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Research into the efficacy of photobiomodulation therapy (PBMT) in reducing inflammation has been ongoing for years, but standards for irradiation methodology still need to be developed. This study aimed to test whether PBMT stimulates in vitro human peripheral blood mononuclear cells (PBMCs) to synthesize pro-inflammatory cytokines, including chemokines. PBMCs were irradiated with laser radiation at two wavelengths simultaneously (λ = 808 nm in continuous emission and λ = 905 nm in pulsed emission). The laser radiation energy was dosed in one dose as a whole (5 J, 15 J, 20 J) or in a fractionated way (5 J + 15 J and 15 J + 5 J) with a frequency of 500, 1,500 and 2,000 Hz. The surface power densities were 177, 214 and 230 mW/cm 2 , respectively. A pro-inflammatory effect was observed at both the transcript and protein levels for IL-1β after PBMT at the energy doses 5 J and 20 J (ƒ=500 Hz) and only at the transcript level after application of PBMT at energy doses of 20 J (ƒ= 1,500; ƒ=2,000 Hz) and 5 + 15 J (ƒ=500 Hz). An increase in CCL2 and CCL3 mRNA expression was observed after PBMT at 5 + 15 J (ƒ=1,500 Hz) and 15 + 5 J (ƒ=2,000 Hz) and CCL3 concentration after application of an energy dose of 15 J (frequency of 500 Hz). Even though PBMT can induce mRNA synthesis and stimulate PBMCs to produce selected pro-inflammatory cytokines and chemokines, it is necessary to elucidate the impact of the simultaneous emission of two wavelengths on the inflammatory response mechanisms.

Background Gestational diabetes mellitus (GDM) is the most common metabolic complication, which leads to short and long-term consequences in both mother and fetus exposed to hyperglycemia. The aetiology of this condition is proposed to be based on the dysfunction of the adipose tissue, which is characterised by the aberrant generation of adipokines. One of them is preadipocyte factor-1 (Pref-1), which could mediate controlling the adaptation of the maternal metabolism to pregnancy. Aims The study aims to examine the level of Pref-1 in the cord blood of healthy pregnant women’s neonates and fetuses born to mothers with GDM. Materials and methods Cord blood samples were collected from 30 newborns of mothers with GDM and 40 newborns of healthy pregnant women. Pref-1 concentrations were measured with an ELISA kit. Results Fetal Pref-1 concentrations were significantly lower in newborns of mothers with GDM compared to the normal pregnancy group children (5.32 ± 0.29 vs. 7.38 ± 0.53; p  < 0.001). Mothers with GDM had a significantly higher index of BMI before pregnancy, maternal gestational weight gain, and maternal fasting glucose. In-depth analysis through multiple variant linear regression revealed a significant association between fetal serum Pref-1 levels, exposure to GDM, and gestational age. Conclusion These findings contribute valuable insights into maternal-fetal health and pave the way for more targeted and effective clinical interventions. Highlights Fetal Pref-1 concentration was significantly lower in GDM group. Positive correlation between Pref-1 and exposure to GDM and gestational age Pref-1 as one of mediators increased risk of metabolic diseases in late life. Significant impact of intrauterine hyperglycemia on the offspring’s health.

Fungi are ubiquitous organisms that are capable of transient or persistent colonization in humans. Their polymorphic nature and complex host–mycobiome interactions remain incompletely understood. Emerging evidence highlights the role of resident fungi in modulating immune responses and adapting to host changes, which can trigger a shift from commensalism to parasitism, particularly in immunocompromised individuals. This study evaluated the effects of two major β-glucans—zymosan and curdlan—on the expression of pattern recognition receptors (Dectin1, Dectin2, TLR2, TLR4) in human peripheral blood mononuclear cells (PBMCs). It also examined their impact on reactive oxygen species (ROS) production, cytokine/chemokine gene expression, and antioxidant enzyme expression. Both β-glucans significantly increased the mRNA levels of all tested receptors and enhanced ROS generation. Curdlan downregulated key antioxidant enzymes (SOD1, CAT, GPX1), while zymosan markedly upregulated SOD1. These findings demonstrate that the β-glucans zymosan and curdlan have a substantial influence on PBMC reactivity and oxidative stress responses. Further studies are needed to deepen our understanding of host–fungal interactions and their implications in health and disease.

