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Pentoxifylline treatment of mice with chronic pulmonary tuberculosis accelerates the development of destructive pathology
Author(s) -
Turner J.,
Frank A. A.,
Brooks J. V.,
Marietta P. M.,
Orme I. M.
Publication year - 2001
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2001.01161.x
Subject(s) - pentoxifylline , tuberculosis , tumor necrosis factor alpha , pathological , lung , medicine , cytokine , mycobacterium tuberculosis , disease , immunology , pathology , antibiotics , necrosis , inflammation , biology , microbiology and biotechnology
Summary It is well established in animal models that production of the cytokine tumour necrosis factor‐α (TNF‐α) is essential to the proper expression of acquired specific resistance following infection with Mycobacterium tuberculosis. This gives rise to an apparent state of chronic disease which over the next 100–200 days is characterized by slowly worsening pathological changes in the lung. To determine whether continued TNF‐α production was harmful during this phase mice were treated with a TNF‐α inhibitor, pentoxifylline. It was observed that although this therapy did not alter the numbers of bacteria recovered from the lungs of the infected mice, tissue damage within the lung was accelerated. These data thus demonstrate that production of TNF‐α, already known to be important during the early expression of resistance to tuberculosis, remains important and beneficial during the chronic stage of the disease.