The effect of bacterial toxins, modifying the activity of regulatory N proteins of adenylate cyclase and probably other systems, on the mitogen-induced changes of cytosolic free Ca2+ concentration ([Ca2+]i) has been studied using Ca2+ fluorescent probe quin-2. It is shown that treatment of thymocytes with cholera toxin, E. coli heat-labile (HL) toxin or pertussis toxin abolishes the concanavalin A (con A)-induced rise of [Ca2+]i. The inhibitory effect of cholera and HL toxins can be explained by the toxin-induced rise of intracellular cAMP. The effect of pertussis toxin indicates the involvement of N proteins in the action of con A receptor and in generation of Ca2+-signal during the mitogenic activation of thymocytes.
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Afr J Prim Health Care Fam Med
December 2024
Department of Internal Medicine, Prince Mshiyeni Memorial Hospital, Durban.
Background: Tuberculosis (TB) remains a leading cause of mortality in low-resource settings and poses a diagnostic challenge in human immunodeficiency virus (HIV)-negative populations because of limitations in traditional diagnostic methods such as sputum smear microscopy (SSM) and sputum Xpert Ultra. There is a lack of effective, non-invasive diagnostic options for TB diagnosis in HIV-negative populations. This scoping review explores the potential of urinary lipoarabinomannan (ULAM) as a point-of-care diagnostic tool for Mycobacterium tuberculosis (MTB) in HIV-negative individuals.
View Article and Find Full Text PDFFront Immunol
January 2025
State Key Laboratory of Traditional Chinese Medicine Syndrome, Department of Neurology, Guangdong Provincial Academy of Chinese Medical Sciences, Guangdong Provincial Hospital of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Background: A stable and reproducible experimental bacterial pneumonia model postintracerebral hemorrhage (ICH) is necessary to help investigating the pathogenesis and novel treatments of Stroke-associated pneumonia (SAP).
Aim: To establish a Gram-negative bacterial pneumonia-complicating ICH rat model and an acute lung injury (ALI)-complicating ICH rat model.
Methods: We established two standardized models of post-ICH pneumonia by nasal inoculation with () or intratracheal inoculation with lipopolysaccharide (LPS).
Sci Rep
January 2025
Division of Reproductive Biology, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Tuwima 10, Olsztyn, 10-748, Poland.
An inflammatory response is related to different inflammatory mediators generated by immune and endometrial cells. The links between lipopolysaccharide (LPS), cytokines, and leukotrienes (LTs) in endometrial stromal cells remain unclear. This study aimed to examine the influence of LPS, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-4 and IL-10 on 5-lipooxygenase (5-LO), LTA4 hydrolase (LTAH) and LTC4 synthase (LTCS) mRNA and protein abundances, and LTB4 and cysteinyl (cys)-LTs release including LTC4, by the cultured pig endometrial stromal cells, as well as on cell viability.
View Article and Find Full Text PDFJ Physiol Sci
January 2025
Department of Critical Care Medicine, The Third People's Hospital of Qingdao, No. 29 Yongping Road, Licang District, 266000, Qingdao, Shandong, China. Electronic address:
Background: Sepsis-induced acute lung injury (ALI) accounts for about 40% of ALI, accompanied by alveolar epithelial injury. The study aimed to reveal the role of circular RNA_0114428 (circ_0114428) in sepsis-induced ALI.
Methods: Human pulmonary alveolar epithelial cells (HPAEpiCs) were treated with lipopolysaccharide (LPS) to mimic a sepsis-induced ALI cell model.
Sci Adv
January 2025
Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Mitochondrial electron transport chain (ETC) function modulates macrophage biology; however, mechanisms underlying mitochondria ETC control of macrophage immune responses are not fully understood. Here, we report that mutant mice with mitochondria ETC complex III (CIII)-deficient macrophages exhibit increased susceptibility to influenza A virus (IAV) and LPS-induced endotoxic shock. Cultured bone marrow-derived macrophages (BMDMs) isolated from these mitochondria CIII-deficient mice released less IL-10 than controls following TLR3 or TLR4 stimulation.
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