid-tissue chemokine (SLC)/CCL21 form gradients to facilitate DC trafficking and antigen presentation within secondary lymph nodes and link innate and adaptive responses [121]. Cytokines, like TNF-α, can also induce chemokine production from immune cells, further driving effector cell recruitment to sites of infection and inflammation [122]. Finally, chemokines like thymus and activation-regulated chemokine (TARC)/CCL17 directly modulate antifungal responses [123].
Inflammation and spermatogenesis
Published in C. Yan Cheng, Spermatogenesis, 2018
Maria Susana Theas, Patricia Verónica Jacobo, Cecilia Valeria Pérez, Vanesa Anabella Guazzone, Livia Lustig
Macrophages also play the role of antigen-presenting cells and release inflammatory cytokines and chemokines that contribute to EAO development. In fact, in vivo depletion of these cells with clodronate-containing liposomes in rats undergoing EAO decreased incidence and severity of testicular damage. Testicular macrophage population is heterogeneous; it includes resident macrophages (ED2+ cells), inflammatory monocytes recently arrived from circulation (ED1+ cells), and double-positive (ED1+ ED2+) subpopulation, the major contributor to the macrophage number increase in EAO.46 Inflammatory chemokines CCL2, CCL3, and CCL4 regulate macrophage recruitment within the interstitium via CCR2, CCR1, and CCR5 receptors.47–49
Cell Recruitment for Intervertebral Disc
Published in Raquel M. Gonçalves, Mário Adolfo Barbosa, Gene and Cell Delivery for Intervertebral Disc Degeneration, 2018
Catarina Leite Pereira, Sibylle Grad, Mário Adolfo Barbosa, Raquel M. Gonçalves
CCL3, also known as macrophage inflammatory protein (MIP)-1α, was shown to be upregulated in NP cells isolated from rat and human IVD tissue following treatment with IL-1β or TNF-α. In the same study, CCL3 expression in human samples was shown to be correlated with the grade of tissue degeneration (Wang et al. 2013). This molecule induced macrophage migration after treatment with NP cells conditioned media (previously treated with IL-1β or TNF-α); migration was suggested to occur via CCR1, the primary receptor of CCL3, since its inhibition resulted in cell migration blockage (Wang et al. 2013). CCL2 and CCL3 gene expression were shown to be significantly up-regulated in both human AF and NP cells after treatment with IL-1β (Liu et al. 2017b; Wang et al. 2013). Additionally, some of those chemokines, such as CCL2, CCL7, and CXCL18, have been correlated with histological degenerative tissue changes (Phillips et al. 2013) and are known to be involved in the recruitment of immune cells to inflammatory sites (Luster 1998).
Persistent changes in expression of genes involved in inflammation and fibrosis in the lungs of rats exposed to airborne lunar dust
Published in Inhalation Toxicology, 2023
Ye Zhang, Michael Story, Samrawit Yeshitla, Xiaoyu Wang, Robert R. Scully, Corey Theriot, Honglu Wu, Valerie E. Ryder, Chiu-wing Lam
Expression of the chemokine genes Ccl3, Ccl12, and Cxcl2 was closely correlated with total cell number in the BALF, and even more closely correlated with neutrophil number, especially in the samples collected 13 wk after the LD exposure. The correlation test results were presented in the Supplemental Data Table 7. As an example, the correlation of Ccl3 expression levels to neutrophil numbers (within the control, 20.8 and 60.6 mg/m3 groups) was 0.89 (p < 0.00001) and for macrophages it was 0.36 (p = 0.186) 13 wk after exposure to LD. The overall correlations of Ccl3 expression to neutrophil and macrophage numbers are presented in Figure 6(B). These results suggest that this chemokine might have played a role in recruitment of these cells into the lung in response to LD exposure. In addition, the expression of Cxcl2 was consistent with the dose- and time-dependent increases in oxidative contents of the lavage BAL cells from LD-exposed rats, as assessed by the magnitude of chemiluminescent signal production (Figure 6(C)).
Role of necroptosis of alveolar macrophages in acute lung inflammation of mice exposed to titanium dioxide nanoparticles
Published in Nanotoxicology, 2021
Tomoya Sagawa, Akiko Honda, Raga Ishikawa, Natsuko Miyasaka, Megumi Nagao, Sakiko Akaji, Takashi Kida, Takahiro Tsujikawa, Tatsushi Yoshida, Yutaka Kawahito, Hirohisa Takano
CCL3 is a chemokine secreted by immune cells such as macrophages (Ramos et al. 2005; Reichel et al. 2012) and has been reported to cause leukocyte migration to the lungs in infectious pathogens- and bleomycin-induced pulmonary disease models (Zeng et al. 2003; Bonville et al. 2006; Ishida et al. 2007). Additionally, secretion of CCL3 is increased by TiO2 nanoparticles and CCL3 is one of the important mediators of TiO2-induced lung inflammation (Chen et al. 2006; Numano et al. 2014). Although we found that necroptosis affects the secretion of CCL3 by AMs, other mediators were not exhaustively investigated. However, as indicated by the study showing that CCL3 is involved in promoting TiO2-induced lung carcinogenesis (Xu et al. 2010), CCL3 is an important mediator of the toxicity of TiO2 nanoparticles. The involvement of necroptosis of AMs in regulating CCL3 secretion is an important finding for understanding the properties of TiO2 nanoparticles.
CCL3 augments tumor rejection and enhances CD8+ T cell infiltration through NK and CD103+ dendritic cell recruitment via IFNγ
Published in OncoImmunology, 2018
Frederick Allen, Iuliana D. Bobanga, Peter Rauhe, Deborah Barkauskas, Nathan Teich, Caryn Tong, Jay Myers, Alex Y. Huang
Although our study focuses exclusively on CCL3 which showed a pronounced effect on CT26 rejection in vivo, similar contribution to tumor rejection has been ascribed to CCL4 in melanoma.4 Indeed, CCL4-secreting CT26 (L4TU) also resulted in a significant production of IFNγ at the tumor site compared to WTTU (Supplemental Fig. S5). However, compared to L4TU, L3TU resulted in a more rapid rejection (data not shown). Future studies will exam the mechanisms of s.c. administered CCL3 in mobilizing marrow-derived immune cells to facilitate tumor rejection. Taken together, our current data further support the exploration of CCL3 as an adjuvant for enhancing antitumor immune response.