Pathological and radiological changes in resected lung specimens in Mycobacterium avium intracellulare complex disease

Fujita, Jiro; Ohtsuki, Yuji; Suemitsu, Ichizo; Shigeto, Eriko; Yamadori, Ichiro; Obayashi, Yuka; Mikami, Hiroshi; Dobashi, Naomi; Matsushima, Toshiharu; Takahara, Jiro

doi:10.1183/09031936.99.13353599

Cited by 114 publications

(86 citation statements)

References 12 publications

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“…Immunohistochemistry showed massive infiltration, mostly by macrophages and T cells, which are the characteristic cellular components of granulomas after mycobacterial infection (26,27). We observed a distinct pattern of distribution of macrophages, T cells, and B cells in which a central region of macrophages is interspersed with T cells and the next layer of granulomatous material contains aggregates of T and B cells (27).…”

Section: Discussionmentioning

confidence: 84%

A Rhesus Macaque Model of Pulmonary Nontuberculous Mycobacterial Disease

Winthrop

Rivera

Engelmann

et al. 2016

Am J Respir Cell Mol Biol

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In this study, we sought to develop a nonhuman primate model of pulmonary Mycobacterium avium complex (MAC) disease. Blood and bronchoalveolar lavage fluid were collected from three female rhesus macaques infected intrabronchially with escalating doses of M. avium subsp. hominissuis. Immunity was determined by measuring cytokine levels, lymphocyte proliferation, and antigen-specific responses. Disease progression was monitored clinically and microbiologically with serial thoracic radiographs, computed tomography scans, and quantitative mycobacterial cultures. The animal subjected to the highest inoculum showed evidence of chronic pulmonary MAC disease. Therefore, rhesus macaques could provide a robust model in which to investigate host-pathogen interactions during MAC infection.

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Section: Discussionmentioning

confidence: 84%

A Rhesus Macaque Model of Pulmonary Nontuberculous Mycobacterial Disease

Winthrop

Rivera

Engelmann

et al. 2016

Am J Respir Cell Mol Biol

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“…Pul- (1,10,13). In a previous report, we demonstrated pathological findings of MAC infection (9). Our present study also examined the appearance and distribution of myofibroblasts.…”

Section: Discussionmentioning

confidence: 94%

Immunohistochemical Distribution of Epithelioid Cell, Myofibroblast, and Transforming Growth Factor‐β1 in the Granuloma Caused by Mycobacterium avium intracellulare Complex Pulmonary Infection

Fujita

Ohtsuki²,

Suemitsu

et al. 2002

Microbiology and Immunology

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The present study was designed to evaluate the distribution of epithelioid cells, myofibroblasts, and TGF‐β1 in the formation of granuloma caused by Mycobacterium avium intracellulare complex (MAC) lung infection. A retrospective study was performed for 9 cases of positive MAC culture in which lung resections were performed between January 1989 and August 1999. Resected lung specimens were evaluated histologically and immunohistochemically for CD68 (stain for monocytes and macrophages, and epithelioid cells) and α‐smooth muscle actin as well as vimentin (stain for myofibroblasts), and TGF‐β1 was performed. When granuloma was initially formed, no myofibroblasts were found, but as caseous necrosis appeared, the thin epithelioid cell layer was detected and the outer myofibroblast layer gradually became thick. In the cavitary wall, the layer of epithelioid cells and multinucleated giant cells surrounded necrosis, and was associated with the outer layer of myofibroblasts. In addition, the anti‐TGF‐β1 antibody stained the cytoplasm of epithelioid cells and multinucleated giant cells, preceding the advent of myofibroblasts. In summary, our present study evaluated distributions of epithelioid cells, myofibroblasts, and TGF‐β along with the morphogenesis of granuloma, and clearly demonstrated the immunohistochemical difference between granuloma with caseous necrosis and granulomas without caseous necrosis.

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“…Moreover, all patients in the MAC-culture positive group had findings of small nodules on CCT. Some careful investigation of CCT and histological findings revealed that small nodular lesions were caused by granulomas formed as a specific response to mycobacterial infection [13,14]. Furthermore, the individuals with MAC colonisation, who had a single and small amount of culturepositive MAC but did not have clinical symptoms or abnormal lesions on CCT findings, were excluded from the present study at enrolment.…”

Section: Discussionmentioning

confidence: 99%