Probiotics
Jay R Hoffman in Dietary Supplementation in Sport and Exercise, 2019
Several investigations have indicated that probiotic supplementation may have an important role in exercise recovery. The cytokine response to intense training is often used as an indicator of recovery from high-intensity training (35). Previous studies have demonstrated that probiotic supplementation provides a modulatory effect on both pro- and anti-inflammatory cytokines (25, 29). Carbuhn and colleagues (4) reported enhanced recovery in National Collegiate Athletic Association (NCAA) division 1 female swimmers consuming Bifidobacterium longum 35624 during six weeks of training. These improvements were reflected by a reduction in URTI and enhanced immune function in swimmers consuming the probiotic compared to placebo. Significant increases of interleukin-1 receptor antagonist (IL-1ra) concentrations were also reported in the probiotic group. IL-1ra is an anti-inflammatory cytokine and a natural antagonist to interleukin 1 beta (IL-1β; a pro-inflammatory cytokine) (3).
Cervicogenic Headache
Gary W. Jay in Clinician’s Guide to Chronic Headache and Facial Pain, 2016
Cytokine patterns in CeH patients, like those seen in cluster headache, tend toward an inflammatory status. Interleukin-1 beta (IL-1ß) and tumor necrosis factor-alpha (TNF-a) exert multifunctional biological effects by promoting and increasing the molecular events of cellular inflammation. Higher levels of both IL-1ß and TNF-a were detected in the sera of 15 CeH subjects, both during the natural course of a painful attack and during a phase of mechanically worsened pain, than in that of 15 subjects with migraine without aura during or outside an attack and 15 historically healthy controls. Differences also emerged in CeH between spontaneous and mechanically worsened pain phases (49,50). Although the role of these pro-inflammatory cytokines remains unknown, both IL-1ß and TNF-a may promote hyperalgesia in CeH. While not relevant in clinical laboratory testing, this discovery may lead to a potential therapeutic treatment modality (35).
Genetically Modified Salmonella as Cancer Therapeutics: Mechanisms, Advances, and Challenges
Ananda M. Chakrabarty, Arsénio M. Fialho in Microbial Infections and Cancer Therapy, 2019
Salmonella has an indirect killing impact on tumor cells, which is aided by cooperation with the host’s immune system through recruitment of inflammatory immune cells and cytokines. Lee et al. compared the anticancer activities of Salmonella in wildtype mice and toll-like receptor 4 (TLR4)-deficient mice and found that TLR4 played an important role in Salmonella-induced tumor inhibition [14]. This was later confirmed by Kaimala and colleagues’ work demonstrating that the anticancer capacity of Salmonella relied mostly on the induction of innate immune responses through the TLR-MyD88 signaling pathway [15]. The activation of TLR serves as a priming signal required for the activation of NLRP3 inflammasome. Phan and colleagues reported that Salmonella activated inflammasome pathways, resulting in a marked increase of IL-β in a Salmonella-colonized tumor [16]. Interleukin-1 beta (IL-1β), produced by the infiltrated dendritic cells, played an important role in Salmonella-mediated cancer therapy [17]. Depletion of IL-1β using neutralizing antibodies abrogated the anticancer effects of Salmonella. A similar result was also observed in our study. Three VNP20009 mutants with unchanged tumor targeting ability induced far less IL-1p in tumors and displayed reduced anticancer capacities [18].
Higher perceived stress is associated with lower cortisol concentrations but higher salivary interleukin-1beta in socially evaluated cold pressor test
Published in Stress, 2020
Katarina Buzgoova, Lucia Balagova, Martin Marko, Daniela Kapsdorfer, Igor Riecansky, Daniela Jezova
The release of interleukins is an important component of the response to short-term acute stressors. For example, plasma interleukin-6 is known to respond to acute psychosocial stressors in humans (Quinn, Williams, Sivilli, Raison, & Pace, 2018). Findings on interleukin-1beta are scarce and less consistent. Only few studies evaluating interleukin-1beta in the blood showed a rapid increase in response to psychosocial stressors (Heinz et al., 2003; Yamakawa et al., 2009). Noninvasive measurements of salivary interleukin-1beta showed increased values 10 min (Mastrolonardo, Alicino, Zefferino, Pasquini, & Picardi, 2007) or 40 min (Newton et al., 2017) after the end of a mental stressor. To our knowledge, no data are available on interleukin-1beta in response to socially evaluated CPT.
Role of angiotensin II type 1 (AT1) and type 2 (AT2) receptors in airway reactivity and inflammation in an allergic mouse model of asthma
Published in Immunopharmacology and Immunotoxicology, 2019
Mehaben Patel, Mangesh Kurade, Sahith Rajalingam, Riya Bhavsar, S. Jamal Mustafa, Dovenia S. Ponnoth
Asthma is a chronic lung disease characterized by airway hypersensitivity, inflammation and difficulty in breathing. The renin–angiotensin system (RAS) plays a key role in the regulation of homeostasis and fluid balance [1]. Angiotensin II (Ang II), an effector octa-peptide of RAS, is a potent vasoconstrictor of vascular smooth muscle and causes increased blood pressure, inflammation, and vascular remodeling [2–4]. Ang II exerts its effect by binding to two GPCRs: angiotensin type 1 (AT1) and type 2 (AT2) receptors [5]. Several reports indicate the involvement of AT1 receptors in inflammation. Studies have shown that a number of inflammatory molecules, such as interleukin-1 beta (IL-1β), are induced via AT1 receptors [6]. Ang II stimulation of the AT1 receptor-subtype is known to increase the production of prostaglandins and TLR-4 expression, which initiate the inflammatory response and oxidative injury, as well as exerts its major cardiovascular effects like vasoconstriction [7–9].
Nutraceuticals-based therapeutic approach: recent advances to combat pathogenesis of Alzheimer’s disease
Published in Expert Review of Neurotherapeutics, 2021
Marjan Talebi, Eleni Kakouri, Mohsen Talebi, Petros A. Tarantilis, Tahereh Farkhondeh, Selen İlgün, Ali Mohammad Pourbagher-Shahri, Saeed Samarghandian
Curcumin interferes with Aβ synthesis and τau phosphorylation. In in vitro and in vivo experiments curcumin downregulated early growth response factor 1 (Egr1) in THP-1 monocytic cells by reducing expression of cytokines, extracellular signal-regulated kinase ERK 1/2, and CCR5, a protein implicated in the inflammation process [138]. Furthermore, τau phosphorylation was successfully decreased in 3xTg-AD mice by targeting cyclin-dependent protein kinase 5 (CDK5) and BACE1 activity afterward the Egr-1 silencing [139]. Oxidative and inflammatory damage sequelae on APPSw transgenic mice were addressed with curcumin. The authors examined the role of the compound in inhibiting interleukin 1 beta (IL-1β), a cytokine that mediates inflammation, and showed that in treated animals significantly reduced levels of the cytokine respect to the control group. In addition to this, lower levels of glial fibrillary acidic protein (GFAP), which is overexpressed in the astrocytes of an AD patient, and quantitative changes in the planum temporal area (PT) were observed. Furthermore, Aβ accumulation either soluble or insoluble was reduced, however, the reduction of the insoluble fraction was not APP related [140–142]. Curcumin inhibited inducible nitric oxide synthase (iNOS) expression, cyclooxygenase-2 (COX-2), prostaglandin E-2 (PGE-2), and nitric oxide (NO). Curcumin also inhibited NF-kB transcription factor [143,144].