The dominant lineage of an emerging pathogen harbours contact-dependent inhibition systems.

Bacteria from the complex (Smc) are important multidrug-resistant pathogens that cause a broad range of infections. Smc is genomically diverse and has been classified into 23 lineages. Lineage Sm6 is the most common among sequenced strains, but it is unclear why this lineage has evolved to be dominant.

The Role of Lifestyle and Environmental Factors in the Pathogenesis of Multiple Myeloma.

Objectives: The study evaluated the impact of lifestyle and environmental exposure on the etiology of multiple myeloma (MM).

Methods: A multicenter case-control study was conducted in 20 hematology centers and in 5 outpatient clinics in Poland. The questionnaire on exposure to potential risk factors including sociodemographic data, lifestyle, and environmental factors was completed.

Serotype switching in Pseudomonas aeruginosa ST111 enhances adhesion and virulence.

Evolution of the highly successful and multidrug resistant clone ST111 in Pseudomonas aeruginosa involves serotype switching from O-antigen O4 to O12. How expression of a different O-antigen serotype alters pathogen physiology to enable global dissemination of this high-risk clone-type is not understood. Here, we engineered isogenic laboratory and clinical P.

Intraspecific Diversity of Populations Isolated from Cystic Fibrosis Respiratory Infections.

Chronic bacterial infections are often polymicrobial, comprising multiple bacterial species or variants of the same species. Because chronic infections may last for decades, they have the potential to generate high levels of intraspecific variation through within-host diversification over time, and the potential for superinfections to occur through the introduction of multiple pathogen populations to the ongoing infection. Traditional methods for identifying infective agents generally involve isolating one single colony from a given sample, usually after selecting for a specific pathogen or antibiotic resistance profile.

Pseudomonas aeruginosa elongation factor-Tu (EF-Tu) is an immunogenic protective protein antigen.

Pseudomonas aeruginosa is a Gram-negative, opportunistic pathogen that infects immunocompromised individuals, especially in the hospital setting. This bacterium is an important pathogen in people with weakened immune systems, injuries, and other underlying physiologic dysfunctions. P.

Role of factor H-related protein 3 in bloodstream infections.

Pseudomonas aeruginosa is a leading cause of nosocomial bloodstream infections. The outcome of these infections depends on the virulence of the microorganism as well as host-related conditions and factors. The complement system plays a crucial role in defense against bloodstream infections.

Flagellum-deficient is more virulent than non-motile but flagellated mutants in a cystic fibrosis mouse model.

Loss of the flagellum marks the pathoadaptation of to the cystic fibrosis (CF) airway environment during lung disease. Losing the flagellum is advantageous to the bacterium as the flagellum can be recognized by immune cells. The primary purpose of the flagellum is, however, to provide motility to the bacterium.

Improvement of a mouse infection model to capture chronic physiology in cystic fibrosis.

Laboratory models are central to microbiology research, advancing the understanding of bacterial physiology by mimicking natural environments, from soil to the human microbiome. When studying host-bacteria interactions, animal models enable investigators to examine bacterial dynamics associated with a host, and in the case of human infections, animal models are necessary to translate basic research into clinical treatments. Efforts toward improving animal infection models are typically based on reproducing host genotypes/phenotypes and disease manifestations, leaving a gap in how well the physiology of microbes reflects their behavior in a human host.

Chronic hyperglycemia aggravates lung function in a -Tg murine model.

Cystic fibrosis-related diabetes (CFRD), the most common comorbidity in cystic fibrosis (CF), leads to increased mortality by accelerating the decline in lung function. Tg transgenic mice overexpressing the epithelial sodium channel β subunit exhibit spontaneous CF-like lung disease, including airway mucus obstruction and chronic inflammation. Here, we established a chronic CFRD-like model using Tg mice made diabetic by injection of streptozotocin (STZ).

Antibacterial potential of complex cystic fibrosis isolates.

Unlabelled: Over 160,000 people worldwide suffer from cystic fibrosis (CF), a genetic condition that causes mucus to accumulate in internal organs. Lung decline is a significant health burden for people with CF (pwCF), and chronic bacterial pulmonary infections are a major cause of death. complex (Smc) is an emerging, multidrug-resistant CF pathogen that can cause pulmonary exacerbations and result in higher mortality.

LasR regulates protease IV expression at suboptimal growth temperatures in .

The opportunistic pathogen causes debilitating lung infections in people with cystic fibrosis, as well as eye, burn, and wound infections in otherwise immunocompetent individuals. Many of 's virulence factors are regulated by environmental changes associated with human infection, such as a change in temperature from ambient to human body temperature. One such virulence factor is protease IV (PIV).

