Mycobacterium celatum, an emerging pathogen and cause of false positive amplified Mycobacterium tuberculosis direct test.

Mycobacterium celatum is a recently described organism. Herein we describe a case of M. celatum lymphadenitis in an immunocompetent child and the first reported case of a M. celatum infection (lung abscess) in a transplant recipient. A literature review identified 19 other cases of M. celatum infection. Fifteen occurred in patients with the acquired immunodeficiency syndrome. Of these, nine were disseminated and six were localized (primarily to the lungs). The remaining 4 patients were immunocompetent and had localized infection (pneumonitis or lymphadenitis). Diagnosis of M. celatum infection can be challenging as M. celatum can cause false-positive results with the current version of the Amplified Mycobacterium tuberculosis Direct Test (Gen-Probe, San Diego, CA.). Definitive identification is available by DNA sequencing or high-performance liquid chromatography. M. celatum can cause infection in immunocompromised and immunocompetent hosts.

Cardiotrophin-1 stimulates endothelin-1 via gp130 in vascular endothelial cells.

Endothelin-1 (ET-1) is a vasoconstricting and mitogenic peptide released from vascular endothelial cells under normal and pathophysiological conditions, and synthesis and secretion of ET-1 are stimulated by cytokines. Cardiotrophin-1 (CT-1) is a new member of the interleukin-6-type cytokines that induce biological actions through the glycoprotein (gp) 130. The present study was designed to determine the presence of CT-1 and the gp130 cytokine system in vascular endothelial cells and to investigate whether CT-1 stimulates synthesis and secretion of ET-1 in the vascular endothelial cells. We first sought to determine gene expression and immunoreactivity of CT-1, gp130 and ET-1 in cultured canine aortic endothelial cells (CAECs) using Northern blot analysis and immunocytochemistry, which revealed the presence of CT-1 and gp130 together with ET-1 in CAECs. CT-1 increased ET-1 gene expression in CAECs, and stimulated ET-1 secretion from CAECs in a dose-dependent manner. Furthermore, inhibition of gp130 by monoclonal antibody attenuated ET-1 secretion from CAECs, suggesting that actions of CT-1 on the secretion of ET-1 are mediated through gp130 receptor system. The present study, therefore, reports the presence of CT-1 and gp130 in vascular endothelial cells and mechanisms of secretion of ET-1 related to this cytokine system.