Human T-cell leukemia virus type I infects human lung epithelial cells and induces gene expression of cytokines, chemokines and cell adhesion molecules

<p>Abstract</p> <p>Background</p> <p>Human T-cell leukemia virus type I (HTLV-I) is associated with pulmonary diseases, characterized by bronchoalveolar lymphocytosis, which correlates with HTLV-I proviral DNA in carriers. HTLV-I Tax seems to be involved in the development of such pulmonary diseases through the local production of inflammatory cytokines and chemokines in T cells. However, little is known about induction of these genes by HTLV-I infection in lung epithelial cells.</p> <p>Results</p> <p>We tested infection of lung epithelial cells by HTLV-I by coculture studies in which A549 alveolar and NCI-H292 tracheal epithelial cell lines were cocultured with MT-2, an HTLV-I-infected T-cell line. Changes in the expression of several cellular genes were assessed by reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay and flow cytometry. Coculture with MT-2 cells resulted in infection of lung epithelial cells as confirmed by detection of proviral DNA, HTLV-I Tax expression and HTLV-I p19 in the latter cells. Infection was associated with induction of mRNA expression of various cytokines, chemokines and cell adhesion molecule. NF-κB and AP-1 were also activated in HTLV-I-infected lung epithelial cells. <it>In vivo </it>studies showed Tax protein in lung epithelial cells of mice bearing Tax and patients with HTLV-I-related pulmonary diseases.</p> <p>Conclusion</p> <p>Our results suggest that HTLV-I infects lung epithelial cells, with subsequent production of cytokines, chemokines and cell adhesion molecules through induction of NF-κB and AP-1. These changes can contribute to the clinical features of HTLV-I-related pulmonary diseases.</p

Pneumocystis jirovecii Pneumonia and Alveolar Hemorrhage in a Pregnant Woman with Human T Cell Lymphotropic Virus Type-1 Infection

Acute lung injury during pregnancy results in morbidity and mortality in both the mother and the fetus. Pneumocystis jirovecii pneumonia (PCP) is a rare disease but may occur in pregnant immune-suppressed women. Here, we describe a case of acute lung injury due to PCP and alveolar hemorrhage in a pregnant woman who was a human T lymphotropic virus type-1 (HTLV-1) carrier. PCP should be considered in the differential diagnosis of pulmonary complications during pregnancy in HTLV-1 endemic areas

Elsberg Syndrome with Eosinophilic Meningoencephalitis Caused by Angiostrongylus cantonensis

A 42-year-old man was admitted to our hospital with a history of fever, headache and disorientation. His cerebrospinal fluid revealed eosinophilia and his serum had an antibody against Angiostrongylus cantonensis (A. cantonensis). Then, he was diagnosed as eosinophilic meningoencephalitis caused by A. cantonensis. He was treated with repeated lumbar punctures and oral prednisolone. Although a symptom he had been suffering from at the time of his admission was urinary retention, this symptom disappeared as his general condition improved. Therefore his case was considered to be Elsberg syndrome with eosinophilic meningoencephalitis caused by A. cantonensis

Do infections with disseminated Mycobacterium avium complex precede sweet's syndrome? A case report and literature review

Sweet's syndrome is reportedly associated with preceding nontuberculous mycobacterial infections (NTMIs). Here, we report on a systemic Mycobacterium intracellulare infection in a patient on corticoid therapy for Sweet's syndrome. Literature searches show that 69.1% of patients with Sweet's syndrome and NTMIs developed this syndrome later than NTMIs and 89.3% of them developed during the clinical course of a rapidly growing mycobacterial infection. The residual cases were associated with slow-growing mycobacteria (14.3%), but only three cases of Mycobacterium avium complex (MAC) infections before the onset of Sweet's syndrome have been reported, and all of them were caused by disseminated MAC disease. One of these cases developed during corticoid therapy for Sweet's syndrome, while another case had underlying diabetes mellitus. Hence, the occurrence of systemic MAC disease may be an inevitable consequence of long-term steroid use and underlying diseases. Literature searches also show that cervical lymphadenitis was a predominant symptom in NTMIs (90.5%). The present case did not have cervical lymphadenitis although the previously reported MAC cases did experience it. Therefore, lymphadenitis from NTMIs may be related to the pathogenesis of Sweet's syndrome. Hence, should a patient have systemic infection without lymphadenitis, it will be more difficult to clinically confirm that MAC disease is a predisposing factor for Sweet's syndrome