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M cells and the follicle-associated epithelium
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Hiroshi Ohno, Marian Neutra, Ifor R. Williams
Salmonella species are able to infect many cell types, including epithelial cells and phagocytes. In humans, Salmonella enterica serovar typhimurium causes a mucosa-limited diarrheal disease, but in mice the bacteria spread systemically and cause a lethal septicemia that closely mimics typhoid fever caused by Salmonella enterica serovar Typhi in humans. After adhering to the host-cell membrane, the bacteria use a type III secretion system to deliver proteins into the host cell, inducing massive actin reorganization and macropinocytosis, a process that disrupts normal cell architecture as bacteria are internalized. Because the FAE and M cells are relatively accessible, intestinal Salmonella preferentially adhere to M cells in both mice and humans, rapidly invade Peyer's patches, and are taken up by subepithelial DCs. Uptake of Salmonella has cytotoxic effects that can result in M cell death. In mice, some Salmonella may also be taken up from villus surfaces, captured by DCs that send extensions through tight junctions. Salmonella enterica serovar typhimurium survive in special vacuoles in phagocytes and are carried by these migrating cells via the lymphatic vessels to the spleen, causing murine typhoid fever.
Pseudomonas
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Rajasekharan Sharika, Krishnaswamy Balamurugan
Type III secretion system is a needle-like appendage that forms pores in the eukaryotic membrane and allows the injection of toxins directly, a mechanism used by pathogens like Salmonella, Shigella, and Pseudomonas species to infect the host. This pilus-like structure allows the translocation of effectors such as Exo S, Exo T, Exo Y, and Exo U from bacteria into the host.7,109 Exo S is a cytotoxin with two active domains, a C-terminal ADP-ribosyltransferase domain and an n-terminal Rho GTPase–activating proteins (GAP) domain, that disrupt the normal cytoskeletal organization as well as are capable of modulating host immune and inflammatory response, respectively.110 Exo T is similar to Exo S with dual active domain and has similar effect on cytoskeleton as well as inhibits wound repair in the host. Exo Y is an adenylate cyclase that increases cytosolic cAMP that leads to increased pulmonary microvascular intercellular formation and lung permeability, thus helping in colonization inside the host. Exo U is a potent eukaryotic cell membrane disruptor and a major cytotoxin. It is mainly responsible for the decompartmentalization in acute lung injury model that leads to sepsis.84,111,112
An Outbreak of Pseudomonas Aeruginosa in a Neonatal Intensive Care Unit
Published in Meera Chand, John Holton, Case Studies in Infection Control, 2018
Trupti A. Patel, Michael Kelsey
P. aeruginosa possesses a number of virulence factors, including the production of toxins and enzymes such as proteases and elastases, and phenazine pigments, such as pyocyanin. It possesses several different export systems that are involved in the secretion of virulence factors. Of particular importance is a type III secretion system that enables injection of effector proteins directly into the cytoplasm of host cells. These proteins have significant effects on epithelial barrier function and wound healing.
EspH interacts with the host active Bcr related (ABR) protein to suppress RhoGTPases
Published in Gut Microbes, 2022
Rachana Pattani Ramachandran, Ipsita Nandi, Nir Haritan, Efrat Zlotkin-Rivkin, Yael Keren, Tsafi Danieli, Mario Lebendiker, Naomi Melamed-Book, William Breuer, Dana Reichmann, Benjamin Aroeti
Enteropathogenic Escherichia coli (EPEC), one of the most important human diarrheagenic bacterial pathogens, infects people mainly in low and middle-income countries.1 In contrast, the closely related enterohemorrhagic Escherichia coli (EHEC), which causes hemorrhagic colitis and hemolytic uremic syndrome in humans, is prevalent mainly in the industrial world.2,3Citrobacter rodentium (C. rodentium), a natural mouse pathogen that employs similar strategies of colonization and pathogenesis, serves as an in vivo model for studying EPEC and EHEC infection.4 Following attachment to the host cell surface, these pathogens utilize the type III secretion system (T3SS) to introduce bacterial proteins, termed ‘effector’ proteins, into the host cells.5,6 These effectors specifically target and manipulate host cell organelles and signaling pathways, leading to intimate binding of the bacteria to host enterocytes via the attaching and effacing (A/E) lesion formation,7 modulation of host cell death pathways,4,8 and inhibition of host immune responses.9 Recent in vivo studies using the C. rodentium model have shown that effectors act as a multifunctional and interconnected network within the host cells. These characteristics are essential for inducing the diarrheal disease.10,11
Latent Upregulation of Nlrp3, Nlrc4 and Aim2 Differentiates between Asymptomatic and Symptomatic Trichomonas vaginalis Infection
Published in Immunological Investigations, 2022
Sonal Yadav, Vivek Verma, Rakesh Singh Dhanda, Sumeeta Khurana, Manisha Yadav
NLRC4, also called IPAF, CLAN, and card12; it regulates activation of caspase-1 and IL-1β. Its response is not directly mediated. NAIPs; first, interact with the type III secretion system (T3SS) components like rods and needle and flagellin proteins and then interact with NLRC4 and causing its oligomerization (Hafner-Bratkovič 2017; Paintlia et al. 2002). Tumor necrosis factor-alpha (TNFα), p53, and exposure to UV radiation can directly induce transcription of Ipaf in some human cells compared to un-stimulated cells (Gutierrez et al. 2004; Paintlia et al. 2002; Sutterwala and Flavell 2009). In bacterial infection, NLRC4 leads to IL-1β expression through caspase-1. S. enteric, L. pneumophila, L. monocytogenes activated the NLRC4 pathway and resulted in infection clearance (Skeldon and Saleh 2011). During fungal infection, Tomalka et al. found that NLRC4 played a role in limiting the growth of candida in the mucosal stroma (Tomalka et al. 2011). Sadasivam et al. reported an increased immune-reactivity for p53 in T. vaginalis infected women (Sadasivam et al. 2005). A study reported increased levels of TNF-α in the vaginal–cervical lymphocytes of BALB/c mice infected with T. vaginalis isolates obtained from asymptomatic women as compared to isolates of symptomatic women (Paintlia et al. 2002).
Healthy Intestinal Function Relies on Coordinated Enteric Nervous System, Immune System, and Epithelium Responses
Published in Gut Microbes, 2021
Fatima B. Saldana-Morales, Dasom V. Kim, Ming-Ting Tsai, Gretchen E. Diehl
In contrast with commensals, pathogens have additional functional systems that help them colonize the host tissue. An example is the type III secretion system (T3SS) used by pathogenic Gram-negative bacteria, such as Salmonella, to deliver bacterial proteins directly into the cytoplasm of host cells.38,94Salmonella has two T3SS which allow for epithelial cell uptake and intracellular survival in macrophages.95 Detection of the T3SS is a way for host cells to discriminate between pathogenic and commensal bacteria. T3SS are sensed by NLR family apoptosis inhibitory proteins (NAIPs) to activate NLRC4 inflammasome and induce secretion of IL-1β, leading to programmed cell death of macrophages.95–98 In parallel, intracellular flagellin detection via NLR neuronal apoptosis inhibitory protein 5 (NAIP5) and NAIP6 in the cytosol serves as a secondary signal to further promote the assembly of NLRC4 inflammasome and IL-1β production.99,100