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Nontuberculous mycobacteria (NTM) are an important cause of morbidity and mortality in pulmonary infections. Among them, Mycobacterium avium complex (MAC) is the most common cause of pulmonary NTM disease worldwide., Nrf2 is a redox-sensitive transcription factor that is thought to be important in protection against intracellular pathogens. To determine the protective role of Nrf2 in the host defense against Mycobacterium avium complex (MAC), both wild-type and Nrf2-deficient mice were intranasally infected with MAC bacteria. Nrf2-deficient mice were highly susceptible to MAC bacteria compared with wild-type mice. There were no significant changes in the levels of oxidative stress and Th1 cytokine production between genotypes. Comprehensive transcriptome analysis showed that the expressions of Nramp1 and HO-1 were much lower in the infected lungs, and the expression of Nramp1 was especially lower in alveolar macrophages of Nrf2-deficient mice than of wild-type mice. Electron microscopy showed that many infected alveolar macrophages from Nrf2-deficient mice contained a large number of intracellular MAC bacteria with little formation of phagolysosomes, compared with those from wild-type mice. Treatment with sulforaphane, an activator of Nrf2, increased resistance to MAC with increased lung expression of Nramp1 and HO-1 in wild-type mice. These results indicate that Nramp1 and HO-1, regulated by Nrf2, are essential in defending against MAC infection due to the promotion of phagolysosome fusion and granuloma formation, respectively. Thus, Nrf2 is thought to be a critical determinant of host resistance to MAC infection.

Sherpa, Mingma Thsering, and Raksha Shrestha. Stroke at high altitude in an experienced Sherpa climber: A case report. High Alt Med Biol. 21:406–408, 2020.—A 44-year-old experienced Sherpa climber ...

We present a case of a healthy 22 years old who presented with bruising and hematoma following a minor trauma. Investigations showed severe thrombocytopenia but complete hematological investigations did not reveal a cause. An aggressive treatment with steroids, IVIG, anti-D, splenectomy and immunosuppressant proved to be refractory. A subclinical transaminitis prompted an infectious workup which revealed Cytomegalovirus infection. Platelet count improved and remained stable after eradication of Cytomegalovirus. We conclude that infection with CMV should be ruled out in cases of severe refractory immune thrombocytopenic purpura. DOI: http://dx.doi.org/10.3126/jaim.v3i1.10704 Journal of Advances in Internal Medicine 2014;03(01):42-45