title: Influence of human T lymphotrophic virus type I on diffuse pan-bronchiolitis.
abstract: Human T lymphotrophic virus type-I (HTLV-I), a human retrovirus, infects CD4(+) lymphocytes and is thought to modify their function and a possible association with pulmonary diseases has also been suggested. However, little is known about the influence of HTLV-I on diffuse pan-bronchiolitis (DPB), a chronic inflammatory lung disease with infiltration of lymphocytes and hyperplasia of the bronchus-associated lymphoid tissue. In this study, 35 DPB patients with and without HTLV-I infection were examined. HTLV-I positive DPB patients were likely to have a larger affected area with lower FEV(1). The CD3(+)/CD25(+) lymphocyte percentage was significantly higher in the BALF of HTLV-I positive patients than in negative patients. MIP-1 alpha, IP-10 and levels in BALF were also significantly higher in HTLV-I positive patients than in negative patients. The levels of MCP-1 and IL-8 were not significantly different. In HTLV-I positive patients, the MIP-1 alpha and IP-10 levels showed a significant positive correlation with the percentage of CD3(+)/CD25 lymphocytes. BALF cells of all HTLV-I positive DPB patients showed expression of p40(tax) mRNA. We suggest that HTLV-I infection may modify DPB pathogenesis via activation of T cells. We also found that the frequency of ATL development in HTLV-I positive DPB patients was significantly higher than in all HTLV-I positive patients (OR = 8.22, 95% CI = 2.61-25.9, P < 0.01). The levels of TGF-beta in patients who developed ATL were significantly lower than in patients who did not develop ATL. Sensitivity and specificity were 80% and 85.7%, respectively (cut-off = 20 pg/ml). We also propose that these features should be taken into consideration in the treatment of DPB in HTLV-I infected individuals.
authors.affiliation: Third Department of Internal Medicine, Kagoshima University Faculty of Medicine, Sakuragaoka, Kagoshima, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Yamamoto
authors.forename: W
authors.initials: W
authors.lastname: Matsuyama
authors.forename: K
authors.initials: K
authors.lastname: Oonakahara
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: I
authors.initials: I
authors.lastname: Higashimoto
authors.forename: M
authors.initials: M
authors.lastname: Kawabata
authors.forename: M
authors.initials: M
authors.lastname: Osame
authors.forename: K
authors.initials: K
authors.lastname: Arimura
mesh_terms: D000328:Adult; D000368:Aged; D001988:Bronchiolitis / Q000276:immunology / Q000821:virology*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D018932:Chemokine CCL2 / Q000032:analysis; D054407:Chemokine CCL4; D054357:Chemokine CXCL10 / Q000032:analysis; D016009:Chi-Square Distribution; D002908:Chronic Disease; D005260:Female; D015490:HTLV-I Infections / Q000175:diagnosis / Q000276:immunology*; D015368:Human T-lymphotropic virus 1 / Q000235:genetics / Q000276:immunology*; D006801:Humans; D016209:Interleukin-8 / Q000032:analysis; D008213:Lymphocyte Activation; D019402:Macrophage Inflammatory Proteins / Q000032:analysis; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018709:Statistics, Nonparametric; D016212:Transforming Growth Factor beta / Q000032:analysis
chemical_list: D018932:Chemokine CCL2; D054407:Chemokine CCL4; D054357:Chemokine CXCL10; D016209:Interleukin-8; D019402:Macrophage Inflammatory Proteins; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta