Enhanced inhibition of lymphocyte activation by Mycobacterium avium complex in human T lymphotrophic virus type I carriers

Matsuyama, Wataru; Hamasaki, Takayuki; Mizoguchi, Akira; Iwami, Fumiyuki; Wakimoto, Joeji; Kawabata, Masaharu; Osame, Mitsuhiro

doi:10.1136/thorax.56.5.394

Cited by 4 publications

(6 citation statements)

References 14 publications

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“…In this study, we evaluated clinical and immunological HTLV‐I infection influence on DPB. There have been several reports describing possible association of HTLV‐I infection and pulmonary disorders [12,16,17,30]. Accordingly, a new clinical entity, namely HTLV‐I associated fibrosing alveolitis (HAFA) [22], has been suggested.…”

Section: Discussionmentioning

confidence: 99%

Influence of human T lymphotrophic virus type I on diffuse pan-bronchiolitis

Yamamoto

Matsuyama

Oonakahara

et al. 2004

Clinical and Experimental Immunology

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SUMMARY 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 bronchusassociated 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 a , 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 a 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-b 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.

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Section: Discussionmentioning

confidence: 99%

Influence of human T lymphotrophic virus type I on diffuse pan-bronchiolitis

Yamamoto

Matsuyama

Oonakahara

et al. 2004

Clinical and Experimental Immunology

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“…In this study, we evaluated clinical and immunological HTLV‐I infection influence on CFA. There have been several reports describing possible association of HTLV‐I infection and pulmonary disorders [13,22,23]. Accordingly, a new clinical entity, namely HTLV‐I associated bronchopneumonopathy (HAB), has been suggested [8,13,23].…”

Section: Discussionmentioning

confidence: 99%

“…describing possible association of HTLV-I infection and pulmonary disorders [13,22,23]. Accordingly, a new clinical entity, namely HTLV-I associated bronchopneumonopathy (HAB), has been suggested [8,13,23].…”

Section: Discussionmentioning

confidence: 99%

“…We also examined the affected pulmonary segments on high resolution computed tomography (HRCT) to evaluate the distribution of the lesion in patients with CFA. The ratio of the affected area to the total lung field was judged subjectively by the visual scoring method [22]. Each slice was evaluated individually, and the right and left lungs were graded separately.…”

Section: Methodsmentioning

confidence: 99%

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Influence of human T lymphotrophic virus type I on cryptogenic fibrosing alveolitis − HTLV-I associated fibrosing alveolitis: proposal of a new clinical entity

Matsuyama

Kawabata

Mizoguchi

et al. 2003

Clinical and Experimental Immunology

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SUMMARYHuman T lymphotrophic virus type-I (HTLV-I), a human retrovirus, infects CD4 + lymphocytes and is thought to modify their function; a possible association with pulmonary diseases has also been suggested. However, little is known about the influence of HTLV-I on cryptogenic fibrosing alveolitis (CFA), a chronic inflammatory interstitial lung disease of unknown aetiology. In order to clarify the influence of HTLV-I infection on CFA, 72 CFA patients with and without HTLV-I infection were examined. HTLV-I positive CFA patients were likely to have larger affected areas and to show traction bronchiectasis with honeycombing change. An imbalance of matrix metalloproteinases and tissue inhibitor of metalloproteinases were also observed in the BALF of HTLV-I positive CFA patients. CD3 + /CD25 + lymphocyte percentage was significantly higher in the BALF of HTLV-I positive patients compared to negative patients. MIP-1 a , IP-10 and sICAM 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 a and IP-10 levels showed a significant positive correlation with percentage of CD3 + /CD25 lymphocytes. HTLV-I positive CFA patients showed a larger lesion than negative patients and exhibited increased levels of certain cytokines that correlated with activated T cells in the BALF. We suggest that HTLV-I infection may contribute to the development of CFA via activation of T cells. We also propose that these features should be taken into consideration in the treatment of CFA in HTLV-I infected individuals.

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“…Glycopeptidolipid from M. avium inhibits the lymphocyte blastogenic response to human T-lymphotrophic virus type 1 (77). Conversely, administration of Z-100, an arabinomannan from M. tuberculosis, reduced splenomegaly and increased survival of mice infected with LP-BM5 murine leukemia virus (100).…”

Section: Cryptic Relationships To Other Diseasesmentioning

confidence: 99%

Health Impacts of Environmental Mycobacteria

2004

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SUMMARY Environmental mycobacteria are emerging pathogens causing opportunistic infections in humans and animals. The health impacts of human-mycobacterial interactions are complex and likely much broader than currently recognized. Environmental mycobacteria preferentially survive chlorination in municipal water, using it as a vector to infect humans. Widespread chlorination of water has likely selected more resistant environmental mycobacteria species and potentially explains the shift from M. scrofulaceum to M. avium as a cause of cervical lymphadenitis in children. Thus, human activities have affected mycobacterial ecology. While the slow growth and hydrophobicity of environmental mycobacteria appear to be disadvantages, the unique cell wall architecture also grants high biocide and antibiotic resistance, while hydrophobicity facilitates nutrient acquisition, biofilm formation, and spread by aerosolization. The remarkable stress tolerance of environmental mycobacteria is the major reason they are human pathogens. Environmental mycobacteria invade protozoans, exhibiting parasitic and symbiotic relationships. The molecular mechanisms of mycobacterial intracellular pathogenesis in animals likely evolved from similar mechanisms facilitating survival in protozoans. In addition to outright infection, environmental mycobacteria may also play a role in chronic bowl diseases, allergies, immunity to other pulmonary infections, and the efficacy of bacillus Calmette-Guerin vaccination.

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Enhanced inhibition of lymphocyte activation by Mycobacterium avium complex in human T lymphotrophic virus type I carriers

Cited by 4 publications

References 14 publications

Influence of human T lymphotrophic virus type I on diffuse pan-bronchiolitis

Influence of human T lymphotrophic virus type I on diffuse pan-bronchiolitis

Influence of human T lymphotrophic virus type I on cryptogenic fibrosing alveolitis − HTLV-I associated fibrosing alveolitis: proposal of a new clinical entity

Health Impacts of Environmental Mycobacteria

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