Model-driven characterization of functional diversity of clinical isolates with broadly representative phenotypes.

is a leading cause of infections in immunocompromised individuals and in healthcare settings. This study aims to understand the relationships between phenotypic diversity and the functional metabolic landscape of clinical isolates. To better understand the metabolic repertoire of in infection, we deeply profiled a representative set from a library of 971 clinical isolates with corresponding patient metadata and bacterial phenotypes.

Mutation of , encoding homogentisate 1,2-dioxygenase, is responsible for pyomelanin production but does not impact the virulence of in a chronic granulomatous disease mouse lung infection.

The complex (Bcc) is a group of Gram-negative opportunistic bacteria often associated with fatal pulmonary infections in patients with impaired immunity, particularly those with cystic fibrosis (CF) and chronic granulomatous disease (CGD). Some Bcc strains are known to naturally produce pyomelanin, a brown melanin-like pigment known for scavenging free radicals; pigment production has been reported to enable Bcc strains to overcome the host cell oxidative burst. In this work, we investigated the role of pyomelanin in resistance to oxidative stress and virulence in strains J2315 and K56-2, two epidemic CF isolates belonging to the ET-12 lineage.

Monoclonal antibodies derived from B cells in subjects with cystic fibrosis reduce burden in mice.

(PA) is an opportunistic, frequently multidrug-resistant pathogen that can cause severe infections in hospitalized patients. Antibodies against the PA virulence factor, PcrV, protect from death and disease in a variety of animal models. However, clinical trials of PcrV-binding antibody-based products have thus far failed to demonstrate benefit.

A role for the stringent response in ciprofloxacin resistance in Pseudomonas aeruginosa.

Pseudomonas aeruginosa is a major cause of nosocomial infections and the leading cause of chronic lung infections in cystic fibrosis and chronic obstructive pulmonary disease patients. Antibiotic treatment remains challenging because P. aeruginosa is resistant to high concentrations of antibiotics and has a remarkable ability to acquire mutations conferring resistance to multiple groups of antimicrobial agents.

Factor H-related protein 1 promotes complement-mediated opsonization of .

is an important human opportunistic pathogen responsible for a wide range of infections. The complement system is the main early host defense mechanism to control these infections. counteracts complement attack by binding Factor H (FH), a complement regulator that inactivates C3b, preventing the formation of the C3-convertase and complement amplification on the bacterial surface.

Impact of CFTR Modulation on Pseudomonas aeruginosa Infection in People With Cystic Fibrosis.

Background: Pseudomonas aeruginosa is a multidrug-resistant pathogen causing recalcitrant pulmonary infections in people with cystic fibrosis (pwCF). Cystic fibrosis transmembrane conductance regulator (CFTR) modulators have been developed that partially correct the defective chloride channel driving disease. Despite the many clinical benefits, studies in adults have demonstrated that while P.

Experimentally evolved shows increased survival in the presence of by acquiring mutations in the amino acid transporter, GltT.

When cultured together under standard laboratory conditions has been shown to be an effective inhibitor of . However, and are commonly observed in coinfections of individuals with cystic fibrosis (CF) and in chronic wounds. Previous work from our group revealed that isolates from CF infections are able to persist in the presence of strain PAO1 with a range of tolerances with some isolates being eliminated entirely and others maintaining large populations.

Efficacy of a serogroup O9 vaccine.

There are currently no approved vaccines against the opportunistic pathogen . Among vaccine targets, the lipopolysaccharide (LPS) O antigen of is the most immunodominant protective candidate. There are 20 different O antigens composed of different repeat sugar structures conferring serogroup specificity, and 10 are found most frequently in infection.

The type VI secretion system of the emerging pathogen complex has antibacterial properties.

Infections with the opportunistic pathogen complex can be fatal for immunocompromised patients. The mechanisms used by the bacterium to compete against other prokaryotes are not well understood. We found that the type VI secretion system (T6SS) allows complex to eliminate other bacteria and contributes to the competitive fitness against a co-infecting isolate.

Model-driven characterization of functional diversity of clinical isolates with broadly representative phenotypes.

is a leading cause of infections in immunocompromised individuals and in healthcare settings. This study aims to understand the relationships between phenotypic diversity and the functional metabolic landscape of clinical isolates. To better understand the metabolic repertoire of in infection, we deeply profiled a representative set from a library of 971 clinical isolates with corresponding patient metadata and bacterial phenotypes.