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At least 1,459 records · Page 81Linked to original sources
PubMed2001

TREM-1 amplifies inflammation and is a crucial mediator of septic shock.

Host innate responses to bacterial infections are primarily mediated by neutrophils and monocytes/macrophages. These cells express pattern recognition receptors (PRRs) that bind conserved molecular structures shared by groups of microorganisms. Stimulation of PRR signalling pathways initiates secretion of proinflammatory mediators, which promote the elimination of infectious agents and the induction of tissue repair. Excessive inflammation owing to bacterial infections can lead to tissue damage and septic shock. Here we show that inflammatory responses to microbial products are amplified by a pathway mediated by triggering receptor expressed on myeloid cells (TREM)-1. TREM-1 is an activating receptor expressed at high levels on neutrophils and monocytes that infiltrate human tissues infected with bacteria. Furthermore, it is upregulated on peritoneal neutrophils of patients with microbial sepsis and mice with experimental lipopolysaccaride (LPS)-induced shock. Notably, blockade of TREM-1 protects mice against LPS-induced shock, as well as microbial sepsis caused by live Escherichia coli or caecal ligation and puncture. These results demonstrate a critical function of TREM-1 in acute inflammatory responses to bacteria and implicate TREM-1 as a potential therapeutic target for septic shock.

Animals↗
PubMed2004

Frontal and stealth attack strategies in microbial pathogenesis.

Interactions between microbes and human hosts can range from a benign, even symbiotic collaboration to a competition that may turn fatal--resulting in death of the host, the microbe or both. Despite advances that have been made over the past decades in understanding microbial pathogens, more people worldwide still die every year from infectious disease than from any other cause. This highlights the relevance of continuing to probe the mechanisms used by microorganisms to cause disease, and emphasizes the need for new model systems to advance our understanding of host-pathogen interactions.

Bartonella↗
PubMed2005

[Cat-scratch disease as cause of Lymphadenitis colli].

Cat-scratch Disease as Cause of Lymphadenitis colli. Cat-scratch disease is a frequent cause of lymphadenitis colli. It mainly affects children and adolescents younger than 21 years. Since the clinical picture is not characteristic, a history of contact to cats or kittens is highly valuable for diagnosing the disease. Major aspects of the disease concerning epidemiology, diagnostic procedures, clinical presentation and therapy are discussed.

Adolescent↗
PubMed1996

[Cat scratch disease. An overview for the ENT physician].

BACKGROUND: Cat scratch disease (CSD) is a relatively common cause of chronic lymphadenopathy in the USA. In the present paper the authors describe recent advances in the understanding of this disorder focusing on etiology, clinical aspects, diagnostic management, and therapy. ETIOLOGY: Rochalimaea henselae and Afipia felis, two gram-negative bacteria, have recently been isolated from lymph node tissue of patients suffering from CSD. The current literature reveals that Rochalimaea henselae seems to be the most probable agent responsible for CSD. Serum samples from CSD patients' cats have shown titers of 1:64 or higher for antibodies to Rochallmaea henselae. EPIDEMIOLOGY: The incidence of CSD in the USA is between 0.77 and 9.3 per 100,000 per year. The incidence of CSD in Europe is unknown, but the prevalence of antibodies to Rochalimaea henselae among cats is comparable. CLINICAL MANIFESTATIONS: Most common symptoms of CSD are regional lymphadenopathy, fever, and malaise. Other manifestations occur in about 5% of patients and include encephalitis, granulomatous hepatitis, and Parinaud's oculoglandular syndrome. Fatal complications and irreversible sequelae have not been reported. DIAGNOSIS: To establish the diagnosis of CSD, the presence of regional lymphadenopathy, cat contact, and papula are required. Additional procedures include indirect fluorescent antibody assays and PCR. THERAPY: Up to now there is no standard therapy for CSD. Antibiotic treatment, however, might be considered for CSD patients with severe symptoms. Rifampicin, ciprofloxacin, trimethoprim sulfamethoxazole, and gentamicin are known to be effective antibiotic agents.

Adolescent↗