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Specific Host Restance: The Effector Mechanisms
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Chemotactic factors are substances that attract leukocytes. Under their influence polymorphonuclear leukocytes are induced to adhere to vascular endothelial cells, pass through the spaces between the endothelial cells of the capillaries (extravasation), and move into the inflamed site by moving up the concentration gradient of the factor. The presence of additional leukocytes increases the likelihood of phagocytosis of any parasites present. and 67 are weakly chemotactic; is strongly chemotactic.
Innate and Adaptive Immune Dysfunction and Necrotizing Enterocolitis
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Paula Osterhout, Christina S. Kim, Erika C. Claud
Macrophages are mature in terms of numbers and function by midgestation; however, while adult intestinal macrophages exhibit inflammatory anergy and do not secrete cytokines to induce a local inflammatory response, it has been shown that fetal macrophages do express inflammatory cytokines at levels that developmentally decrease toward term (55). TGFβ2 suppresses this inflammatory cytokine production (55). The migration of macrophages to the site of intestinal injury is regulated by the chemokine CXCL5 found in the epithelial and muscular layers of the intestine, which attracts myeloid cells and is also elevated in immature intestinal tissue (56). In contrast, neutrophils have limited chemotactic ability until post-term (57). Thus, intestinal inflammatory infiltrates in preterm infants have a macrophage predominance.
The Hematologic System and its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Neutrophils protect the body against acute invasion by bacteria and are the most numerous of the leukocytes. When bacteria pause tissue damage, the tissues release chemotactic substances, one of which is leukotaxine (-taxis = movement). These substances diffuse in all
Enhanced healing efficacy of an optimized gabapentin-melittin nanoconjugate gel-loaded formulation in excised wounds of diabetic rats
Published in Drug Delivery, 2022
Hani Z. Asfour, Nabil A. Alhakamy, Osama A. A. Ahmed, Usama A. Fahmy, Shadab Md, Mohamed A. El-Moselhy, Waleed Y. Rizg, Adel F. Alghaith, Basma G. Eid, Ashraf B. Abdel-Naim
Inflammation is considered a nonspecific immune reaction, involving the degeneration of tissue, that usually resolves after infiltrated leukocytes revert to their pre-inflammatory condition. A chemotactic response in leukocytes by inflammatory cytokines enhances the inflammation phase (Henry & Garner, 2003). Therefore, inflammation represents the first phase of wound healing. Our data indicate that treatment GPN–MLT significantly expedited the inflammatory phase as indicated by the reduced expression of IL-6, and TNF-α (Figure 5). Experimentally, GPN anti-inflammatory activity has been previously shown (Abdel-Salam & El-Batran, 2005; Motavallian et al., 2021). On the other side, MLT anti-inflammatory properties have been reported (Park et al., 2007; Kim et al., 2018; Motavallian et al., 2021). In particular, its anti-inflammatory actions in wounded skin have been proven in rats (Alhakamy et al., 2021a, 2021b). MLT antioxidant and anti-inflammatory have been reported to involve modulation of TLR4/TRAF6 mediated NF-κB and p38MAPK pathways (Ahmedy et al., 2020). Similarly, the anti-inflammatory activity of GPN has been attributed to the modulation of NF-κB (Li et al., 2022b). These data give a base for explaining the observed enhancement of the anti-inflammatory effects of the nanoconjugate formula.
Diet-Derived Gallated Catechins Prevent TGF-β-Mediated Epithelial-Mesenchymal Transition, Cell Migration and Vasculogenic Mimicry in Chemosensitive ES-2 Ovarian Cancer Cells
Published in Nutrition and Cancer, 2021
Audrey-Ann Sicard, Tiziana Dao, Narjara Gonzalez Suarez, Borhane Annabi
TGF-β signaling was reported to promote single-cell migration of mammary tumor cells and to contribute to EMT (21, 22). However, it is unclear whether this chemotactic response applies to a chemoresistant phenotype. We thus first assessed the extent of TGF-β-mediated Smad-3 phosphorylation status in serum-starved chemosensitive ES-2 ovarian cancer cells, and compared it to that of chemoresistant SKOV-3 ovarian cancer cells (Fig. 1A). We found that Smad-3 phosphorylation occurred within the first 20 mins, of TGF-β treatment in ES-2 cells, whereas it was undetectable in SKOV-3 cells although TGF-βR1 expression was detected in both cell lines (Fig. 1B). The chemotactic response was further assessed using exposure to various concentrations of TGF-β; the cytokine was found to significantly trigger ES-2 cell migration, whereas SKOV-3 chemotaxis remained low in response to TGF-β (Fig. 1C).
Nanobodies in Human Infections: Prevention, Detection, and Treatment
Published in Immunological Investigations, 2020
Marzieh Sanaei, Neda Setayesh, Zargham Sepehrizadeh, Mehdi Mahdavi, Mohammad Hossein Yazdi
Chemokines or chemotactic cytokines have multiple roles in the immune system organization during infection. A crucial role of chemokines is the different types of leukocyte recruitment from the blood to the inflammation sites. Typical inflammatory chemokines include CCL2, CCL3, CCL5, CXCL1, CXCL2, and CXCL8. They act by binding to chemokine receptors associated with G-proteins. Therefore, antagonizing the chemokine–receptor interaction could be considered as beneficial in inflammation control (Blanchetot et al. 2013). For example, a research was conducted on a nanobody against inflammatory chemokine CXCL10, recently, which directs chemotaxis of Th1 into the central nervous system (CNS) using its receptor CXCR3. This nanobody was able to block the CXCL10-CXCR3 binding, so it has been put forward as a potential therapeutic target in the multiple sclerosis treatment (Sadeghian-Rizi et al. 2019).