Recognition of by Toll-like receptor 9 is altered during persistence.

Toll-like receptor 9 (TLR9) is an innate immune receptor that localizes to endosomes in antigen presenting cells and recognizes single stranded unmethylated CpG sites on bacterial genomic DNA (gDNA). Previous bioinformatic studies have demonstrated that the genome of the human pathogen contains TLR9 stimulatory motifs, and correlative studies have implied a link between human TLR9 (hTLR9) genotype variants and susceptibility to infection. Here, we present our evaluation of the stimulatory potential of gDNA and its recognition by hTLR9- and murine TLR9 (mTLR9)-expressing cells.

Recognition of by Toll-Like Receptor 9 is altered during persistence.

Toll-like receptor 9 (TLR9) is an innate immune receptor that localizes to endosomes in antigen presenting cells and recognizes single stranded unmethylated CpG sites on bacterial genomic DNA. Previous bioinformatic studies have indicated that the genome of the human pathogen contains TLR9 stimulatory motifs, and correlative studies have implied a link between human TLR9 (hTLR9) genotype variants and susceptibility to infection. Here we present our evaluation of the stimulatory potential of gDNA and its recognition by hTLR9- and murine TLR9 (mTLR9)-expressing cells.

Polyamines and hypusination are important for toxin B (TcdB)-mediated activation of group 3 innate lymphocytes (ILC3s).

is the most common cause of nosocomial gastrointestinal tract bacterial infections. We lack fully effective reliable treatments for this pathogen, and there is a critical need to better understand how interacts with our immune system. Group 3 innate lymphocytes (ILC3s) are rare immune cells localized within mucosal tissues that protect against bacterial infections.

Modulation of innate lymphoid cells by enteric bacterial pathogens.

Innate lymphoid cells (ILCs) are key regulators of tissue homeostasis, inflammation, and immunity to infections. ILCs rapidly respond to environmental cues such as cytokines, microbiota and invading pathogens which regulate their function and phenotype. Even though ILCs are rare cells, they are enriched at barrier surfaces such as the gastrointestinal (GI) tract, and they are often critical to the host's immune response to eliminate pathogens.

Corrigendum: Genetic inactivation of inclusion membrane protein CT228 alters MYPT1 recruitment, extrusion production, and longevity of infection.

[This corrects the article DOI: 10.3389/fcimb.2018.

The Polyamine Putrescine Is a Positive Regulator of Group 3 Innate Lymphocyte Activation.

Group 3 innate lymphocytes (ILC3s) rapidly respond to invading pathogens or inflammatory signals, which requires shifting cellular metabolic demands. Metabolic adaptations regulating ILC3 function are not completely understood. Polyamines are polycationic metabolites that have diverse roles in cellular functions and in immunity regulate immune cell biology, including Th17 cells.

Clostridioides difficile Toxin B Activates Group 3 Innate Lymphocytes.

Group 3 innate lymphocytes (ILC3s) are rare immune cells localized in mucosal tissues, especially the gastrointestinal (GI) tract. Despite their rarity, they are a major source of the cytokine interleukin-22 (IL-22), which protects the GI epithelium during inflammation and infection. Although ILC3s have been demonstrated to be important for defense against Clostridioides difficile infection, the exact mechanisms through which they sense productive infection and become activated to produce IL-22 remain poorly understood.

Group 3 innate lymphocytes (ILC3s) upregulate IL-22 in response to elevated intracellular cAMP levels.

Group 3 innate lymphocytes (ILC3s) are important immune cells within mucosal tissues and protect against bacterial infections. They can be activated in response to the innate cytokines IL-23 or IL-1β, which rapidly increases their production of effector molecules that regulate barrier functions. Pathogens can subvert these anti-bacterial effects to evade mucosal defenses to infect the host.

Eumelanin-Inspired Antimicrobial with Biocidal Activity against Methicillin-Resistant .

The reliance on antibiotics and antimicrobials to treat bacterial infectious diseases is threatened by the emergence of antibiotic resistance and multi-drug-resistant organisms, thus having the potential to greatly impact human health. Thus, the discovery and development of antimicrobials capable of acting on antibiotic-resistant bacteria is a major area of significance in scientific research. Herein, we present the development of a eumelanin-inspired antimicrobial capable of killing methicillin-resistant (MRSA).

Hijacking and Use of Host Kinases by Chlamydiae.

species are causative agents of sexually transmitted infections, blinding trachoma, and animal infections with zoonotic potential. Being an obligate intracellular pathogen, relies on the host cell for its survival and development, subverting various host cell processes throughout the infection cycle. A key subset of host proteins utilized by include an assortment of host kinase signaling networks which are vital for many chlamydial processes including entry, nutrient acquisition, and suppression of host cell apoptosis.

Chlamydia trachomatis recruits protein kinase C during infection.

Chlamydia trachomatis is a significant pathogen with global and economic impact. As an obligate intracellular pathogen, C. trachomatis resides inside the inclusion, a parasitophorous vacuole, and depends on the host cell for survival and transition through a biphasic development cycle.

Genetic Inactivation of Inclusion Membrane Protein CT228 Alters MYPT1 Recruitment, Extrusion Production, and Longevity of Infection.

is an obligate intracellular pathogen with global health and economic impact. Upon infection, resides within a protective niche, the inclusion, wherein it replicates and usurps host cell machinery and resources. The inclusion membrane is the key host-pathogen interface that governs specific protein-protein interactions to manipulate host signaling pathways.

Nasal carriage of methicillin resistant Staphylococcus aureus among health care workers at a tertiary care hospital in Western Nepal.

Background: Staphylococcus aureus is a frequent cause of infections in both the community and hospital. Methicillin-resistant Staphylococcus aureus continues to be an important nosocomial pathogen and infections are often difficult to manage due to its resistance to multiple antibiotics. Healthcare workers are important source of nosocomial transmission of MRSA.