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Unlabelled: Crosstalk between autophagy, host cell death, and inflammatory host responses to bacterial pathogens enables effective innate immune responses that limit bacterial growth while minimizing coincidental host damage. ( ) thwarts innate immune defense mechanisms in alveolar macrophages (AMs) during the initial stages of infection and in recruited bone marrow-derived cells during later stages of infection. However, how protective inflammatory responses are achieved during infection and the variation of the response in different macrophage subtypes remain obscure.
View Article and Find Full Text PDFUnlabelled: Guanosine triphosphate (GTP) is essential for macromolecular biosynthesis, and its intracellular levels are tightly regulated in bacteria. Loss of the alarmone (p)ppGpp disrupts GTP regulation in , causing cell death in the presence of exogenous guanosine and underscoring the critical importance of GTP homeostasis. To investigate the basis of guanosine toxicity, we performed a genetic selection for spontaneous mutations that suppress this effect, uncovering an unexpected link between GTP synthesis and glycolysis.
View Article and Find Full Text PDFMechanisms of Keap1/Nrf2 modulation in bacterial infections: implications in persistence and clearance.
Front Immunol
December 2024
Centro Multidisciplinario de Estudios en Biotecnología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Mexico.
Pathogenic bacteria trigger complex molecular interactions in hosts that are characterized mainly by an increase in reactive oxygen species (ROS) as well as an inflammation-associated response. To counteract oxidative damage, cells respond through protective mechanisms to promote resistance and avoid tissue damage and infection; among these cellular mechanisms the activation or inhibition of the nuclear factor E2-related factor 2 (Nrf2) is frequently observed. The transcription factor Nrf2 is considered the regulator of several hundred cytoprotective and antioxidant genes.
View Article and Find Full Text PDFNatural Mutation of PrfA K10N/T151A Enhances Serotype 4h Virulence.
Foodborne Pathog Dis
January 2025
College of Biological Sciences and Technology, Yangzhou University, Yangzhou, China.
PrfA is a key virulence regulator for (Lm) responding to host environment. Here we report that the natural mutation in PrfA enhanced the pathogenicity of hypervirulent serotype 4h . We characterized the phylogenetic tree of PrfA, and found that PrfA prevalently distributed in all serotype 4h isolates.
View Article and Find Full Text PDFspp., and Threats to the Food Industry and Public Health.
Foodborne Pathog Dis
January 2025
Departamento de Alimentos e Nutrição Experimental, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, São Paulo, Brazil.
Foodborne pathogens have always been of public health concern and represent safety issues for food processors. These pathogens develop new ways to overcome antibiotics, survive in different environmental conditions, and the ability to reproduce in many hostile environments configure them as serious health hazards. Considering the huge number of microorganisms, three bacterial representatives were selected to provide a better knowledge about the question of which one is the worst enemy for humans, from the food industry point of view, taking into consideration their multiplication specificity, virulence, and resistance.
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