Редактирование: NTM

Neurotrimin precursor (hNT) (IgLON family member 2) [IGLON2] [NT] [UNQ297/PRO337]

==Publications==

{{medline-entry
|title=Attenuated heme oxygenase-1 responses predispose the elderly to pulmonary nontuberculous mycobacterial infections.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27694475
|abstract=Pulmonary infections with nontuberculous mycobacteria (P-[[NTM]]), such as by Mycobacterium avium complex (M. avium), are increasingly found in the elderly, but the underlying mechanisms are unclear. Recent studies suggest that adaptive immunity is necessary, but not sufficient, for host defense against mycobacteria. Heme oxygenase-1 (HO-1) has been recognized as a critical modulator of granuloma formation and programmed cell death in mycobacterial infections. Old mice (18-21 mo) infected with M. avium had attenuated HO-1 response with diffuse inflammation, high burden of mycobacteria, poor granuloma formation, and decreased survival (45%), while young mice (4-6 mo) showed tight, well-defined granuloma, increased HO-1 expression, and increased survival (95%). To further test the role of HO-1 in increased susceptibility to P-[[NTM]] infections in the elderly, we used old and young HO-1  and HO-1  mice. The transcriptional modulation of the JAK/STAT signaling pathway in HO-1  mice due to M. avium infection demonstrated similarities to infected wild-type old mice with upregulation of [[SOCS3]] and inhibition of Bcl2. Higher expression of [[SOCS3]] with downregulation of Bcl2 resulted in higher macrophage death via cellular necrosis. Finally, peripheral blood monocytes (PBMCs) from elderly patients with P-[[NTM]] also demonstrated attenuated HO-1 responses after M. avium stimulation and increased cell death due to cellular necrosis (9.69% ± 2.02) compared with apoptosis (4.75% ± 0.98). The augmented risk for P-[[NTM]] in the elderly is due, in part, to attenuated HO-1 responses, subsequent upregulation of [[SOCS3]], and inhibition of Bcl2, leading to programmed cell death of macrophages, and sustained infection.
|mesh-terms=* Aged
* Aging
* Animals
* Cell Death
* Disease Susceptibility
* Gene Expression Regulation, Enzymologic
* Granuloma
* Heme Oxygenase-1
* Humans
* Leukocytes, Mononuclear
* Mice, Inbred C57BL
* Mycobacterium Infections, Nontuberculous
* Mycobacterium avium
* Proto-Oncogene Proteins c-bcl-2
* Respiratory Tract Infections
* Suppressor of Cytokine Signaling 3 Protein
* Transcription, Genetic
|keywords=* SOCS3
* aging
* cell death
* heme oxygenase 1
* nontuberculosis mycobacterium
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5504405
}}