Search

Background: Using genetic enhancement techniques has led to the development of poultry capable of fulfilling significant portions of human dietary requirements through meat and egg production. Maximizing genetic potential necessitates the provision of conducive environmental conditions. Heat stress poses a substantial challenge within the poultry sector, detrimentally impacting poultry production and growth, there by diminishing breeders' economic returns. Adaptation to heat stress is contingent upon a multitude of factors. The capacity to establish homeostasis through alterations in gene expression serves to mitigate extracellular damage and restore physiological equilibrium upon reversion to favorable temperature ranges. Domestic birds thrive within a temperature spectrum of 18-24 °C, with any deviation beyond this range precipitating elevated mortality rates. Elevated mortality is attributed to heat-induced suppression of the immune system and compromised resilience. Moreover, heat stress amplifies the secretion of the corticotropin-releasing hormone, subsequently elevating blood corticosterone levels, thereby instigating molecular alterations under stress conditions. Hence, a comprehensive examination of this challenge from diverse perspectives holds significant promise. Consequently, the present study endeavors to delineate protein complexes and pivotal signaling pathways regulated by distinct genes expressed in response to heat stress within the hypothalamus of broiler chickens. Methods: The systemic response of chickens' hypothalamus transcripts to heat stress was comprehensively examined in this investigation. Transcript expression profiles from eight chicken hypothalamus tissues, including four subjected to thermal stress and four under non-stress conditions, were retrieved from the GEO database (accession number GSE37400). The raw microarray data underwent rigorous quality control measures and normalization using GEO2R software to ensure reliability and consistency. Genes with discernible expression changes were identified based on a stringent criterion of P-value > 0.05 and (LogFC < 0.5-0.5). Subsequently, a gene expression regulatory network was constructed to elucidate the interplay among genes implicated in broiler heat stress, employing Cytoscape software in conjunction with the STRING database. The network visualization facilitated the identification of protein clusters, representing areas of high density, which were further analyzed using the CytoCluster plugin renowned for its efficacy in detecting such densely interconnected regions. Following the delineation and characterization of genes within these clusters, the DAVID database was utilized to elucidate the relevant biological pathways associated with the identified genes. This comprehensive approach enabled a detailed exploration of the molecular mechanisms underlying the hypothalamic response to heat stress in chickens. Results: The analysis of microarray data unveiled a comprehensive portrait of the molecular response to heat stress in chickens. Among the 43,607 initially examined probes, 593 differentially expressed genes were identified after rigorous curation involving the elimination of duplicate genes and application of a significance threshold. A network encompassing 149 genes with a minimum interaction score of 0.4 was constructed utilizing the STRING software, shedding light on the intricate interplay among these genes. Subsequent investigations honed in on genes exerting significant regulatory effects in response to heat stress, elucidating their pivotal roles in orchestrating physiological processes. Functional assessment of the networked genes revealed their involvement in diverse biological activities, including the positive regulation of T cell- mediated immunity, WNT and MAPK signaling pathways, as well as phagocytosis and natural killer (NK) cell activity. Particularly noteworthy was the observation of suppressed NK cell activity in broilers under heat stress, likely influenced by heightened corticosterone levels and subsequent inhibition of thyroid hormone secretion, thereby impacting temperature regulation and metabolism. Moreover, the elevation in blood glucose levels observed in stressed chicks may contribute to their adaptive survival response. Importantly, heat stress was observed to disrupt cellular homeostasis and molecular pathways, manifesting in alterations in biological processes such as the cell cycle. This disruption in the cell cycle may signify a novel mechanism of stress resistance in vertebrates, further underscoring the complexity of the physiological response to thermal stress in chickens. Conclusion: The analysis of gene functionality within the network underscores the intricate nature of the innate immune response and cellular demise elicited by heat stress. Notably, certain genes identified in this analysis participate in positively regulating T cell-mediated immunity, vascular endothelial growth factor (VEGF), WNT signaling, and mitogen-activated protein kinase (MAPK) pathways. Introducing a biomarker panel comprising genes, such as MAPK14, NT3, SOX2, YAP1, FGF2, LRRK1, LEF1, and TLE1, holds promise for advancing our understanding of the underlying molecular mechanisms governing stress responses in poultry. Furthermore, this approach may facilitate the discovery of novel genes whose modulation could mitigate the effects of thermal stress. [ABSTRACT FROM AUTHOR]

Background and Aim Fennel with phytoestrogenic, antioxidant and anti-diabetic properties is used in traditional Iranian medicine to treat Polycystic Ovarian Syndrome (PCOS). Chronic inflammation is a new proposed mechanism in PCOS pathogenesis that suggests the role of immune system in this disease. Due to the main role of Treg cells in maintaining immune homeostasis, their impaired function, along with increased production of inflammatory compounds such as nitric oxide, can lead to persistent inflammation. Methods & Materials In this experimental study, 18 BALB/c mice were randomly divided into three groups including control group, untreated PCOS-induced group, and fennel-treated group. The control group received 0.1 ml sesame oil for 21 days. PCOS was induced by subcutaneous injection of Dehydroepiandrosterone (60 mg/kg/day) plus 0.1 mL sesame oil for 21 days. Mice in third group were treated by intraperitoneal injection of 500 mg/kg/day fennel extract after 21 days. The regulatory of T cells (Tregs) were analyzed by flow cytometry method and nitric oxide level determination was performed by Griess Reaction method. Ferric Reducing/ Antioxidant Power (FRAP) assay was used to measure the total antioxidant power. Ethical Considerations This study was approved by the Ethical Committee of Arak University of Medical Sciences (Code: IR.ARAKMU.REC.1397.312). Results The estrous cycle was normalized after treatment with fennel. Fennel significantly reduced the number of ovarian cysts. Nitric oxide concentration decreased significantly while FRAP concentrations did not significantly alter. The number of Treg cells was also increased significantly. Conclusion Due to the role of immune system in the incidence of inflammation, concurrent modulation of both immune and endocrine systems may open new horizons in the design of new therapeutic interventions for PCOS. [ABSTRACT FROM AUTHOR]

Background and Objective: Many different factors and problems can cause infertility. This study carried out to compare NK, T and B lymphocyte populations in peripheral blood of fertile and infertile women. Materials and Methods: In this case - control study 30 infertile women and 15 non pregnant women participated. The non pregnant women had a history of at least two alive children as a control group. The monoclonal antibodies and flowcytometry were used for evaluation of T cell subpopulations (CD3, CD4, CD8), Bcells (CD22) and NK cells (CD56) in fertile and infertile women. Results: NK cells (CD56) significantly increased in infertile women compared with control groups (P=0.009) and T lymphocytes CD3, CD4 significantly reduced in infertile women compared with fertile women (P=0.013, P=0.004, respectively). CD4/CD8 ratio reduced in infertile women compared with fertile women (P=0.05). There was no difference in B cells and CD8 T cells in infertile women compared with controls. Conclusion: This study showed that NK cells increase and CD4 T lymphocytes reduce in infertile women. Our results suggest the immunological alterations may be related to infertility. [ABSTRACT FROM AUTHOR]