Cathelicidins, like other antimicrobial peptides, exhibit direct antimicrobial activities against a broad spectrum of microbes, including both Gram-positive and Gram-negative bacteria, enveloped viruses, and fungi. These host-derived peptides kill the invaded pathogens by perturbing their cell membranes and can neutralize biological activities of endotoxin. Nowadays, more and more data indicate that these peptides, in addition to their antimicrobial properties, possess various immunomodulatory activities. Cathelicidins have the potential to influence and modulate, both directly and indirectly, the activity of various cell populations involved in inflammatory processes and in host defense against invading pathogens. They induce migration of neutrophils, monocytes/macrophages, eosinophils, and mast cells and prolong the lifespan of neutrophils. These peptides directly activate inflammatory cells to production and release of different pro-inflammatory and immunoregulatory mediators, cytokines, and chemokines, however cathelicidins might mediate the generation of anti-inflammatory cytokines as well. Cathelicidins also modulate epithelial cell/keratinocyte responses to infecting pathogens. What is more, they affect activity of monocytes, dendritic cells, keratinocytes, or epithelial cells acting in synergy with cytokines or -defensins. In addition, these peptides indirectly balance TLR-mediated responses of monocytes, macrophages, dendritic cells, epithelial cells, and keratinocytes. This review discusses the role and significance of cathelicidins in inflammation and innate immunity against pathogens.

Damaged cells release endogenous molecules known as alarmins into the extracellular space following cellular injury. Alarmins may function as adjuvants by interacting with PRRs to indicate danger and initiate a localized sterile inflammatory response, which facilitates tissue regeneration. A pivotal alarmin is HMGB1, which is internalized through the RAGE to notify adjacent cells about compromised homeostasis. Given the significant role of mast cells (MCs) in inflammatory processes and the critical nature of alarmins as indicators of danger, this study evaluates the hypothesis that MCs serve as essential sensors of cellular injury. The present study investigates whether HMGB1 affects the expression levels of specific PRRs in mature MCs. These receptors include Dectin-1 and Dectin-2, TLR2, NOD1, and RIG-I. Furthermore, this study aims to determine whether HMGB1 modulates the inflammatory response of these cells, which encompasses the production of cytokines, chemokines, ROS, histamine, and cysLTs, as well as their migration patterns. Moreover, the research aims to investigate the role of RAGE and the involvement of signaling molecules in the activation of MCs mediated by HMGB1. All experiments were carried out using differentiated, mature tissue MCs freshly isolated from the rat peritoneal cavity. The potency of HMGB1 to provoke MC PRR expression, generation, and/or release of a panel of mediators and migration was investigated. HMGB1 markedly enhances the expression of Dectin-1, RIG-I, and NOD1, while simultaneously stimulating MCs to produce CCL3, IL-1β, TNF, cysLTs, histamine, and ROS. This protein acts as a potent chemoattractant for MCs. The administration of RAGE antagonist to MCs significantly attenuated the generation of mediators and the migratory response, thereby confirming the receptor's involvement in the response of HMGB1-treated cells. Intracellular signaling in MCs activated by HMGB1 involves ERK1/2, p38 MAPK, PI3K, NF-κB, and, in part, JAK2. The data robustly support the notion that HMGB1 is an important endogenous alarmin that promotes and enhances MC activity in inflammatory processes. These insights highlight HMGB1 as a potential therapeutic target for regulating MC-driven inflammatory disorders, which encompass allergy, autoimmune diseases, and chronic conditions.

Background Our study aimed to assess the level of IL-1β, CXCL8, and TNF-α in peri-implant sulcular fluid (PISF) collected from patients with no clinical symptoms of mucositis or peri-implantitis and compare them with cytokine concentration in gingival crevicular fluid (GCF) acquired from patients with healthy periodontium and those with varying severity of periodontitis. Methods A total of 189 subjects were included in the study, and GCF/PISF samples were checked for IL-1β, CXCL8, and TNF-α levels using an ELISA test. Results The IL-1β level in PISF in patients with implants was significantly lower than in GCF in patients with mild, moderate, or severe periodontitis. The CXCL8 level in PISF was considerably lower than in patients with moderate periodontitis. The TNF-α level in PISF in patients with implants was markedly higher compared to subjects with healthy periodontium or patients with mild periodontitis. Conclusion Analysis of cytokine levels may help describe the pathogenesis and early diagnosis of peri-implantitis and prevision in high-risk patients.

Undoubtedly, mast cells take part in host defense against microorganisms as they are numerous at the portal of infection, they release many proinflammatory and antimicrobial mediators, and they express pattern recognition receptors, such as TLRs. These receptors play a key role in recognition and binding molecules associated with microorganisms and molecules associated with damage. Cathelicidins exhibit direct antimicrobial activities against a broad spectrum of microbes by perturbing their cell membranes. Accumulating evidence suggests a role for these molecules in supporting cell activation. We examined the impact of human cathelicidin LL-37 on tissue mast cell TLR expression and distribution. Depending on context, we show that LL-37 stimulation resulted in minor to major effects on TLR2, TLR3, TLR4, TLR5, TLR7, and TLR9 expression. Confocal microscopy analysis showed that, upon stimulation, TLRs may translocate from the cell interior to the surface and conversely. FPR2 and EGFR inhibitors reduced the increase in expression of selected receptors. We also established that LL-37 acts as a powerful inducer of CCL3 and ROS generation. These results showed that in response to LL-37, mast cells enhance the capability to detect invading pathogens by modulation of TLR expression in what may be involved FPR2 or EGFR molecules.

