Development of a newly immunoassay specific for mouse presepsin (sCD14-ST).

Presepsin (sCD14-ST) is used as a marker for sepsis diagnosis. The production mechanism of presepsin is unique in that it is produced through phagocytosis of microorganisms. However, some studies have demonstrated that non-infected patients had increased presepsin levels and that presepsin is related to the risk or severity of diseases. This study was designed to describe a sensitive sandwich enzyme-linked immunosorbent assay for mouse presepsin developed to investigate the association of presepsin with diseases. Polyclonal antibodies were generated from peptide-immunized rabbit antiserum. Mouse presepsin standard was prepared using the recombinant method as an Fc-fusion protein. The linear detection range of the method was 4.7-300 pg/mL with a detection limit of 1.4 pg/mL. The assay detected mouse presepsin where mouse soluble CD14 (sCD14) was digested by cathepsin D proteinase and the cross-reactivity of sCD14 was not observed. The normal levels of mouse presepsin and sCD14 were compared; 65.9 ± 21.4 pg/mL and 43.2 ± 7.2 ng/mL were determined, respectively. Moreover, the levels of presepsin and sCD14 were compared with a lipopolysaccharide (LPS)-injected sepsis mouse model. The newly developed analytical method had high specificity to presepsin and is an efficient tool for studying the association between presepsin and diseases.

Lemierre's syndrome with isolated external jugular vein thrombosis caused by Streptococcus intermedius.

An 85-year-old woman with a history of rheumatoid arthritis fell due to unsteadiness and visited our emergency room due to head injury. The patient had minor head trauma and lip and oral cavity injuries, and she presented with fever. Laboratory tests showed high inflammatory marker levels. Moreover, there were indicative of urinary tract infection. Thus, the patient was admitted to our hospital. Blood cultures performed upon admission revealed the presence of Streptococcus intermedius, and contrast-enhanced computed tomography scan showed solitary right external jugular vein thrombosis and multiple abscesses in both lungs. Hence, the patient was diagnosed with Lemierre's syndrome, and antimicrobial agents and anticoagulants were administered. The patient developed left pleurisy due to inflammation caused by lung abscesses, which improved with thoracic drainage. Her condition improved satisfactorily, and she was then discharged. There are only few studies about Lemierre's syndrome caused by S. intermedius and even lesser cases involving external jugular vein thrombosis. Herein, we report a relatively rare case of Lemierre's syndrome with isolated external jugular vein thrombosis.

Severe leptospirosis infection in a non-epidemic area.

A 39-year-old man visited our hospital with lower leg pain and fever. We suspected sepsis because of an infectious disease. He was hospitalized, and treatment was initiated. After admission, we received information that mice were present in his living environment. Moreover, we considered leptospirosis in the differential diagnosis and started the administration of ceftriaxone and minocycline. On the 10th day after admission, after examination by the National Institute on Infectious Diseases, we diagnosed him with leptospirosis. The patient was transferred to the hospital for rehabilitation on day 23 after admission. It is important to consider leptospirosis even in non-epidemic area.

Mitigation of tight junction protein dysfunction in lung microvascular endothelial cells with pitavastatin.

BACKGROUND: Statin use in individuals with chronic obstructive pulmonary disease (COPD) with coexisting cardiovascular disease is associated with a reduced risk of exacerbations. The mechanisms by which statin plays a role in the pathophysiology of COPD have not been defined. To explore the mechanisms involved, we investigated the effect of statin on endothelial cell function, especially endothelial cell tight junctions. METHOD: We primarily assessed whether pitavastatin could help mitigate the development of emphysema induced by continuous cigarette smoking (CS) exposure. We also investigated the activation of liver kinase B1 (LKB1)/AMP-activated protein kinase (AMPK) signaling, which plays a role in maintaining endothelial functions, important tight junction proteins, zonula occludens (ZO)-1 and claudin-5 expression, and lung microvascular endothelial cell permeability. RESULTS: We found that pitavastatin prevented the CS-induced decrease in angiomotin-like protein 1 (AmotL1)-positive vessels via the activation of LKB1/AMPK signaling and IFN-γ-induced hyperpermeability of cultured human lung microvascular endothelial cells by maintaining the levels of AmotL1, ZO-1, and claudin-5 expression at the tight junctions. CONCLUSION: Our results indicate that the maintenance of lung microvascular endothelial cells by pitavastatin prevents tight junction protein dysfunctions induced by CS. These findings may ultimately lead to new and novel therapeutic targets for patients with COPD.