Mast cells (MCs) are found mainly at the anatomical sites exposed to the external environment; thus, they are localized close to blood vessels, lymphatic vessels, and a multitude of immune cells. Moreover, those cells can recognize invading pathogens through a range of surface molecules known as pathogen recognition receptors (PRRs), mainly Toll-like receptors (TLRs). MCs are extensively engaged in the control and clearance of bacterial infections, but much less is known about their contribution to antiviral host response as well as pathomechanisms of virus-induced diseases. In the study, we employed in vivo differentiated mature tissue mast cells freshly isolated from rat peritoneal cavity. Here, we demonstrated that rat peritoneal mast cells (rPMCs) express viral dsRNA-specific TLR3 molecule (intracellularly and on the cell surface) as well as other proteins associated with cellular antiviral response: IRF3, type I and II IFN receptors, and MHC I. We found that exposure of rPMCs to viral dsRNA mimic, i.e., poly(I:C), induced transient upregulation of surface TLR3 (while temporarily decreased TLR3 intracellular expression), type II IFN receptor, and MHC I. TLR3 ligand-stimulated rPMCs did not degranulate but generated and/or released type I IFNs (IFN-α and IFNβ) as well as proinflammatory lipid mediators (cysLTs), cytokines (TNF, IL-1β), and chemokines (CCL3, CXCL8). We documented that rPMC priming with poly(I:C) did not affect FcεRI-dependent degranulation. However, their costimulation with TLR3 agonist and anti-IgE led to a significant increase in cysLT and TNF secretion. Our findings confirm that MCs may serve as active participants in the antiviral immune response. Presented data on modulated FcεRI-mediated MC secretion of mediators upon poly(I:C) treatment suggests that dsRNA-type virus infection could influence the severity of allergic reactions.

Mast cells (MCs) play an essential role in host defense, primarily because of their location, their ability to pathogen destruction via several mechanisms, and the pattern recognition receptors they express. Even though most data is available regarding MC activation by various bacteria- or virus-derived molecules, those cells’ activity in response to constituents associated with fungi is not recognized enough. Our research aimed to address whether Saccharomyces cerevisiae-derived zymosan, i.e., β-(1,3)-glucan containing mannan particles, impacts MC activity aspects. Overall, the obtained results indicate that zymosan has the potential to elicit a pro-inflammatory response of rat peritoneal MCs. For the first time ever, we provided evidence that zymosan induces fully mature MC migration, even in the absence of extracellular matrix (ECM) proteins. Moreover, the zymosan-induced migratory response of MCs is almost entirely a result of directional migration, i.e., chemotaxis. We found that zymosan stimulates MCs to degranulate and generate lipid mediators (cysLTs), cytokines (IFN-α, IFN-β, IFN-γ, GM-CSF, TNF), and chemokine (CCL2). Zymosan also upregulated mRNA transcripts for several cytokines/chemokines with pro-inflammatory/immunoregulatory activity. Moreover, we documented that zymosan activates MCs to produce reactive oxygen species (ROS). Lastly, we established that the zymosan-induced MC response is mediated through activation of the Dectin-1 receptor. In general, our results strongly support the notion that MCs contribute to innate antifungal immunity and bring us closer to elucidate their role in host-pathogenic fungi interactions. Besides, provided findings on IgE-sensitized MCs appear to indicate that exposure to fungal zymosan could affect the severity of IgE-dependent disorders, including allergic ones.

Objective The aim of this study was to determine whether leptin, a member of the adipocytokines involved in immune and inflammatory response regulation, may influence some aspects of mast cell biology. Materials and methods Experiments were done in vitro on fully mature tissue rat mast cells isolated from the peritoneal cavity, and leptin was used at concentrations 0.001–100 ng/ml. The effect of leptin on mast cell degranulation (histamine release assay), intracellular Ca 2+ level (fluorimetry), pro-inflammatory mediator release (ELISA technique), surface receptor expression (flow cytometry and confocal microscopy), and migration (Boyden microchamber assay) was estimated. Results Leptin was found to stimulate mast cells to degranulation and histamine release. It induced the intracellular Ca 2+ increase, as well. In response to leptin stimulation, mast cells generated and released cysLTs and chemokine CCL3. Leptin-induced upregulation of CYSLTR1 and CYSLTR2 surface expression was observed. Moreover, this adipocytokine stimulated mast cells to migratory response, even in the absence of extracellular matrix (ECM) proteins. Conclusions Our observations clearly documented that leptin promotes the pro-inflammatory activity of mast cells, and it thereby engages these cells in the inflammatory processes.